| First Author | Noto Llana M | Year | 2012 |
| Journal | Infect Immun | Volume | 80 |
| Issue | 6 | Pages | 2231-9 |
| PubMed ID | 22493084 | Mgi Jnum | J:186521 |
| Mgi Id | MGI:5432466 | Doi | 10.1128/IAI.00324-12 |
| Citation | Noto Llana M, et al. (2012) Salmonella enterica induces joint inflammation and expression of interleukin-17 in draining lymph nodes early after onset of enterocolitis in mice. Infect Immun 80(6):2231-9 |
| abstractText | 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 mug of streptomycin 24 h before intragastric inoculation of a low dose (3 x 10(3) to 4 x 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-alpha) 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 DeltainvG 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 DeltainvG enterocolitis. Neutralization of IL-17 in mice infected with S. Enteritidis prevented both synovitis and the increment of TNF-alpha in the joints, suggesting that IL-17 participates in the generation of Salmonella-induced ReA through the induction of TNF-alpha in the joints. |
