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

ELICABE J; GUTIERREZ Y; CASTRO D; CARGNELUTTI D.E.; AGUILERA C; BERNARDI A; GOMEZ N; STEFANINI DE GUZMAN A; DI GENARO S

San Luis –Argentina

Congreso; XXII Annual Scientific Meeting, Cuyo Biology Ssociety; 2004

Sociedad de Biología de Cuyo

Interleukin 12 (IL-12) is a cytokine which plays an important role in early innate resitance to bacterial infection. Yersinia enterocolitica causes reactive arthritis (ARe) as a complication of the gastrointestinal infection. Y. enterocolitica O:3 is the most frequent Yersinia arthritogenic serotype in human. This work studied the impact of IL-12 deficiency on early stage of Y. enterocolitica O:3 arthritis. IL-12 knockout (IL-12 -/-) 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  joint and bacterial clearance. Spleen cell proliferation in response to Yersinia lipopolisaccharide (LPS), concanavalin A (ConA) or heat-killed Yersiniae (HKY) were studied. Histological analysis showed histopathological changes in the joints of IL-12 -/- mice. In these animals, dilations 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, Peyers patches and mesenteric lymphid 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 plays a role in early protective host responses after  Y. enterocolitica O:3 infection.