Abstract
We have examined soluble sonic extracts of Actinobacillus actinomycetemcomitans (Aa) for their ability to alter human lymphocyte function. This microorganism has been isolated from a variety of clinical abcesses and is the suspected etiologic agent in certain forms of both periodontal disease and bacterial endocarditis. We have found that soluble sonic extracts of all Aa strains examined suppressed HPBL responsiveness to Con A, PHA, PWM, and the antigen, SKSD, in a dose-dependent fashion; whereas other Gram-negative organisms (Capnocytophaga, Leptotrichia, Hemophilus aphrophilus, and Veillonella parvula) grown under similar conditions failed to have a suppressive effect. Aa suppression involved effects on DNA, RNA, and protein synthesis and was not due to cytotoxic effects. The suppressive factor is heat labile and appears to function early in the process of lymphocyte activation, because maximum inhibition requires that cells be exposed for 90 min before the addition of mitogen and suppression could not be reversed by washing after an incubation of only 30 min. Finally, the data are consistent with the generation of suppressor cells, probably of lymphocyte origin.Although it is not clear how Aa acts to cause disease, several investigators have proposed that impaired host defenses may play a pivotal role. Several studies have demonstrated defects in PMN, monocyte, and lymphocyte function in patients with periodontal disease. These findings, along with the data presented in this paper, support the hypothesis that patients who harbor Aa could suffer from local and/or immune suppression. The effects of this suppression may be to enhance the pathogenicity of Aa itself or that of some other opportunistic organism.
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CITATION STYLE
Shenker, B. J., McArthur, W. P., & Tsai, C. C. (1982). Immune suppression induced by Actinobacillus actinomycetemcomitans . I. Effects on human peripheral blood lymphocyte responses to mitogens and antigens. The Journal of Immunology, 128(1), 148–154. https://doi.org/10.4049/jimmunol.128.1.148
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