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

ZAP-70 BALB/c (SKG) mice develop reactive arthritis (ReA) after Chlamydia muridarum (Cmu) infection. Since intracellular pathogens enhance their replicative fitness in stressed host cells, we examined how myeloid cells taking up Cmu drive arthritis. Female SKG, Il17a-deficient SKG and were genitally infected with or Luciferase. dissemination was assessed by vivo imaging genomic DNA amplification. Macrophages depleted using clodronate liposomes. Anti-TNF, anti-IL-23p19 administered infection onset. Hspa5, Tgtp1, Il23a, Il17a, Il12b Tnf expression compared mice. One-week post infection, macrophages neutrophils infiltrated the uterus; both carried to spleen. load higher than BALB/c. Macrophage depletion reduced prevented Compared BALB/c, of Il23a Il17a increased uterine splenic neutrophils. Anti-IL-23p19 during deficiency suppressed over-expressed joints within one-week persisted. TNF inhibition at onset Endoplasmic reticulum stress constitutively but induced, immunity-related GTPase, uterus. The is While proinflammatory IL-23 produced contributes initiation Cmu-mediated ReA, macrophage reduces other tissues, tissue burden, suppresses Our data suggest that enhanced bacterial drives production required for persistent