Articular expresion of TLR2 and TLR4 mRNA in Yersinia induced arthritis

JAVIER ELICABE, DIEGO CASTRO, DIEGO CARGNELUTTI, JÈSICA GUTIÈRREZ, SILVIA DI GENARO.

Salvador Bahia, Brasil

Congreso; Recent Advances in Pattern Recognition. Toll 2006; 2006

University of Massachusetts Medical School

Reactive arthritis (ReA) is a chronic, sterile synovitis that develops after infections such as by Yersinia enterocolitica. The pathogenesis of ReA is incompletely understood. We studied the role of IL-12p40 in Yersinia-induced ReA, and investigated the presence of microbial antigens and expression of TLR2, TLR4 and TNF-a mRNA in the joint. Wild-type and IL-12p40 deficient (IL-12p40-/-) C57BL/6 mice were orogastrically infected with Y. enterocolitica O:3. The number of bacteria was determined in Peyer’s patches (PP), mesenteric lymph nodes (MLN), spleen and joint. Histologic changes in the joint were examined. Antibodies against collagens and Yersinia were measured by ELISA. Induction of articular mRNA of TLR2, TLR4, and TNF-a was analyzed by RT-PCR. Yersinia antigens in the joint were studied by dot-blot. At day 3, bacterial recovery in spleen, PP and MLN was significantly increased in IL-12p40-/- mice. Histopathological changes were observed in IL-12p40-/- mice at day 21, and correlated with higher anti-type II collagen antibody response. Although live bacteria could not be isolated at day 21, Yersinia outer membrane (OM) antigens were detected in the joint. Articular antibodies to Yersinia antigens were significantly higher in IL-12p40-/- mice. Expression of TLR2, TLR4 and TNF-a mRNA was increased in joints from infected IL-12p40-/- mice. We concluded that IL-12 influences the resistance against Yersinia-triggered ReA. Bacterial products in the joint could contribute to ReA by induction of TLR expression.