Degradation in vivo of the C3 protein of guinea‐pig complement by a pathogenic strain of Bacteroides gingivalis
作者:
GÖRAN K. SUNDQVIST,
JAN CARLSSON,
BJÖRN F. HERRMANN,
JOSÉ F. HÖFLING,
ANNA VÄÄTÄINEN,
期刊:
European Journal of Oral Sciences
(WILEY Available online 1984)
卷期:
Volume 92,
issue 1
页码: 14-24
ISSN:0909-8836
年代: 1984
DOI:10.1111/j.1600-0722.1984.tb00854.x
出版商: Blackwell Publishing Ltd
关键词: Bacteroides;C3 protein;microbiology
数据来源: WILEY
摘要:
Abstract –The pathogenicity of five black‐pigmented strains of Bacteroides was tested in subcutaneously implanted Teflon cages in guinea pigs. The tissue reaction around the cages was registered and the contents of the fluid of the cages were analyzed. Two strains of B. intermedius produced a localized abscess around the cages, while one strain (381) of B. gingivalis and an asaccharolytic strain (BN11a‐f) different from B. gingivalis did not induce any signs of abscess formation. One strain (W83) of B. gingivalis caused extensive purulent breakdown of the tissues. When the inoculum of strain VV83 contained more than 109 cells, the animals were killed. Strain W83 was the only strain that increased in number in the cage. The fluid of cages inoculated with strain W83 was also remarkably different from the fluid of cages inoculated with the other strains. The fluid had a high proteolytic activity. No C3 protein of complement and only traces of immunoglobulins could be detected in the fluid. Both strain W83 and strain 381 had a high proteolytic activity against whole guinea‐pig serum and when bacteria of these two strains were incubated with guinea‐pig serum for 24 h, almost all serum proteins, including the C3 protein, were degraded. These two strains might thus have similar capacity in perturbing the host defence when inoculated into the tissue cages. The actual difference in pathogenicity between the strains might be explained by a recent finding that the pathogenic strain W83, but not strain 381, requires complement in activating polymorphonuclear leukocytes. The degradation of the C3 protein by the pathogenic strain W83 of B. gingivalis thus may be the crucial event in its perturbation of the host defence. A degradation of the C3 protein by strain 381 would be of no help in eluding the host defence, since this strain activates polymorphonuclear leukocytes in the absence of c
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