FIG. 3.

Proposed model of intra-abdominal abscess formation. The CPC of B. fragilis interacts with cells of the host immune system within the peritoneal cavity. This interaction (i) allows for the localization of B. fragilis within the abdominal cavity, thus resulting in enhanced adherence to the mesothelial surface and the ability to resist clearance from the peritoneum, and (ii) stimulates proinflammatory cytokines and chemokines, the production of which stimulates the expression of CAMs (such as ICAM-1) on host cells and the recruitment of PMNs to the abdominal cavity. Infiltration and sequestration of PMNs within the peritoneal cavity are the hallmark of intra-abdominal abscess formation. The CPC of B. fragilis interacts with T cells, peritoneal macrophages, and PMNs. In response to this interaction, these cells produce TNF-α and IL-8, which serve to recruit activated PMNs to the peritoneal cavity and upregulate ICAM-1 expression on mesothelial cells. The production of ICAM-1 by mesothelial cells serves as a functional ligand for infiltrating PMNs. The recruitment of PMNs into the peritoneal cavity and subsequent adherence of these cells to activated mesothelial tissue form the first stages of intra-abdominal abscess formation in the infected host.