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J. Biol. Chem., Vol. 278, Issue 3, 2043-2050, January 17, 2003
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From the Infiltration of the lungs with
neutrophils promotes respiratory failure during severe
Pneumocystis carinii (PC) pneumonia. Recent studies have
shown that alveolar epithelial cells (AECs), in addition to
promoting PC attachment, also participate in lung inflammation by the
release of cytokines and chemokines. Herein, we demonstrate that a PC
Pneumocystis carinii Cell Wall
-Glucan Induces
Release of Macrophage Inflammatory Protein-2 from Alveolar
Epithelial Cells via a Lactosylceramide-mediated Mechanism*
,,,,§, and§¶
Thoracic Diseases Research Unit,
Division of Pulmonary, Critical Care, and Internal Medicine, and the
§ Department of Biochemistry and Molecular Biology, Mayo
Clinic and Foundation, Rochester, Minnesota 55905
-glucan rich cell wall isolate (PCBG) stimulates the release of
macrophage inflammatory protein-2 (MIP-2) from isolated AECs through a
lactosylceramide-dependent mechanism. The results
demonstrate that MIP-2 mRNA and protein production is significantly
increased at both early and late time points after PCBG challenge.
Although CD11b/CD18 (Mac-1, CR3) is the most widely studied -glucan
receptor, we demonstrate that CD11b/CD18 is not present on AECs. This
study instead demonstrates that preincubation of AECs with an antibody
directed against the membrane glycosphingolipid lactosylceramide
(CDw17) results in a significant decrease in MIP-2 secretion.
Preincubation of the anti-CDw17 antibody with solubilized
lactosylceramide reverses this effect. Furthermore, incubation of AECs
with inhibitors of glycosphingolipid biosynthesis, including
N-butyldeoxyno jirimycin and
D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol-HCl, also results in a significant decrease in AEC MIP-2 production following challenge with PCBG. These data demonstrate that PC -glucan induces significant production of MIP-2 from AECs and that
CDw17 participates in the glucan-induced inflammatory signaling in lung
epithelial cells during PC infection.
*
This work was supported in part by National Institutes of
Health Grants HL55934, HL57125, and HL62150 (to A. H. L.) and GM22942 (to R. E. P.) and a grant from the Robert N. Brewer Family Foundation to Thoracic Disease Research Unit.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.
Copyright © 2003 by The American Society for Biochemistry and Molecular Biology, Inc.
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