Biomedical subjects
Publications and source records attributed to R Finberg.
Total hemolytic complement activity (CH50) and levels of C4, C5, and Factor B determined by commercially available radial immunodiffusion plates were compared in sera from patients with systemic lupus erythematosus. There was a significant correlation between CH50, C4 and C5, but no correlation between Factor B and any of the other indices of complement activity measured.
Experimental animal model systems have been used by many investigators to explore the pathogenicity of obligate anaerobes. During the last 15 years, research in our laboratory has utilized an experimental model for intraabdominal sepsis to define the contribution of obligate anaerobes to the infectious process. These studies have shown that obligate anaerobes are important components of the polymicrobic flora present during such infection. Moreover, certain anaerobes, such as Bacteroides fragilis, possess specific virulence factors, such as the capsular polysaccharide, that appear to be important to the infectious process. More recent research has used modifications of the original model system to evaluate the host immune response to B. fragilis. These studies indicate that immunization with the capsular polysaccharide provides a T cell-dependent immunity to abscess development when animals are challenged with B. fragilis. It has also been shown that the killing of B. fragilis is T cell dependent. The observations made with regard to B. fragilis in this animal model system are discussed.
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Intraabdominal abscesses (IAA) caused by Bacteroides fragilis are a major sequela to colonic spillage into the peritoneum. The development of an animal model that closely reproduces the disease observed in humans permitted careful inspection of the cellular and/or humoral contributions to the development and control of this disease. The results obtained thus far describe an immunoregulatory T cell circuit that governs both the development of and the immunity against these abscesses. T cells of CD4+8+ phenotype induce the development of IAA in response to B. fragilis. CD8+ T cells generated in response to immunization with the B. fragilis capsular polysaccharide confer protection against the development of IAA. These cells elaborate an antigen-specific factor that mediates the observed protection by these cells. Moreover, a third type of T cell, a CD8+ cell that is also present in nonimmune individuals, is required for the immune T cell or its factor to confer protection. Thus, in the specific disease process of IAA induced by the encapsulated microorganism B. fragilis, immunity proceeds by cellular and not humoral mechanisms.