engleski

Experimental campylobacteriosis in C57Bl/6 mice

Campylobacter jejuni is, today, recognized as one of the most frequently reported cause of acute inflammatory gastroenteritis in man. Because the lack of appropriate animal model the mechanisms involved in the pathogenesis and immunological response of the host to campylobacteriosis are still poorly understood. In this study, on the established experimental model of murine campylobacteriosis, we investigated the role of T lymphocytes and NK cells in the course of primary C. jejuni infection. We enumerated bacteria in the livers and spleens of challanged control and mice which were, in vivo, depleted of either CD4+, CD8+ or NK cells by intraperitoneal administration of appropriate monoclonal antibodies (mAb). In the immunocompetent animals the sterile clearance of bacteria from their spleens was achieved ten days and from the livers two weeks after infection. Results after in vivo administration of anti-CD4 mAb, anti-CD8 mAb or anti-NK 1.1.+ mAb showed that mice remained capable of resolving primary C. jejuni infection, but the duration was prolonged and bacterial titres were significantlly higher in livers, especially in the case of NK cells depletion. Lack of CD8+ lymphocytes and NK cells prolonged the course and increased the number of C. jejuni in the spleen of infected mice. The results show that cellular immunity may play a role in host defence against C. jejuni what has to be futher elucidated.

Campylobacter; mice; experimental

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