Salmonella enterica induces joint inflammation and the expression of IL-17 in draining lymph nodes early after the onset of enterocolitis in mice.

MARIANGELES NOTO LLANA; SEBASTIAN HERNAN SARNACKI; MARIA VICTORIA VAZQUEZ; ALEJANDRA SONIA GARTNER; MONICA NANCY GIACOMODONATO; MARIA CRISTINA CERQUETTI

INFECTION AND IMMUNITY

AMER SOC MICROBIOLOGY

Lugar: Washington; Año: 2012 vol. 80 p. 2231 - 2239

0019-9567

In developing countries, one third of reactive arthritis (ReA) cases are associated with Salmonella enterocolitis, nevertheless there is no animal model for studying this pathology. Here we induced a self-limiting Salmonella enterica serovar Enteritidis enterocolitis in mice to analyze the onset of ReA. BALB/c mice received orally 20 ug of streptomycin 24 h before intragastric inoculation of a low dose (3-4 x 103 CFU) of S. Enteritidis. In response to Salmonella infection, a 30-fold increase in the expression of  IL-17, measured by qPCR, was observed in mesenteric lymph nodes 5 days post infection. At this time synovitis was already evident and concomitantly a significant increase in joint TNF-á was detected by ELISA. The early development of joint lesions was accompanied by an increased expression of IL-17 in inguinal and popliteal lymph nodes. Infection with 107 CFU of an isogenic ÄinvG mutant bearing a defective TTSS- 1 induced enterocolitis histologically similar to that triggered by the wild type strain. Interestingly, despite the higher infective dose used, the mutant did not trigger intestinal IL-17. Moreover, no synovitis was observed in mice suffering ÄinvG enterocolitis. Neutralization of IL-17 in mice infected with S. Enteritidis prevented both synovitis and the increment of TNF-á in the joints suggesting that IL-17 participates in the generation of Salmonella-induced ReA through the induction of TNF-á in the joints.