Present addresses: David K. O'Brien, Division of Bacteriology, United States Army Medical Research Institute for Infectious Diseases, Fort Detrick, 1425 Porter Street, Frederick, MD 21702, USA. Michael E. Woodman, Department of Microbiology, Immunology, and Molecular Genetics, University of Kentucky College of Medicine, Lexington, KY 40536-0298, USA.
The role of neutrophils and monocytic cells in controlling the initiation of Clostridium perfringens gas gangrene
Article first published online: 11 APR 2007
FEMS Immunology & Medical Microbiology
Volume 50, Issue 1, pages 86–93, June 2007
How to Cite
O'Brien, D. K., Therit, B. H., Woodman, M. E. and Melville, S. B. (2007), The role of neutrophils and monocytic cells in controlling the initiation of Clostridium perfringens gas gangrene. FEMS Immunology & Medical Microbiology, 50: 86–93. doi: 10.1111/j.1574-695X.2007.00235.x
Editor: Patrik Bavoil
- Issue published online: 11 APR 2007
- Article first published online: 11 APR 2007
- Received 17 December 2006; revised 9 February 2007; accepted 18 February 2007.First published online 11 April 2007.
- Clostridium perfringens;
- gas gangrene;
Clostridium perfringens is a common cause of the fatal disease gas gangrene (myonecrosis). Established gas gangrene is notable for a profound absence of neutrophils and monocytic cells (phagocytes), and it has been suggested that the bactericidal activities of these cells play an insignificant role in controlling the progression of the infection. However, large inocula of bacteria are needed to establish an infection in experimental animals, suggesting phagocytes may play a role in inhibiting the initiation of gangrene. Examination of tissue sections of mice infected with a lethal (1 × 109) or sublethal (1 × 106) inoculum of C. perfringens revealed that phagocyte infiltration in the first 3 h postinfection was inhibited with a lethal dose but not with a sublethal dose, indicating that exclusion of phagocytes begins very early in the infection cycle. Experiments in which mice were depleted of either circulating monocytes or neutrophils before infection with C. perfringens showed that monocytes play a role in inhibiting the onset of gas gangrene at intermediate inocula but, although neutrophils can slow the onset of the infection, they are not protective. These results suggest that treatments designed to increase monocyte infiltration and activate macrophages may lead to increased resistance to the initiation of gas gangrene.