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The Journal of Immunology, 1998, 160: 5000-5006.
Copyright © 1998 by The American Association of Immunologists

Cellular Mechanism of Intraabdominal Abscess Formation by Bacteroides fragilis1

Frank C. Gibson, III2,*, Andrew B. Onderdonk{dagger}, Dennis L. Kasper* and Arthur O. Tzianabos*

Channing Laboratory, Departments of * Medicine and {dagger} Pathology, Brigham and Women’s 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-{alpha} 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-{alpha} or ICAM-1. Mice treated with TNF-{alpha}- 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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