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J Biol Chem, Vol. 274, Issue 16, 10689-10692, April 16, 1999
From the Division of TLR4 is a member of the recently identified
Toll-like receptor family of proteins and has been putatively
identified as Lps, the gene necessary for potent responses
to lipopolysaccharide in mammals. In order to determine whether TLR4 is
involved in lipopolysaccharide-induced activation of the nuclear
factor- Lipopolysaccharide
(LPS),1 a component of the
outer membrane of Gram-negative bacteria, is a potent activator of a
variety of mammalian cell types (1, 2). Activation by LPS constitutes the first step in a cascade of events believed to lead to the manifestation of Gram-negative sepsis, a condition that results in
approximately 20,000 annual deaths in the United States (3). Activation
of LPS-responsive cells, such as monocytes and macrophages, occurs
rapidly after LPS interacts with circulating LPS-binding protein and
CD14, a glycosylphosphatidylinositol-linked cell surface glycoprotein
necessary for sensitive responses to LPS (1, 2). LPS has been shown to
initiate multiple intracellular signaling events (4), including the
activation of NF- Toll is a transmembrane receptor in Drosophila that is
involved in dorsal-ventral patterning in embryos and in the induction of an anti-fungal response (5, 6). Activation of the Toll receptor by
its ligand Spätzle results in the interaction and stimulation of
several signaling molecules that are homologous to proteins involved in
NF- Several lines of evidence suggest that one or more members of the TLR
family is the cell-surface receptor for LPS, the prototypical activator
of NF- Materials--
Human TLR4 cDNA was provided by Dr. Charles
A. Janeway, Jr. (Yale University). The ELAM-1-luciferase reporter
plasmid, pELAM-luc, was generated by cloning a fragment ( Cell Culture and Transfections--
HEK 293 cells (ATCC,
Rockville, MD) were cultured in Dulbecco's modified Eagle's medium
(ATCC, Rockville, MD) supplemented with 10% fetal bovine serum (Life
Technologies, Inc.). Cells were plated in 12-well tissue culture plates
(3 × 105 cells/well) and maintained in the above
medium for 24 h. Cells were transfected using the CalPhos
Maximizer protocol (CLONTECH) with 250 ng of TLR4
cDNA or vector DNA (pcDNA3, Invitrogen, Inc.) and 100 ng of
pELAM-luc. All cells were also transfected with a Purification of Soluble CD14 (sCD14) from Transfected CHO
Cells--
CHO cells expressing CD14 were cultured in suspension under
serum-free conditions (EX-CELL 301 medium supplemented with
L-glutamine). The culture supernatant was collected,
filtered through a 0.22-µm nitrocellulose filter, and concentrated
5-fold in a protein concentrator (Amicon Diaflo, PM30) with a 30-kDa
cut-off filter under pressure at 4 °C. This concentrate was then
loaded onto an anti-CD14 affinity column. The column was washed twice
with wash buffer before eluting with 0.1 M glycine, pH 2.8. The fractions were immediately neutralized with 1 M
Tris-HCl, pH 9.5, and an aliquot of each fraction was mixed with 2 × SDS loading buffer (Novex, San Diego, CA) and heated for 5 min at
95 °C. Expression and purification of sCD14 was verified by
SDS-polyacrylamide gel electrophoresis followed by silver stain and
immunoblotting with MEM-18 anti-CD14 antibody. Immunoreactive proteins
were visualized using enhanced chemiluminescence detection reagents
(Amersham Pharmacia Biotech).
Statistical Analysis--
Quantitative data are presented as
mean ± S.E. and analyzed using a statistical model based on a
one-way classification analysis of variance. Tests of significance for
all possible comparisons were determined by Student Newman-Keuls test
or unpaired t test (GraphPad Prism, version 2.0a).
To determine whether TLR4 mediates LPS-induced activation of
NF- In order to further examine whether TLR4 is involved in LPS
signaling at the cell surface, HEK 293 cells were transfected with TLR4
or empty vector and the NF- Although it has been proposed previously that LPS interacts
with a transmembrane receptor or recognition molecules on the surface
of plasma membranes of responsive cell types (2), strong evidence for
this hypothesis has only recently become available. First, Medzhitov
et al. (11) identified a human homolog of
Drosophila Toll, later designated TLR4 (9), with signaling
properties similar to those observed for the IL-1 receptor. These
properties include the activation of the transcription factor NF- In the experiments presented here, transfection of HEK 293 cells using
a construct containing the full-length cDNA for TLR4 was sufficient
to elicit a significant response with LPS in the presence of soluble
CD14. The reporter construct utilized in these experiments contained a
region of the promoter for the E-selectin gene, which is absolutely
dependent upon NF- Kirschning et al. (13) failed to observe LPS-inducible NF-kB
activation in HEK 293 cells transfected with human TLR4. The reasons
for this are unclear, but might reflect the differences inherent in HEK
293 cell lines. For example, we have found that one stock of HEK 293 cells responded to LPS, as evidenced by inducible NF- E5531 is a potent synthetic lipid A analog that acts as an
antagonist of LPS-induced activation (16). The compound inhibits the
effects of LPS in monocytes, macrophages, animal models of sepsis and
infection (16), as well as the effects of low amounts of LPS
administered to humans (22). Based on LPS binding studies, it is
believed that E5531 antagonizes LPS activity at its cell-surface receptor, leading to inhibition of transmembrane signal transduction (16). Consistent with this hypothesis, E5531 inhibits the stimulation of TLR4 transfected cells by LPS plus CD14 in a
dose-dependent manner with an IC50 of ~30
nM, comparable with its effects in other cell based assays
(23). Since E5531 did not affect activation of the NF- In light of the recent identification of the lesion in C3H/HeJ and
C57BL/10ScCr LPS-resistant mice as a mutation in the tlr4 gene (14), the results presented here are particularly significant. These data demonstrate that TLR4 behaves as a functional LPS receptor when transfected into cells that are otherwise LPS-insensitive. This
cell-based result is consistent with the observation made by Poltorak
et al. (14) in C3H/HeJ mice. These data do not exclude a
role for TLR2 in LPS signal transduction under certain conditions or in
specific cell types, but support the hypothesis that TLR4 is essential
in LPS signaling in vitro and in vivo. Finally, the characterization of TLR4 as a receptor for the LPS antagonist is an
important development for understanding the mechanistic steps and will
enable further improvements in the discovery of anti-endotoxin agents.
We thank Hua Yang and Melissa Ferrin for
excellent technical assistance and Samantha Roberts for assisting in
the preparation of the manuscript.
*
The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
§
To whom correspondence should be addressed: Eisai Research
Institute, 100 Research Dr., Wilmington, MA 01887. Tel.: 978-661-7276; Fax: 978-657-7715.
**
Supported by National Institutes of Health Grant RO1 GM54060.
2
E. Lien and D. T. Golenbock, unpublished observations.
3
J. C. Chow and F. Gusovsky, unpublished observations.
The abbreviations used are:
LPS, lipopolysaccharide;
TLR, toll-like receptor;
IL, interleukin;
NF-
COMMUNICATION
Toll-like Receptor-4 Mediates Lipopolysaccharide-induced Signal
Transduction*
§,,
, and
Inflammatory Diseases and
Synthetic Chemistry, Eisai Research Institute, Andover,
Massachusetts 01810 and the ¶ Boston University School of
Medicine, Boston Medical Center, The Maxwell Finland Laboratory for
Infectious Diseases, Boston, Massachusetts 02118
ABSTRACT
TOP
ABSTRACT
INTRODUCTION
EXPERIMENTAL PROCEDURES
RESULTS
DISCUSSION
REFERENCES
B (NF-B) pathway, HEK 293 cells were transiently
transfected with human TLR4 cDNA and an
NF-B-dependent luciferase reporter plasmid followed by
stimulation with lipopolysaccharide/CD14 complexes. The results
demonstrate that lipopolysaccharide stimulates NF-B-mediated gene
expression in cells transfected with the TLR4 gene in a dose- and
time-dependent fashion. Furthermore, E5531, a
lipopolysaccharide antagonist, blocked TLR4-mediated transgene
activation in a dose-dependent manner (IC50
~30 nM). These data demonstrate that TLR4 is involved in
lipopolysaccharide signaling and serves as a cell-surface co-receptor for CD14, leading to lipopolysaccharide-mediated NF-B activation and
subsequent cellular events.
INTRODUCTION
TOP
ABSTRACT
INTRODUCTION
EXPERIMENTAL PROCEDURES
RESULTS
DISCUSSION
REFERENCES
B, which ultimately leads to the synthesis and
release of a number of proinflammatory mediators, including
interleukin-1 (IL-1), interleukin-6 (IL-6), interleukin-8 (IL-8), and
tumor necrosis factor-
(1). However, since CD14 is not a
transmembrane protein, it lacks the ability to transduce cytoplasmic
signals (2), and before the recent discovery of Toll-like receptors
(TLRs), the identity of a transmembrane protein that could relay
LPS-induced signals across the cell-surface membrane remained elusive.
B activation by the IL-1 receptor in mammalian cells (7, 8). The
cloning of a family of human receptors structurally related to
Drosophila Toll revealed five proteins that have
extracellular domains that contain multiple leucine-rich repeats and
cytoplasmic domains with sequence homology to the intracellular portion
of the IL-1 receptor (9). Furthermore, constitutively active mutants of
TLR2, TLR4, and TLR5 can induce the activation of NF-B (10, 11), and
the active form of TLR4 increases the expression of NF-B-regulated
genes for the inflammatory cytokines IL-1, IL-6, and IL-8 (11).
B and other proinflammatory responses. TLR2 and TLR4 are
highly expressed in cells that respond to LPS, such as peripheral blood
leukocytes, macrophages, and monocytes (11, 12). Also, heterologously
expressed TLR2 mediates LPS-induced NF-B activation and IL-8
mRNA expression in HEK 293 cells (12, 13). However, TLR2 is not the
only potential LPS signal transducer. The C3H/HeJ mouse is a
spontaneous LPS resistant mutant. Poltorak et al. (14)
mapped the Lps gene, which has been shown previously to be
necessary for LPS responses in LPS nonresponder C3H/HeJ mice, to TLR4.
TLR4 from the C3H/HeJ mouse has a single point mutation at amino acid
712 (Pro to His) that changes the function of the receptor dramatically
(14); furthermore, the LPS-resistant C57/10ScCr mouse appears to be
null for the TLR4 locus. These observations strongly support the
concept that TLR4, and not TLR2, is the dominant LPS receptor in
mammals and the hypothesis that TLR4 is a cell-surface component of the
LPS signaling pathway. Thus, the present study was conducted to
investigate whether TLR4 is involved in mediating the actions of
LPS.
EXPERIMENTAL PROCEDURES
TOP
ABSTRACT
INTRODUCTION
EXPERIMENTAL PROCEDURES
RESULTS
DISCUSSION
REFERENCES
241 to 54
base pairs) of the human E-selectin promoter into the pGL3 reporter
plasmid (Promega, Inc.). All plasmid constructs were confirmed by
automated sequencing analysis. Lipopolysaccharide was purchased from
Sigma. The human embryonic kidney cell line HEK 293 (CRL-1573) was from
American Type Culture Collection (Rockville, MD). The Chinese hamster
ovary (CHO) cell line expressing CD14 was engineered and maintained as
described (15). The LPS antagonist (E5531) was synthesized as described
previously (16). Plasmid DNA was isolated with Qiagen
Endo-freeTM Maxi-prep columns (Chatsworth, CA). MEM-18
anti-CD14 antibody was purchased from Accurate Chemicals & Scientific
Corp. (Westbury, NY). Phorbol 12-myristate 13-acetate (PMA) and IL-1
were purchased from Calbiochem and Endogen (Woburn, MA), respectively.
Luciferase activity was assayed using a commercial luciferase assay kit
(Stratagene, La Jolla, CA).
-galactosidase
control plasmid for normalizing transfection efficiencies. After
transfection, cells were maintained in Dulbecco's modified Eagle's
medium supplemented with 1% fetal bovine serum overnight (18 h). The
following day, cells were either left untreated or incubated with the
indicated amount of ligand and/or compound E5531. After the indicated
treatment period, cells were harvested in lysis buffer and assayed for
luciferase activity per the manufacturer's protocol. The amount of
luciferase activity in each sample was quantified by a Wallac 1450 MicroBetaTrilux counter.
RESULTS
TOP
ABSTRACT
INTRODUCTION
EXPERIMENTAL PROCEDURES
RESULTS
DISCUSSION
REFERENCES
B, HEK 293 cells were transiently transfected with TLR4 cDNA or empty vector control (pcDNA3) and an
NF-B-dependent ELAM-1-luciferase reporter plasmid
(pELAM-luc). Twenty-four hours post-transfection, cells were left
untreated or incubated with either LPS (1 µg/ml or indicated
concentrations), sCD14 (10 nM) or both for an additional 6 h. Cells were then lysed and assayed for luciferase activity. Expression of TLR4 in HEK 293 cells induced activation of the NF-B
reporter gene 2.5-fold above controls (cells transfected with empty
vector and the pELAM-luc reporter gene) in the absence of stimuli (Fig.
1). Soluble CD14 alone did not have a
significant effect on NF-B activity in the presence or absence of
TLR4. LPS treatment alone (1 µg/ml) was sufficient to elicit an
increase (1.6-fold) in luciferase activity after incubation with TLR4
transfected cells, and this increase was not observed in vector
controls (Fig. 1). However, when cells were stimulated with LPS in the
presence of sCD14, there was a marked increase in TLR4-mediated
activation of NF-B that was not observed in cells treated with LPS
or CD14 alone (Fig. 1). Stimulation of TLR4-mediated NF-B activation by LPS plus CD14 was 5-fold higher than levels produced by TLR4 expression in unstimulated controls or with CD14 alone. LPS-induced reporter activity occurred in a dose-dependent fashion,
increasing 2-fold above controls at 10 ng/ml LPS and reaching maximal
levels at 1 µg/ml LPS (Fig.
2A). Furthermore, stimulation
of NF-B activity by LPS was time-dependent and reached
maximal levels at 18-24 h after LPS addition (Fig. 2B).
View larger version (27K):
[in a new window]
Fig. 1.
LPS increases TLR4-mediated
NF- B activation via a CD-14 dependent
mechanism. HEK 293 cells were plated at a density of 3 × 105 cells/well in 12-well plates and maintained in
Dulbecco's modified Eagle's medium containing 10% fetal bovine serum
for 24 h. Cells were transiently transfected with TLR4 cDNA or
vector DNA and the ELAM-1-luciferase reporter plasmid as described
under "Experimental Procedures." Cells were either left untreated
or stimulated with CD14 (10 nM), LPS (1 µg/ml), or the
combination of CD14 plus LPS for 6 h. After cell lysis, luciferase
activity was as described under "Experimental Procedures." These
data represent the mean ± S.E. from seven independent
experiments. Means with different superscripts are significantly
different from one another, p < 0.05.
View larger version (34K):
[in a new window]
Fig. 2.
LPS increases TLR4-mediated
NF- B activation in a dose- and
time-dependent manner. HEK 293 cells were transiently
transfected with TLR4 cDNA or vector DNA and pELAM-luc. Cells were
either left untreated or exposed to sCD14 (10 nM) and the
indicated concentration of LPS for 6 h (A) or 1 µg of
LPS/ml for the indicated amount of time (B) as described in
the legend to Fig. 1. After cell lysis, the amount of luciferase
activity in each sample was quantified. These data represent the
mean ± S.E. from three independent experiments. Means with
different superscripts are significantly different from one another,
p < 0.05.
B reporter plasmid. Subsequently, cells
were co-incubated with LPS (plus CD14) and increasing concentrations of
E5531, an LPS antagonist that has been shown to inhibit LPS-induced cytokine synthesis in macrophages and in vivo (16).
Measurements of cellular luciferase activity after these treatments
indicated that E5531 inhibits TLR4-mediated NF-B activation in a
dose-dependent manner (Fig.
3A). At 10 nM,
E5531 significantly reduced NF-B-dependent gene
activation by LPS, and at higher drug concentrations (1 and 10 µM), NF-B reporter activities in TLR4 expressing cells
were similar to unstimulated controls. In contrast to LPS-stimulated TLR4-expressing cells, 1 µM E5531 did not affect PMA- or
IL-1-induced NF-B gene activation in these cells (Fig.
3B), indicating that the drug selectively inhibited
TLR4-mediated NF-B activation in response to LPS.
View larger version (43K):
[in a new window]
Fig. 3.
E5531, an LPS antagonist, inhibits
TLR4-mediated NF- B activation by LPS. HEK
293 cells were transiently transfected as described in the legend to
Fig. 1. The next day, cells were stimulated with 10 nM CD14
plus 1 µg/ml LPS (A and B) or 400 nM PMA or 20 ng/ml IL-1 (B) in the absence or
presence of the indicated concentration of E5531 for 6 h. Cells
were lysed, and the amount of luciferase activity in each sample was
quantified. These data represent the mean ± S.E. from three
independent experiments. Means with different superscripts are
significantly different from one another, p < 0.05.
DISCUSSION
TOP
ABSTRACT
INTRODUCTION
EXPERIMENTAL PROCEDURES
RESULTS
DISCUSSION
REFERENCES
B
and induction of mRNA for several proinflammatory cytokines (11),
both of which were also observed when responsive cells are activated
with LPS (1). Second, reports by Yang et al. (12) and
Kirschning et al. (13) demonstrate the ability of TLR2 to
signal in the presence of LPS and CD14, strongly suggesting a role for
this protein in LPS action. Kirschning et al. (13) also
reported that TLR1 and TLR4 failed to increase NF-B reporter
activity in the presence of LPS, further supporting the notion that
TLR2 is a specific component of the cellular receptor for LPS. However, the recent report by Poltorak et al. (14), which identifies the genetic lesion in the LPS-resistant C3H/HeJ mice as a mutation in
the tlr4 gene (14), prompted us to examine the role of TLR4 in LPS signaling.
B activation for activity (17). Thus, LPS-induced
stimulation of our ELAM-1 reporter gene in TLR4 expressing cells is
predominantly mediated via the NF-B signaling pathway. Previous
studies have shown that constitutively active TLR4 constructs can
activate proximal components (MyD88, IL-1 receptor-associated kinase,
tumor necrosis factor receptor-associated factor-6, and NF-B
inducing kinase) of the IL-1 signaling pathway that lead to NF-B
activation (18, 19). Although we demonstrate a link between LPS
signaling and TLR4 expression in this study, it remains to be
determined whether the effects of LPS utilize the same subsequent
signaling proteins as the IL-1 receptor (4).
B
translocation, in the absence of transfection. In order to perform
these studies, we were forced to locate an alternative stock of HEK 293 cells, as this particular lot, acquired directly from the distributor
(ATCC, Rockville, MD), expressed high levels of TLR2
mRNA.2 Like the IL-1
receptor, TLRs might require the formation of heterodimeric signaling
complexes with highly homologous proteins (such as another TLR) upon
ligand binding (20). A testable hypothesis that might explain the
differences in outcome between seemingly identical experiments is that
the background expression of TLRs determines which heterodimers can be
formed after gene transfer and that all strains of HEK 293 cells are
not equivalent in this respect. Other experimental differences might
also affect results obtained in these types of experiments, such as the
nature of the TLR4 construct, the amount of DNA utilized in
transfections, or other conditions that may influence TLR4 expression.
For example, we have shown that the amount of TLR4 expression vector
transfected into cells influences the regulation of pELAM-luc activity
by LPS.3 This was presumably
due to elevated basal-specific activity of pELAM-luc that was increased
when higher amounts of TLR4 were expressed. A similar effect has been
reported in HEK 293 cells expressing IB kinase- (21). In support
of Yang et al. (12) and Kirschning et al. (13),
we have shown that our HEK 293 cells transfected with a construct
containing TLR2 are also responsive to LPS plus
CD14.3
B reporter
gene induced by IL-1 or the actions of interferon-
in murine
macrophages (16), this indicates that the inhibitory activity of E5531
is closely linked to and specific to cell-surface components utilized
by LPS. In these experiments, TLR4 is the only protein whose expression
can account for the LPS responsiveness observed in transfected cells.
Therefore, based on these results, it is very likely that TLR4 is a
receptor for LPS and that E5531 acts as an antagonist of this interaction.
ACKNOWLEDGEMENTS
FOOTNOTES
ABBREVIATIONS
B, nuclear factor-B;
sCD14, soluble CD14;
CHO, Chinese hamster ovary;
PMA, phorbol 12-myristate 13-acetate;
pELAM-luc, ELAM-1-luciferase
reporter plasmid.
REFERENCES
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ABSTRACT
INTRODUCTION
EXPERIMENTAL PROCEDURES
RESULTS
DISCUSSION
REFERENCES
Copyright © 1999 by The American Society for Biochemistry and Molecular Biology, Inc.
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Y. Wang, X. Zhu, G. Wu, L. Shen, and B. Chen Effect of lipid-bound apoA-I cysteine mutants on lipopolysaccharide-induced endotoxemia in mice J. Lipid Res., August 1, 2008; 49(8): 1640 - 1645. [Abstract] [Full Text] [PDF]
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 C. Fontaine, E. Rigamonti, B. Pourcet, H. Duez, C. Duhem, J.-C. Fruchart, G. Chinetti-Gbaguidi, and B. Staels The Nuclear Receptor Rev-erb{alpha} Is a Liver X Receptor (LXR) Target Gene Driving a Negative Feedback Loop on Select LXR-Induced Pathways in Human Macrophages Mol. Endocrinol., August 1, 2008; 22(8): 1797 - 1811. [Abstract] [Full Text] [PDF]
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S. Machata, S. Tchatalbachev, W. Mohamed, L. Jansch, T. Hain, and T. Chakraborty Lipoproteins of Listeria monocytogenes Are Critical for Virulence and TLR2-Mediated Immune Activation J. Immunol., August 1, 2008; 181(3): 2028 - 2035. [Abstract] [Full Text] [PDF]
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G. Fedele, M. Nasso, F. Spensieri, R. Palazzo, L. Frasca, M. Watanabe, and C. M. Ausiello Lipopolysaccharides from Bordetella pertussis and Bordetella parapertussis Differently Modulate Human Dendritic Cell Functions Resulting in Divergent Prevalence of Th17-Polarized Responses J. Immunol., July 1, 2008; 181(1): 208 - 216. [Abstract] [Full Text] [PDF]
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 H. S. Kim, P. A. Loughran, J. Rao, T. R. Billiar, and B. S. Zuckerbraun Carbon monoxide activates NF-{kappa}B via ROS generation and Akt pathways to protect against cell death of hepatocytes Am J Physiol Gastrointest Liver Physiol, July 1, 2008; 295(1): G146 - G152. [Abstract] [Full Text] [PDF]
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M. M. Hipp, N. Hilf, S. Walter, D. Werth, K. M. Brauer, M. P. Radsak, T. Weinschenk, H. Singh-Jasuja, and P. Brossart Sorafenib, but not sunitinib, affects function of dendritic cells and induction of primary immune responses Blood, June 15, 2008; 111(12): 5610 - 5620. [Abstract] [Full Text] [PDF]
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 C.-S. Lin, J. G. Wann, C.-W. Hsiao, D. W. Tai, J.-S. Chen, Y.-H. Hsu, H.-C. Huang, and C.-F. Chao Intracellular acidification enhances neutrophil phagocytosis in chronic haemodialysis patients: possible role of CD11b/CD18 Nephrol. Dial. Transplant., May 1, 2008; 23(5): 1642 - 1649. [Abstract] [Full Text] [PDF]
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V. Jain, A. Halle, K. A. Halmen, E. Lien, M. Charrel-Dennis, S. Ram, D. T. Golenbock, and A. Visintin Phagocytosis and intracellular killing of MD-2 opsonized Gram-negative bacteria depend on TLR4 signaling Blood, May 1, 2008; 111(9): 4637 - 4645. [Abstract] [Full Text] [PDF]
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 S. W. Waldo, Y. Li, C. Buono, B. Zhao, E. M. Billings, J. Chang, and H. S. Kruth Heterogeneity of Human Macrophages in Culture and in Atherosclerotic Plaques Am. J. Pathol., April 1, 2008; 172(4): 1112 - 1126. [Abstract] [Full Text] [PDF]
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 C.-H. Lee, C.-L. Wu, and A.-L. Shiau Toll-like Receptor 4 Mediates an Antitumor Host Response Induced by Salmonella choleraesuis Clin. Cancer Res., March 15, 2008; 14(6): 1905 - 1912. [Abstract] [Full Text] [PDF]
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K. Ueno, T. Koga, K. Kato, D. T. Golenbock, S. J. Gendler, H. Kai, and K. C. Kim MUC1 Mucin Is a Negative Regulator of Toll-Like Receptor Signaling Am. J. Respir. Cell Mol. Biol., March 1, 2008; 38(3): 263 - 268. [Abstract] [Full Text] [PDF]
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P. Rallabhandi, A. Awomoyi, K. E. Thomas, A. Phalipon, Y. Fujimoto, K. Fukase, S. Kusumoto, N. Qureshi, M. B. Sztein, and S. N. Vogel Differential Activation of Human TLR4 by Escherichia coli and Shigella flexneri 2a Lipopolysaccharide: Combined Effects of Lipid A Acylation State and TLR4 Polymorphisms on Signaling J. Immunol., January 15, 2008; 180(2): 1139 - 1147. [Abstract] [Full Text] [PDF]
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I. Dunn-Siegrist, O. Leger, B. Daubeuf, Y. Poitevin, F. Depis, S. Herren, M. Kosco-Vilbois, Y. Dean, J. Pugin, and G. Elson Pivotal Involvement of Fc{gamma} Receptor IIA in the Neutralization of Lipopolysaccharide Signaling via a Potent Novel Anti-TLR4 Monoclonal Antibody 15C1 J. Biol. Chem., November 30, 2007; 282(48): 34817 - 34827. [Abstract] [Full Text] [PDF]
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G. L. Morefield, L. D. Hawkins, S. T. Ishizaka, T. L. Kissner, and R. G. Ulrich Synthetic Toll-Like Receptor 4 Agonist Enhances Vaccine Efficacy in an Experimental Model of Toxic Shock Syndrome Clin. Vaccine Immunol., November 1, 2007; 14(11): 1499 - 1504. [Abstract] [Full Text] [PDF]
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E. Ostrowska, E. Sokolova, and G. Reiser PAR-2 activation and LPS synergistically enhance inflammatory signaling in airway epithelial cells by raising PAR expression level and interleukin-8 release Am J Physiol Lung Cell Mol Physiol, November 1, 2007; 293(5): L1208 - L1218. [Abstract] [Full Text] [PDF]
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 X. Huang, W. Du, R. P. Barrett, and L. D. Hazlett ST2 Is Essential for Th2 Responsiveness and Resistance to Pseudomonas aeruginosa Keratitis Invest. Ophthalmol. Vis. Sci., October 1, 2007; 48(10): 4626 - 4633. [Abstract] [Full Text] [PDF]
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S. Young Goo, Y. S. Han, W. H. Kim, K.-H. Lee, and S.-J. Park Vibrio vulnificus IlpA-induced Cytokine Production Is Mediated by Toll-like Receptor 2 J. Biol. Chem., September 21, 2007; 282(38): 27647 - 27658. [Abstract] [Full Text] [PDF]
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 H. MacLeod and L. M. Wetzler T Cell Activation by TLRs: A Role for TLRs in the Adaptive Immune Response Sci. Signal., September 4, 2007; 2007(402): pe48 - pe48. [Abstract] [Full Text] [PDF]
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 K. L. Lohmann, M. L. Vandenplas, M. H. Barton, C. E. Bryant, and J. N. Moore The equine TLR4/MD-2 complex mediates recognition of lipopolysaccharide from Rhodobacter sphaeroides as an agonist Innate Immunity, August 1, 2007; 13(4): 235 - 242. [Abstract] [PDF]
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H. L. Wang, I. O. Akinci, C. M. Baker, D. Urich, A. Bellmeyer, M. Jain, N. S. Chandel, G. M. Mutlu, and G. R. S. Budinger The Intrinsic Apoptotic Pathway Is Required for Lipopolysaccharide-Induced Lung Endothelial Cell Death J. Immunol., August 1, 2007; 179(3): 1834 - 1841. [Abstract] [Full Text] [PDF]
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A. V. Gafencu, M. R. Robciuc, E. Fuior, V. I. Zannis, D. Kardassis, and M. Simionescu Inflammatory Signaling Pathways Regulating ApoE Gene Expression in Macrophages J. Biol. Chem., July 27, 2007; 282(30): 21776 - 21785. [Abstract] [Full Text] [PDF]
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A. Zanin-Zhorov, G. Tal-Lapidot, L. Cahalon, M. Cohen-Sfady, M. Pevsner-Fischer, O. Lider, and I. R. Cohen Cutting Edge: T Cells Respond to Lipopolysaccharide Innately via TLR4 Signaling J. Immunol., July 1, 2007; 179(1): 41 - 44. [Abstract] [Full Text] [PDF]
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M. B. B. McCall, M. G. Netea, C. C. Hermsen, T. Jansen, L. Jacobs, D. Golenbock, A. J. A. M. van der Ven, and R. W. Sauerwein Plasmodium falciparum Infection Causes Proinflammatory Priming of Human TLR Responses J. Immunol., July 1, 2007; 179(1): 162 - 171. [Abstract] [Full Text] [PDF]
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O.-L. Brekke, D. Christiansen, H. Fure, M. Fung, and T. E. Mollnes The role of complement C3 opsonization, C5a receptor, and CD14 in E. coli-induced up-regulation of granulocyte and monocyte CD11b/CD18 (CR3), phagocytosis, and oxidative burst in human whole blood J. Leukoc. Biol., June 1, 2007; 81(6): 1404 - 1413. [Abstract] [Full Text] [PDF]
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 M. G. Flynn, B. K. McFarlin, and M. M. Markofski State of the Art Reviews: The Anti-Inflammatory Actions of Exercise Training American Journal of Lifestyle Medicine, May 1, 2007; 1(3): 220 - 235. [Abstract] [PDF]
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M. W. Laschke, M. D. Menger, Y. Wang, G. Lindell, B. Jeppsson, and H. Thorlacius Sepsis-associated cholestasis is critically dependent on P-selectin-dependent leukocyte recruitment in mice Am J Physiol Gastrointest Liver Physiol, May 1, 2007; 292(5): G1396 - G1402. [Abstract] [Full Text] [PDF]
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 D. Droemann, J. Rupp, T. Goldmann, U. Uhlig, D. Branscheid, E. Vollmer, P. Kujath, P. Zabel, and K. Dalhoff Disparate Innate Immune Responses to Persistent and Acute Chlamydia pneumoniae Infection in Chronic Obstructive Pulmonary Disease Am. J. Respir. Crit. Care Med., April 15, 2007; 175(8): 791 - 797. [Abstract] [Full Text] [PDF]
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N. Foster, S. R. Lea, P. M. Preshaw, and J. J. Taylor Pivotal Advance: Vasoactive intestinal peptide inhibits up-regulation of human monocyte TLR2 and TLR4 by LPS and differentiation of monocytes to macrophages J. Leukoc. Biol., April 1, 2007; 81(4): 893 - 903. [Abstract] [Full Text] [PDF]
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 R. Labrum, S. Bevan, M. Sitzer, M. Lorenz, and H. S. Markus Toll Receptor Polymorphisms and Carotid Artery Intima-Media Thickness Stroke, April 1, 2007; 38(4): 1179 - 1184. [Abstract] [Full Text] [PDF]
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S. M. Janciauskiene, I. M. Nita, and T. Stevens {alpha}1-Antitrypsin, Old Dog, New Tricks: {alpha}1-ANTITRYPSIN EXERTS IN VITRO ANTI-INFLAMMATORY ACTIVITY IN HUMAN MONOCYTES BY ELEVATING cAMP J. Biol. Chem., March 23, 2007; 282(12): 8573 - 8582. [Abstract] [Full Text] [PDF]
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S. M. Sacre, A. M. C. Lundberg, E. Andreakos, C. Taylor, M. Feldmann, and B. M. Foxwell Selective Use of TRAM in Lipopolysaccharide (LPS) and Lipoteichoic Acid (LTA) Induced NF-{kappa}B Activation and Cytokine Production in Primary Human Cells: TRAM Is an Adaptor for LPS and LTA Signaling J. Immunol., February 15, 2007; 178(4): 2148 - 2154. [Abstract] [Full Text] [PDF]
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M. A. Wolfert, A. Roychowdhury, and G.-J. Boons Modification of the Structure of Peptidoglycan Is a Strategy To Avoid Detection by Nucleotide-Binding Oligomerization Domain Protein 1 Infect. Immun., February 1, 2007; 75(2): 706 - 713. [Abstract] [Full Text] [PDF]
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C. Nishitani, H. Mitsuzawa, H. Sano, T. Shimizu, N. Matsushima, and Y. Kuroki Toll-like Receptor 4 Region Glu24-Lys47 Is a Site for MD-2 Binding: IMPORTANCE OF CYS29 AND CYS40 J. Biol. Chem., December 15, 2006; 281(50): 38322 - 38329. [Abstract] [Full Text] [PDF]
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D. D. Bolz, R. S. Sundsbak, Y. Ma, S. Akira, J. H. Weis, T. G. Schwan, and J. J. Weis Dual Role of MyD88 in Rapid Clearance of Relapsing Fever Borrelia spp. Infect. Immun., December 1, 2006; 74(12): 6750 - 6760. [Abstract] [Full Text] [PDF]
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A. Visintin, K. A. Halmen, N. Khan, B. G. Monks, D. T. Golenbock, and E. Lien MD-2 expression is not required for cell surface targeting of Toll-like receptor 4 (TLR4) J. Leukoc. Biol., December 1, 2006; 80(6): 1584 - 1592. [Abstract] [Full Text] [PDF]
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H. Mitsuzawa, C. Nishitani, N. Hyakushima, T. Shimizu, H. Sano, N. Matsushima, K. Fukase, and Y. Kuroki Recombinant Soluble Forms of Extracellular TLR4 Domain and MD-2 Inhibit Lipopolysaccharide Binding on Cell Surface and Dampen Lipopolysaccharide-Induced Pulmonary Inflammation in Mice J. Immunol., December 1, 2006; 177(11): 8133 - 8139. [Abstract] [Full Text] [PDF]
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 A. Sato, M. M. Linehan, and A. Iwasaki Dual recognition of herpes simplex viruses by TLR2 and TLR9 in dendritic cells PNAS, November 14, 2006; 103(46): 17343 - 17348. [Abstract] [Full Text] [PDF]
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J. W. Du, F. Zhang, J. E. Capo-Aponte, S. D. Tachado, J. Zhang, F.-S. X. Yu, R. A. Sack, H. Koziel, and P. S. Reinach AsialoGM1-Mediated IL-8 Release by Human Corneal Epithelial Cells Requires Coexpression of TLR5 Invest. Ophthalmol. Vis. Sci., November 1, 2006; 47(11): 4810 - 4818. [Abstract] [Full Text] [PDF]
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 W. Koch, P. Hoppmann, A. Pfeufer, A. Schomig, and A. Kastrati Toll-like receptor 4 gene polymorphisms and myocardial infarction: no association in a Caucasian population Eur. Heart J., November 1, 2006; 27(21): 2524 - 2529. [Abstract] [Full Text] [PDF]
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K.-Y. Lee, S.-C. Ho, H.-C. Lin, S.-M. Lin, C.-Y. Liu, C.-D. Huang, C.-H. Wang, K. F. Chung, and H.-P. Kuo Neutrophil-Derived Elastase Induces TGF-beta1 Secretion in Human Airway Smooth Muscle via NF-{kappa}B Pathway Am. J. Respir. Cell Mol. Biol., October 1, 2006; 35(4): 407 - 414. [Abstract] [Full Text] [PDF]
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 B. M. Arafah Hypothalamic Pituitary Adrenal Function during Critical Illness: Limitations of Current Assessment Methods J. Clin. Endocrinol. Metab., October 1, 2006; 91(10): 3725 - 3745. [Abstract] [Full Text] [PDF]
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C. Yamada, H. Sano, T. Shimizu, H. Mitsuzawa, C. Nishitani, T. Himi, and Y. Kuroki Surfactant Protein A Directly Interacts with TLR4 and MD-2 and Regulates Inflammatory Cellular Response: IMPORTANCE OF SUPRATRIMERIC OLIGOMERIZATION J. Biol. Chem., August 4, 2006; 281(31): 21771 - 21780. [Abstract] [Full Text] [PDF]
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Y. Wakabayashi, M. Kobayashi, S. Akashi-Takamura, N. Tanimura, K. Konno, K. Takahashi, T. Ishii, T. Mizutani, H. Iba, T. Kouro, et al. A Protein Associated with Toll-Like Receptor 4 (PRAT4A) Regulates Cell Surface Expression of TLR4 J. Immunol., August 1, 2006; 177(3): 1772 - 1779. [Abstract] [Full Text] [PDF]
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A. Nencioni, K. Schwarzenberg, K. M. Brauer, S. M. Schmidt, A. Ballestrero, F. Grunebach, and P. Brossart Proteasome inhibitor bortezomib modulates TLR4-induced dendritic cell activation Blood, July 15, 2006; 108(2): 551 - 558. [Abstract] [Full Text] [PDF]
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P. Rallabhandi, J. Bell, M. S. Boukhvalova, A. Medvedev, E. Lorenz, M. Arditi, V. G. Hemming, J. C. G. Blanco, D. M. Segal, and S. N. Vogel Analysis of TLR4 Polymorphic Variants: New Insights into TLR4/MD-2/CD14 Stoichiometry, Structure, and Signaling J. Immunol., July 1, 2006; 177(1): 322 - 332. [Abstract] [Full Text] [PDF]
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X. Huang, L. D. Hazlett, W. Du, and R. P. Barrett SIGIRR Promotes Resistance against Pseudomonas aeruginosa Keratitis by Down-Regulating Type-1 Immunity and IL-1R1 and TLR4 Signaling J. Immunol., July 1, 2006; 177(1): 548 - 556. [Abstract] [Full Text] [PDF]
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A. E. Medvedev, I. Sabroe, J. D. Hasday, and S. N. Vogel Invited review: Tolerance to microbial TLR ligands: molecular mechanisms and relevance to disease Innate Immunity, June 1, 2006; 12(3): 133 - 150. [Abstract] [PDF]
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 Y.-H. Huang, P.-S. Tsai, Y.-F. Kai, C.-H. Yang, and C.-J. Huang Lidocaine inhibition of inducible nitric oxide synthase and cationic amino Acid transporter-2 transcription in activated murine macrophages may involve voltage-sensitive na+ channel. Anesth. Analg., June 1, 2006; 102(6): 1739 - 1744. [Abstract] [Full Text] [PDF]
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H. Fang, L. Xu, T. Y. Chen, J. M. Cyr, and D. M. Frucht Anthrax Lethal Toxin Has Direct and Potent Inhibitory Effects on B Cell Proliferation and Immunoglobulin Production J. Immunol., May 15, 2006; 176(10): 6155 - 6161. [Abstract] [Full Text] [PDF]
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M. Kobayashi, S.-i. Saitoh, N. Tanimura, K. Takahashi, K. Kawasaki, M. Nishijima, Y. Fujimoto, K. Fukase, S. Akashi-Takamura, and K. Miyake Regulatory Roles for MD-2 and TLR4 in Ligand-Induced Receptor Clustering J. Immunol., May 15, 2006; 176(10): 6211 - 6218. [Abstract] [Full Text] [PDF]
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K. Thorlacius, J. E. Slotta, M. W. Laschke, Y. Wang, M. D. Menger, B. Jeppsson, and H. Thorlacius Protective effect of fasudil, a Rho-kinase inhibitor, on chemokine expression, leukocyte recruitment, and hepatocellular apoptosis in septic liver injury J. Leukoc. Biol., May 1, 2006; 79(5): 923 - 931. [Abstract] [Full Text] [PDF]
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 S. W. Ryter, J. Alam, and A. M. K. Choi Heme Oxygenase-1/Carbon Monoxide: From Basic Science to Therapeutic Applications Physiol Rev, April 1, 2006; 86(2): 583 - 650. [Abstract] [Full Text] [PDF]
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K. Nakai, M. B. Kadiiska, J.-J. Jiang, K. Stadler, and R. P. Mason Free radical production requires both inducible nitric oxide synthase and xanthine oxidase in LPS-treated skin PNAS, March 21, 2006; 103(12): 4616 - 4621. [Abstract] [Full Text] [PDF]
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J. S. Yang, H. J. Kim, Y. H. Ryu, C.-H. Yun, D. K. Chung, and S. H. Han Endotoxin contamination in commercially available pokeweed mitogen contributes to the activation of murine macrophages and human dendritic cell maturation. Clin. Vaccine Immunol., March 1, 2006; 13(3): 309 - 313. [Abstract] [Full Text] [PDF]
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R. Higgs, P. Cormican, S. Cahalane, B. Allan, A. T. Lloyd, K. Meade, T. James, D. J. Lynn, L. A. Babiuk, and C. O'Farrelly Induction of a Novel Chicken Toll-Like Receptor following Salmonella enterica Serovar Typhimurium Infection Infect. Immun., March 1, 2006; 74(3): 1692 - 1698. [Abstract] [Full Text] [PDF]
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C. Zhang, S.-H. Wang, M. E. Lasbury, D. Tschang, C.-P. Liao, P. J. Durant, and C.-H. Lee Toll-Like Receptor 2 Mediates Alveolar Macrophage Response to Pneumocystis murina Infect. Immun., March 1, 2006; 74(3): 1857 - 1864. [Abstract] [Full Text] [PDF]
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 J. S. Park, F. Gamboni-Robertson, Q. He, D. Svetkauskaite, J.-Y. Kim, D. Strassheim, J.-W. Sohn, S. Yamada, I. Maruyama, A. Banerjee, et al. High mobility group box 1 protein interacts with multiple Toll-like receptors Am J Physiol Cell Physiol, March 1, 2006; 290(3): C917 - C924. [Abstract] [Full Text] [PDF]
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P. Massari, A. Visintin, J. Gunawardana, K. A. Halmen, C. A. King, D. T. Golenbock, and L. M. Wetzler Meningococcal Porin PorB Binds to TLR2 and Requires TLR1 for Signaling J. Immunol., February 15, 2006; 176(4): 2373 - 2380. [Abstract] [Full Text] [PDF]
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N. Mookherjee, K. L. Brown, D. M. E. Bowdish, S. Doria, R. Falsafi, K. Hokamp, F. M. Roche, R. Mu, G. H. Doho, J. Pistolic, et al. Modulation of the TLR-Mediated Inflammatory Response by the Endogenous Human Host Defense Peptide LL-37 J. Immunol., February 15, 2006; 176(4): 2455 - 2464. [Abstract] [Full Text] [PDF]
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Y. Rosenfeld, N. Papo, and Y. Shai Endotoxin (Lipopolysaccharide) Neutralization by Innate Immunity Host-Defense Peptides: PEPTIDE PROPERTIES AND PLAUSIBLE MODES OF ACTION J. Biol. Chem., January 20, 2006; 281(3): 1636 - 1643. [Abstract] [Full Text] [PDF]
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C. M. O'Connell, I. A. Ionova, A. J. Quayle, A. Visintin, and R. R. Ingalls Localization of TLR2 and MyD88 to Chlamydia trachomatis Inclusions: EVIDENCE FOR SIGNALING BY INTRACELLULAR TLR2 DURING INFECTION WITH AN OBLIGATE INTRACELLULAR PATHOGEN J. Biol. Chem., January 20, 2006; 281(3): 1652 - 1659. [Abstract] [Full Text] [PDF]
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R. P. Deering and J. S. Orange Development of a Clinical Assay To Evaluate Toll-Like Receptor Function Clin. Vaccine Immunol., January 1, 2006; 13(1): 68 - 76. [Abstract] [Full Text] [PDF]
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P. B. Mann, D. Wolfe, E. Latz, D. Golenbock, A. Preston, and E. T. Harvill Comparative Toll-Like Receptor 4-Mediated Innate Host Defense to Bordetella Infection Infect. Immun., December 1, 2005; 73(12): 8144 - 8152. [Abstract] [Full Text] [PDF]
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Z. Zhang, J.-P. Louboutin, D. J. Weiner, J. B. Goldberg, and J. M. Wilson Human Airway Epithelial Cells Sense Pseudomonas aeruginosa Infection via Recognition of Flagellin by Toll-Like Receptor 5 Infect. Immun., November 1, 2005; 73(11): 7151 - 7160. [Abstract] [Full Text] [PDF]
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J. S. Hadley, J. E. Wang, S. J. Foster, C. Thiemermann, and C. J. Hinds Peptidoglycan of Staphylococcus aureus Upregulates Monocyte Expression of CD14, Toll-Like Receptor 2 (TLR2), and TLR4 in Human Blood: Possible Implications for Priming of Lipopolysaccharide Signaling Infect. Immun., November 1, 2005; 73(11): 7613 - 7619. [Abstract] [Full Text] [PDF]
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D. R. Blais, S. G. Vascotto, M. Griffith, and I. Altosaar LBP and CD14 Secreted in Tears by the Lacrimal Glands Modulate the LPS Response of Corneal Epithelial Cells Invest. Ophthalmol. Vis. Sci., November 1, 2005; 46(11): 4235 - 4244. [Abstract] [Full Text] [PDF]
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 X. Yang, D. Coriolan, K. Schultz, D. T. Golenbock, and D. Beasley Toll-Like Receptor 2 Mediates Persistent Chemokine Release by Chlamydia pneumoniae-Infected Vascular Smooth Muscle Cells Arterioscler. Thromb. Vasc. Biol., November 1, 2005; 25(11): 2308 - 2314. [Abstract] [Full Text] [PDF]
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 A. Razmara, D. N. Krause, and S. P. Duckles Testosterone augments endotoxin-mediated cerebrovascular inflammation in male rats Am J Physiol Heart Circ Physiol, November 1, 2005; 289(5): H1843 - H1850. [Abstract] [Full Text] [PDF]
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A. Srivastava, P. Henneke, A. Visintin, S. C. Morse, V. Martin, C. Watkins, J. C. Paton, M. R. Wessels, D. T. Golenbock, and R. Malley The Apoptotic Response to Pneumolysin Is Toll-Like Receptor 4 Dependent and Protects against Pneumococcal Disease Infect. Immun., October 1, 2005; 73(10): 6479 - 6487. [Abstract] [Full Text] [PDF]
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S. R. Coats, T.-T. T. Pham, B. W. Bainbridge, R. A. Reife, and R. P. Darveau MD-2 Mediates the Ability of Tetra-Acylated and Penta-Acylated Lipopolysaccharides to Antagonize Escherichia coli Lipopolysaccharide at the TLR4 Signaling Complex J. Immunol., October 1, 2005; 175(7): 4490 - 4498. [Abstract] [Full Text] [PDF]
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G. Mancuso, A. Midiri, C. Biondo, C. Beninati, M. Gambuzza, D. Macri, A. Bellantoni, A. Weintraub, T. Espevik, and G. Teti Bacteroides fragilis-Derived Lipopolysaccharide Produces Cell Activation and Lethal Toxicity via Toll-Like Receptor 4 Infect. Immun., September 1, 2005; 73(9): 5620 - 5627. [Abstract] [Full Text] [PDF]
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K. B. Goralski, D. Abdulla, C. J. Sinal, A. Arsenault, and K. W. Renton Toll-like receptor-4 regulation of hepatic Cyp3a11 metabolism in a mouse model of LPS-induced CNS inflammation Am J Physiol Gastrointest Liver Physiol, September 1, 2005; 289(3): G434 - G443. [Abstract] [Full Text] [PDF]
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J. D. Savov, D. M. Brass, B. L. Lawson, E. McElvania-Tekippe, J. K. L. Walker, and D. A. Schwartz Toll-like receptor 4 antagonist (E5564) prevents the chronic airway response to inhaled lipopolysaccharide Am J Physiol Lung Cell Mol Physiol, August 1, 2005; 289(2): L329 - L337. [Abstract] [Full Text] [PDF]
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