Clostridial Gas Gangrene: Evidence That α and θ Toxins Differentially Modulate the Immune Response and Induce Acute Tissue Necrosis

The rapid extension of necrosis and an absence of polymorphonuclear leukocytes (PMNL) at the site of infection are two hallmarks of Clostridium perfringens gas gangrene. While both a and u toxins profoundly affect PMNL function and viability in vitro, their roles in muscle destruction and impairment...

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Bibliographic Details
Published in:The Journal of infectious diseases 1997-07, Vol.176 (1), p.189-195
Main Authors: Stevens, Dennis L., Tweten, Rodney K., Awad, Milena M., Rood, Julian I., Bryant, Amy E.
Format: Article
Language:English
Subjects:
Animals
Bacterial Toxins - immunology
Bacterial Toxins - toxicity
Bacteriology
Biological and medical sciences
Calcium-Binding Proteins
Clostridium perfringens
Female
Fundamental and applied biological sciences. Psychology
Fundamental immunology
Gas gangrene
Gas Gangrene - immunology
Gas Gangrene - pathology
Hemolysin Proteins
Immunization
Immunobiology
Infections
Major Articles
Mice
Microbiology
Modulation of the immune response (stimulation, suppression)
Monoclonal antibodies
Mortality
Muscle tissues
Necrosis
Neutrophils
Neutrophils - physiology
Pathogenicity, virulence, toxins, bacteriocins, pyrogens, host-bacteria relations, miscellaneous strains
Toxins
Transcriptional regulatory elements
Type C Phospholipases
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Summary:The rapid extension of necrosis and an absence of polymorphonuclear leukocytes (PMNL) at the site of infection are two hallmarks of Clostridium perfringens gas gangrene. While both a and u toxins profoundly affect PMNL function and viability in vitro, their roles in muscle destruction and impairment of the inflammatory response in vivo have not been investigated. Comparative histopathologic examinations were performed on animals infected with either wild-type C. perfringens, or isogenic, toxin-deficient mutants of C. perfringens. Tissue destruction was modest in animals infected with the α toxin-deficient mutant; destruction was more pronounced in tissues infected with the θ toxin-deficient mutant or the wild-type strain. α and θ toxins also displayed differing abilities to modulate the inflammatory response. Histopathologic studies in which recombinant toxins were injected together with killed, washed C. perfringens further substantiated these tissue-destructive and differential antiinflammatory effects.
ISSN:0022-1899
1537-6613
DOI:10.1086/514022