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 μg of
streptomycin 24 h before intragastric inoculation of a low dose (3 × 10(3) to 4 × 10(3) CFU) of S. Enteritidis. In response to
Salmonella infection, a 30-fold increase in the expression of
interleukin-17 (IL-17), measured by quantitative PCR, was observed in mesenteric lymph nodes 5 days postinfection. At this time
synovitis was already evident, and concomitantly, a significant increase in joint
tumor necrosis factor alpha (TNF-α) was detected by
enzyme-linked
immunosorbent assay (ELISA). The early development of joint lesions was accompanied by an increased expression of
IL-17 in inguinal and popliteal lymph nodes.
Infection with 10(7) CFU of an isogenic ΔinvG mutant bearing a defective
type III secretion system of Salmonella encoded in the pathogenicity island 1 apparatus (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 ΔinvG
enterocolitis. Neutralization of
IL-17 in mice infected with S. Enteritidis prevented both
synovitis and the increment of TNF-α in the joints, suggesting that
IL-17 participates in the generation of Salmonella-induced ReA through the induction of TNF-α in the joints.