Activation of iNKT cells confers protection against Salmonella Enteritidis- induced Reactive Arthritis

NOTO LLANA M; MORALES AL ; SARNACKI SH ; AYA CASTAÑEDA MDR ; GIACOMODONATO MN; CERQUETTI MC

Buenos Aires

Congreso; LXIII Congreso Anual de la Sociedad Argentina de Inmunología.; 2015

BackgroundReactive arthritis (ReA) is a sterile joint inflammation as a sequel to Salmonella gut infection. We have previously 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 has been suggested that Th17 responses are modulated by iNKT cells, therefore, here we analyze the involvement 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 the gastrointestinal route. Studies were performed 5 days after infection. Mesenteric lymph node Th17 population was achieved by flow cytometry after enterocolitis onset. iNKT cell activation and inhibition was studied using alpha-galactosylceramide (a-GalCer) and anti-CD1d monoclonal antibody, respectively. Then, histological tissue evaluation, spleen bacterial load and mesenteric IL-17 expression by qPCR were assessed. Results We found that during S. Enteritidis infection the total number of Th17 cells is increased in mesenteric lymph 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. This beneficial effect of a-GalCer treatment would be related to the decrease in IL-17 produced by cells other than Th17 or iNKT, such as gamma-delta cells.