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J Biol Chem, Vol. 275, Issue 5, 3057-3064, February 4, 2000
From the Division of Newborn Medicine, Department of Medicine,
Children's Hospital and Microbial pathogens frequently take advantage of
host systems for their pathogenesis. Shedding of cell surface molecules
as soluble extracellular domains (ectodomains) is one of the host responses activated during tissue injury. In this study, we examined whether pathogenic bacteria can modulate shedding of syndecan-1, the
predominant syndecan of host epithelia. Our studies found that
overnight culture supernatants of Pseudomonas aeruginosa and Staphylococcus aureus enhanced the shedding of
syndecan-1 ectodomains, whereas culture supernatants of several other
Gram-negative and Gram-positive bacteria had only low levels of
activity. Because supernatants from all tested strains of P. aeruginosa (n = 9) enhanced syndecan-1 shedding
by more than 4-fold above control levels, we focused our attention on
this Gram-negative bacterium. Culture supernatants of P. aeruginosa increased shedding of syndecan-1 in both a
concentration- and time-dependent manner, and augmented shedding by various host cells. A 20-kDa shedding enhancer was partially purified from the supernatant through ammonium sulfate precipitation and gel chromatography, and identified by N-terminal sequencing as LasA, a known P. aeruginosa virulence factor.
LasA was subsequently determined to be a syndecan-1 shedding enhancer from the findings that (i) immunodepletion of LasA from the partially purified sample resulted in abrogation of its activity to enhance shedding and (ii) purified LasA increased shedding in a
concentration-dependent manner. Our results also indicated
that LasA enhances syndecan-1 shedding by activation of the host
cell's shedding mechanism and not by direct interaction with
syndecan-1 ectodomains. Enhanced syndecan-1 shedding may be a means by
which pathogenic bacteria take advantage of a host mechanism to promote
their pathogenesis.
Syndecan-1 Shedding Is Enhanced by LasA, a Secreted Virulence
Factor of Pseudomonas aeruginosa*
,, Channing Laboratory, Department
of Medicine, Brigham and Women's Hospital, Harvard Medical School,
Boston, Massachusetts 02115
*
This work was supported by the Parker B. Francis Foundation
Fellowship (to P. W. P.) and National Institutes of Health
Grants AI22535 (to G. B. P.), CA28735 (to M. B.),
HL569398 (to M. B.), and HL58346 (to M. J. P.).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.
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