Impact of IL-12 deficiency in early stage of Yersinia enterocolitica O:3 arthritis.

ELICABE J; GUTIERREZ J; CASTRO D,; CARGNELUTTI D; AGUILERA C; BERNARDI A; GOMEZ N; STEFANINI DE GUZMÁN A; DI GENARO S

Merlo, San Luis

Congreso; XXII Reunión anual de la Sociedad de Biología de Cuyo; 2004

Sociedad de Biología de Cuyo

Interleuquina 12 (IL-12) is a cytokine, playing an important role in early innate resistance to bacterial infection. Yersinia enterocolitica  causes reactive arthritis (ReA) as a complication of the gastrointestinal infection. Y. enterocolitica O:3 has been described as the most frequent Yersinia arthritogenic  serotype  in humans. The objective of the present work was to study the impact of  IL-12 deficiency in early stage of Y. enterocolitica O:3 arthritis.  IL-12 knockout (IL12--/-) mice and normal C57BL/6 mice were orogastrically infected  with 7 x 108 UFC of Y. enterocolitica O:3. Mice were sacrificed at day 3 postinfection for examination of histopathology of joints and bacterial clearance. Spleen cell proliferation in response to Yersinia lipopolisaccharide (LPS), concanavalin A (ConA) or heat-killed yersiniae (HKY) was studied.  The histological analysis showed histopathological changes in the joints of  IL-12-/- mice. In these animals, dilation of the joint cavity, luminal disorganization and desquamation of the synovial membrane, decrease in synoviocyte number, and  slight mononuclear infiltration were observed. Joint pathology in IL-12-/- correlated with higher bacterial load in the spleen, Peyer‘s patches and mesenteric lymphoid nodes. Impaired proliferation in response to ConA, LPS or HKY  was observed in IL-12-/-.  This study indicates that IL-12 controls the severity of Yersinia-induced arthritis and play a role in early protective host responses after Y. enterocolitica O:3 infection.