| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Department of Biology, Virginia Tech, 2119 Derring Hall, Blacksburg, VA 24061-0406, USA
Correspondence
Stephen B. Melville
melville{at}vt.edu
Clostridium perfringens is a Gram-positive, anaerobic bacterium that is the most common cause of gas gangrene (clostridial myonecrosis) in humans. C. perfringens produces a variety of extracellular toxins that are thought to be the major virulence factors of the organism. However, C. perfringens has recently been shown to have the ability to survive in a murine macrophage-like cell line, J774-33, even under aerobic conditions. In J774-33 cells, C. perfringens can escape the phagosome and gain access to the cytoplasm. Since the receptor that is used for phagocytosis can determine the fate of an intracellular bacterium, we used a variety of inhibitors of specific receptors to identify those used by J774-33 cells to phagocytose C. perfringens. It was found that the scavenger receptor and mannose receptor(s) were involved in the phagocytosis of C. perfringens. In the presence of complement, the complement receptor (CR3) was also involved in the binding and/or uptake of C. perfringens. Since the receptor inhibition studies indicated that the scavenger receptor played a major role in phagocytosis, C. perfringens binding studies were performed with a Chinese hamster ovary (CHO) cell line expressing the mouse SR-A receptor. The cell line expressing the SR-A receptor showed a significant increase in C. perfringens binding in comparison to the non-transfected CHO cells. In the absence of opsonizing antibodies, the Fc receptor was not used to phagocytose C. perfringens. Forcing the macrophages to use a specific receptor by using combinations of different receptor inhibitors led to only a slight increase in co-localization of intracellular C. perfringens with the late endosome-lysosome marker LAMP-1. Carbohydrate analysis of C. perfringens strain 13 extracellular polysaccharide confirmed the presence of mannose and negatively charged residues of glucuronic acid, which may provide the moieties that promote binding to the mannose and scavenger receptors, respectively.
This article has been cited by other articles:
|
|
 |
|
  D. M. Aronoff, Y. Hao, J. Chung, N. Coleman, C. Lewis, C. M. Peres, C. H. Serezani, G.-H. Chen, N. Flamand, T. G. Brock, et al. Misoprostol Impairs Female Reproductive Tract Innate Immunity against Clostridium sordellii J. Immunol., June 15, 2008; 180(12): 8222 - 8230. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. Haberzettl, R. P. F. Schins, D. Hohr, V. Wilhelmi, P. J. A. Borm, and C. Albrecht Impact of the Fc{gamma}II-receptor on quartz uptake and inflammatory response by alveolar macrophages Am J Physiol Lung Cell Mol Physiol, June 1, 2008; 294(6): L1137 - L1148. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. S.A. Myers, D. A. Rasko, J. K. Cheung, J. Ravel, R. Seshadri, R. T. DeBoy, Q. Ren, J. Varga, M. M. Awad, L. M. Brinkac, et al. Skewed genomic variability in strains of the toxigenic bacterial pathogen, Clostridium perfringens Genome Res., August 1, 2006; 16(8): 1031 - 1040. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. A. Champion and S. Mitragotri From the Cover: Role of target geometry in phagocytosis PNAS, March 28, 2006; 103(13): 4930 - 4934. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. K. O'Brien and S. B. Melville Effects of Clostridium perfringens Alpha-Toxin (PLC) and Perfringolysin O (PFO) on Cytotoxicity to Macrophages, on Escape from the Phagosomes of Macrophages, and on Persistence of C. perfringens in Host Tissues Infect. Immun., September 1, 2004; 72(9): 5204 - 5215. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| INT J SYST EVOL MICROBIOL | MICROBIOLOGY | J GEN VIROL |
| J MED MICROBIOL | ALL SGM JOURNALS | |
