Inflammatory processes in a murine model of intra-abdominal abscess formation

Abscess formation has been viewed as a host defense strategy to contain the spread of infection. However, abscesses are also serious and life-threaten ing manifestations of persisting microbial infection, The initiation of abs cess formation, both clinically and experimentally, involves the release of bacteria and an abscess-potentiating agent (e.g., fecal fiber or an analog ) into a sterile site, with host defense mechanisms being unable to elimina te the infecting organisms, Abscess formation is aided by a combination of factors that share a common feature: impairment of phagocytic killing and h ence clearance of microorganisms, These include bacterial virulence factors (e.g., capsule formation, succinic acid production); complement activation by the abscess potentiating agent; fibrin deposition; and microbial seques tration within abscess neutrophils, Recruitment of cells into the peritonea l cavity follows mast cell activation in the pathogenesis of infection: his tamine and tumor necrosis factor or can be detected in the peritoneal cavit y within minutes of challenge with an abscess-inducing mixture. However, th e role of mast cells in host defense is made less clear by the finding of d iminished abscess formation (but no mortality or increased morbidity) in ma st-cell-depleted mice. This may indicate that mast cell products have a rol e in not only the initiation of an inflammatory response but also the promo tion of fibrin deposition and abscess formation.