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Channing Laboratory, Departments of
*
Medicine and
Pathology, Brigham and Womens Hospital and Harvard Medical School, Boston, MA 02115
We investigated the cellular mechanism by which Bacteroides
fragilis promotes the development of intraabdominal abscesses in
experimental models of sepsis. B. fragilis, as well as
purified capsular polysaccharide complex (CPC) from this organism,
adhered to primary murine mesothelial cells (MMCs) in vitro. The
binding of CPC to murine peritoneal macrophage stimulated TNF-
production, which when transferred to monolayers of MMCs elicited
significant ICAM-1 expression by these cells. This response resulted in
enhanced polymorphonuclear leukocyte attachment to MMCs that could be
inhibited by Abs specific for TNF-
or ICAM-1. Mice treated with
TNF-
- or ICAM-1-specific Abs failed to develop intraabdominal
abscesses following challenge with purified CPC. These results
illustrated the role of the CPC in promoting adhesion of B.
fragilis to the peritoneal wall and coordinating the cellular
events leading to the development of abscesses associated with
experimental intraabdominal sepsis.
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