Activation of iNKT cells confers protection against Salmonella enterica- induced arthritis

NOTO LLANA M; MORALES, ANDREA; AYA CASTAÑEDA, MR; SARNACKI SH; GIACOMODONATO; CERQUETTI MC

Congreso; Congreso Internacional LASID encuentro IV; 2015

BackgroundReactive arthritis (ReA) is a sterile joint inflammation as a sequel to Salmonella gut infection. We havepreviously demonstrated that the severity of joint lesions is directly related with the intestinal levels of IL-17 generated during S. Enteritidis infection. Th17 lymphocytes are a possible source of IL-17. It hasbeen suggested that Th17 responses are modulated by iNKT cells, therefore, here we analyze theinvolvement of Th17 and iNKT cells on Salmonella-induced ReA.MethodsAdult female BALB/c mice received 3-4 x 103 colony forming units of S. Enteritidis by thegastrointestinal route. Studies were performed 5 days after infection.Mesenteric lymph node Th17 population was achieved by flow cytometry after enterocolitis onset. iNKTcell activation and inhibition was studied using alpha-galactosylceramide (a-GalCer) and anti-CD1dmonoclonal antibody, respectively. Then, histological tissue evaluation, spleen bacterial load andmesenteric IL-17 expression by qPCR were assessed. Results We found that during S. Enteritidis infection the total number of Th17 cells is increased in mesentericlymph nodes. Infected mice treated with a-GalCer showed a reduction in spleen bacterial load,diminished intestinal and joint lesions concomitantly with a significant decrease in mesenteric IL-17.Surprisingly, mesenteric Th17 population was augmented in these animals. ConclusionsOur results indicate that activation of iNKT cells renders protection against Salmonella ReA. Thisbeneficial effect of a-GalCer treatment would be related to the decrease in IL-17 produced by cells otherthan Th17 or iNKT, such as gamma-delta cells.