RESUMO
AIM: To assess the role of thermolabile enterotoxin of Enterobacter cloacae on level of caspases 3, 7, and 10 in experiment. MATERIALS AND METHODS: Observation of apoptosis in mice splenocytes and peritoneal exudate cells. Experimental infection was created by intraperitoneal injection of live bacteria and cultural fluid of E. cloacae producing thermolabile enterotoxin. RESULTS: The study showed that thermolabile enterotoxin of E. cloacae does not have equal effect on apoptosis of studied cells: it slows apoptosis of splenocytes and virtually does not have any influence on peritoneal phagocytes. CONCLUSION: Apoptosis of infected cells is a protective reaction of microorganism to invasion of infectious agent. Cell death leads to rapid elimination of pathogenic agent. Furthermore, cell death by apoptosis compared to necrosis is more favorable for bacteria because it is not induce inflammatory reactions. In our experiments thermolabile enterotoxin of E. cloacae had had antiapoptogenic effect on mice splenocytes that could be a key element in pathogenesis of diseases caused by enterotoxin-producing strains of Enterobacter.
