RT Journal Article
SR Electronic
T1 Repression of Bleomycin-Induced Pneumopathy by TNF
JF The Journal of Immunology
JO J. Immunol.
FD American Association of Immunologists
SP 567
OP 574
DO 10.4049/jimmunol.170.1.567
VO 170
IS 1
A1 Kuroki, Misuzu
A1 Noguchi, Yuji
A1 Shimono, Michihide
A1 Tomono, Kazunori
A1 Tashiro, Takayoshi
A1 Obata, Yuichi
A1 Nakayama, Eiichi
A1 Kohno, Shigeru
YR 2003
UL http://www.jimmunol.org/content/170/1/567.abstract
AB Idiopathic pulmonary fibrosis is a chronic inflammatory lung disease with interstitial fibrosis. As a potent proinflammatory cytokine, TNF has been suggested to play critical roles in the pathogenesis of the human disease and its animal model, bleomycin-induced pneumopathy. However, studies using TNF-deficient mice have demonstrated that TNF also has an anti-inflammatory function. To determine the role of TNF in pulmonary inflammation induced by bleomycin, we injected bleomycin intratracheally into TNF-deficient mice. In this study, we demonstrated persistent and intense inflammation in TNF-deficient mice due to reduced apoptosis of inflammatory cells. We also showed that in TNF-deficient mice, challenge via airways with murine, but not human rTNF, efficiently eliminated inflammatory cells from the bronchoalveolar space by apoptosis, and thus promoted tissue repair of damaged lungs. Contrary to previous reports that showed that TNF was a central mediator of pulmonary inflammation, we have demonstrated that TNF is essential for repressing pulmonary inflammation in bleomycin-induced pneumopathy.