Apoptosis and Proinflammatory Cytokines Induced in Peyer?s Patches by Attenuated Strains of Salmonella enteritidis.

CERQUETTI MC, GOREN NB, VACCARO MI, SORDELLI DO, GRASSO D, ROPOLO A, AND GIACOMODONATO MN.

Orlando, USA

Congreso; 101st General Meeting of American Society for Microbiology; 2001

American Society for Microbiology

  Temperature sensitive (ts) mutants of S. enteritidis have been used in different animal models to induce protection. C/2/2 and E/1/3 ts mutants of S. enteritidis are highly innocuous when administered orally to mice. Both mutants are able to invade murine Peyer?s Patches (PP), but only E/1/3 strain is protective. In this study we investigated the capacity of protective and non protective mutants of S. enteritidis to induce apoptosis and the release of proinflammatory cytokines in murine PP. Balb/c mice were inoculated orally with 109 CFU/ animal of each mutant, 6 hs later mice were sacrificed and the intestines were removed aseptically. NOS activity was determined by measuring the production of 14C citrulline from 14C arginine. Apoptosis in PP was analyzed using the TUNEL assay. Interleukin (IL) 12, IL18 and IFN-gamma were determined by ELISA. Hyperplasic PP were found in mice inoculated with either strains of S. enteritidis. Apoptosis was observed in PP of inoculated animals as well as in control mice although there were differences in localization. In control mice, apoptosis cells appeared evenly distributed whereas mice inoculated with Salmonella showed apoptosis in the germinal centers. Affected foci in PP of animals inoculated with the protective strain E/1/3 were larger than those observed in mice receiving the non protective mutant C/2/2. The NOS activity measured in animals inoculated with the protective E/1/3 mutant has higher (p<0.05) to that found in mice given the non protective one (706 + 25 vs 318 + 114 pmol/g). The non protective mutant C/2/2 seems to induce a lower or delayed inflammatory response since all cytokines measured 6 hs after inoculation were diminished. Our results suggest that early induction of mucosal inflammatory response may be a main feature of the protective phenotypes of ts mutants of S. enteritidis.