Tumor necrosis factor receptor p55 deficiency affects the severity of post-Yersinia reactive arthritis

CARGNELUTTI D; ELICABE J; STEFANINI DE GUZMÁN A; DI GENARO S

Mendoza

Congreso; XXIII Reunión Anual de la Sociedad de Biología de Cuyo-2005; 2005

Sociedad de Biología de Cuyo

Tumor necrosis factor (TNF)-a is associated with protection against Yersinia. TNF receptor (TNFR) p55 is the dominant pathway in the majority of known TNF effects. The objective of the present work was to study the role of tumor necrosis factor receptor (TNFR) p55 in the Yersinia-associated arthritis by the use of a murine model of oral Yersinia infection. TNFRp55 deficient (TNFRp55-/-) and C57BL/6 mice were orally infected with 1x107 colony-forming units (CFU) of  Y. enterocolitica serotype O:3. Mice were daily observed and arthritis development was monitored by clinical score, joint assessment, x-ray and examination of histopathology of joints. Higher susceptibility to the infection was observed in TNFRp55-/- mice. In addition, TNFRp55-/- mice developed arthritis since day 14 postinfection with severe inflammation and tarsus deformation on day 55 p.i. Erosion of cartilage and bone was observed in knockout mice on day 39 p.i. Differences in the local and systemic expression of cytokine mRNA was found in TNFRp55-/- mice. The results suggest that TNF signaling through TNFRp55 has a protective role in arthritis induced by oral Yersinia infection. A better understanding of the host factors predisposing to disease will help to the development of specific treatments for reactive arthritis.