Beneficial effect on Salmonella Enteritidis- induced Reactive Arthritis after iNKT cell activation

SARNACKI S; BLANCO G; MORALES, ANDREA; GIACOMODONATO M; CERQUETTI M; NOTO LLANA M; AYA CASTAÑEDA M

Saint malo

Simposio; International Symposium Salmonella and Salmonellosis (I3S); 2016

I3S

Background: Reactive 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.Methods: Adult 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. In addition, mesenteric Th17 population was decreased in number in these animals. Conclusions: Our 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 mainly by Th17 cells.