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

John J. Finlay-Jones, Kate V.L. Davies, Lana P. Sturm, Peter A. Kenny, Prue H. Hart

Research output: Contribution to journalReview article

22 Citations (Scopus)

Abstract

Abscess formation has been viewed as a host defense strategy to contain the spread of infection. However, abscesses are also serious and life- threatening manifestations of persisting microbial infection. The initiation of abscess 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 eliminate the infecting organisms. Abscess formation is aided by a combination of factors that share a common feature: impairment of phagocytic killing and hence 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 sequestration within abscess neutrophils. Recruitment of cells into the peritoneal cavity follows mast cell activation in the pathogenesis of infection: histamine and tumor necrosis factor a can be detected in the peritoneal cavity within minutes of challenge with an abscess-inducing mixture. However, the role of mast cells in host defense is made less clear by the finding of diminished abscess formation (but no mortality or increased morbidity) in mast-cell-depleted mice. This may indicate that mast cell products have a role in not only the initiation of an inflammatory response but also the promotion of fibrin deposition and abscess formation.

Original languageEnglish
Pages (from-to)583-587
Number of pages5
JournalJournal of Leukocyte Biology
Volume66
Issue number4
DOIs
Publication statusPublished - 1 Jan 1999
Externally publishedYes

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