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-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 alpha 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.
Finlay-Jones
J J
JJ
Department of Microbiology and Infectious Diseases, School of Medicine, Flinders University, Adelaide, Australia. John.Finlay-Jones@flinders.edu.au
Davies
K V
KV
Sturm
L P
LP
Kenny
P A
PA
Hart
P H
PH
D018784:Abdominal Abscess / Q000209:etiology* / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D000818:Animals; D004195:Disease Models, Animal; D005337:Fibrin / Q000378:metabolism; D006801:Humans; D007249:Inflammation; D008407:Mast Cells / Q000276:immunology; D051379:Mice; D018805:Sepsis / Q000209:etiology* / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D013997:Time Factors
D005337:Fibrin