Mediation of Interleukin‐23 and Tumor Necrosis Factor–Driven Reactive Arthritis by <i>Chlamydia</i>‐Infected Macrophages in SKG Mice

Abstract

C muridarum load is higher in SKG mice than in BALB/c mice. Whereas proinflammatory IL-23 produced by neutrophils contributes to the initiation of C muridarum-mediated ReA, macrophage depletion reduces C muridarum dissemination to other tissues, tissue burden, and the development of arthritis. TNF inhibition was also shown to suppress arthritis development. Our data suggest that enhanced bacterial dissemination in macrophages of SKG mice drives the TNF production needed for persistent arthritis.