Abstract：
:Obliterative bronchiolitis is the major complication affecting long-term lung transplant survivors. Tumor necrosis factor-alpha (TNF-alpha) promotes inflammation and fibrosis in chronic lung injury models. These experiments defined the role of TNF-alpha in an established model of obliterative airway disease (OAD). Rat tracheas were transplanted from Brown-Norway donors into Lewis recipients, and explanted on days 7 and 14. Treated groups received either anti-TNF-alpha antibodies or a novel TNF-alpha translational inhibitor, RDP-58, beginning either immediately or on post-transplant day 7. Morphometry assessed epithelial loss and luminal obliteration, while separate tracheas were processed for TNF-alpha mRNA expression by RQRT-PCR or protein localization/expression by immunohistochemistry. EMSAs evaluated NFkappaB activation. 14-day control allografts averaged 58% occlusion and 98% epithelial loss. These parameters were significantly improved with TNF-alpha inhibition, averaging 32% luminal obliteration and 37% epithelial preservation. TNF-alpha mRNA expression increased at 14-days relative to native tracheas, and was unchanged by RDP-58 treatment. However, TNF-alpha protein expression, localized to the mucosa/submucosa, was markedly reduced with RDP-58, and resulted in diminished global NFkappaB activation in allografts. Delayed RDP treatment reduced disease progression during the second week, as luminal occlusion increased from 26% to only 35%, while respiratory epithelium persisted at 21%. TNF-alpha promotes the development of OAD in tracheal allografts via an NFkappaB-dependent mechanism, and its inhibition may prove beneficial clinically.
journal_name
Exp Mol Patholjournal_title
Experimental and molecular pathologyauthors
Farivar AS,Mackinnon-Patterson B,McCourtie AS,Namkung J,Ward PA,Mulligan MSdoi
10.1016/j.yexmp.2004.10.008keywords:
subject
Has Abstractpub_date
2005-06-01 00:00:00pages
190-7issue
3eissn
0014-4800issn
1096-0945pii
S0014-4800(04)00111-Xjournal_volume
78pub_type
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