The Journal of Immunology · 1996 · 122 citations · 0 references
Veterinary MedicineImmunologyMicrobiologyHost-pathogen InteractionsImmunopathologyInflammationBacterial ImmunologyBacterial PathogenesisCytokine BiologyGranulomatous InflammationInnate Immune ResponseInnate Immune Signaling PathwaysCorynebacterial InfectionsCytokine Responses To Bacterial InfectionHost Defense Against Bacterial InfectionImmune Response To Bacterial InfectionInfectious Granulomatous InflammationInflammatory Response To Bacterial InfectionMycobacterial Granulomatous InflammationTumor Necrosis Factor-mediated Granuloma Maintenance
The aim of this study was to examine the role of TNF receptor I (TNF-RI) in the pathogenesis of heat-killed Corynebacterium parvum- and live bacillus Calmette-Guerin (BCG)-induced granulomas. Granuloma formation was analyzed in TNF-RI knockout mice and after treatment with soluble TNF-RI (sTNF-RI). TNF-RI knockout mice injected with C. parvum or BCG developed fewer and smaller granulomas than wild-type control mice. Mice treated with sTNF-RI from days 7 to 13 after injection of C. parvum or BCG developed fewer and smaller granulomas than saline-treated control mice. Established granulomas regressed in rats treated with sTNF-RI from days 10 to 13 after injection of C. parvum. In conclusion, TNF signaling via TNF-RI contributes to the pathogenesis of C. parvum- and BCG-induced granulomas. sTNF-RI inhibits the development of granulomas and can cause the regression of established granulomas.