Role of resident macrophages, peripheral neutrophils, and translymphatic absorption in bacterial clearance from the peritoneal cavity

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Abstract
Microbial pathogens within the peritoneal cavity encounter 3 categories of host defense mechanisms: removal mechanisms, which occur via diaphragmatic lymphatic absorption; killing mechanisms, in which host phagocytes act as effector cells; and sequestration mechanism due to fibrin trapping and the formation of adhesions between visceral surfaces. The relative roles of the first 2 components were defined and quantitated in an experimental rat model of Escherichia coli peritonitis in which fibrinous adhesions do not form. Challenge i.p. with .gtoreq. 2 .times. 102 colony-forming units (CFU) of viable E. coli led to an initial decline in bacterial numbers followed by ongoing proliferation and > 50% mortality. With inocula of .ltoreq. 5 .times. 107 CFU, elimination of bacteria occurred after moderate initial proliferation, and no mortality ensured. Nonviable, radiolabled E coli organisms were utilized to examine bacterial clearance via translymphatic absorption and phagocytosis. Both processes were extremely rapid, serving to eliminate free bacteria rapidly within the peritoneal cavity. Although macrophages and polymorphonuclear leukocytes within the peritioneal cavity demonstrated similar phagocytic capacities, the predominance of macrophages at the time of the initial bacteria insult led to the conclusion that these cells, in addition to translymphatic absorption, represent the 1st line of host defenses, acting to eliminate bacteria in the incipient stages of infection.