ArticleThe Journal of experimental medicine2002
Recipient iNOS but not eNOS deficiency reduces luminal narrowing in tracheal allografts.
Article in The Journal of experimental medicine, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
13 citing papers in PubMed, 34 citations in OpenAlex.
- The Role of the Endothelium as a Key Regulator of Chronic Transplant Rejection.Results and problems in cell differentiation · 2026Review
- A bio-adaptive physical hydrogel enables dynamic tissue engineering for tracheal reconstruction.Nature communications · 2025Article
- Monotherapy With Anti-CD70 Antibody Causes Long-Term Mouse Cardiac Allograft Acceptance With Induction of Tolerogenic Dendritic Cells.Frontiers in immunology · 2020Article
- Working toward immune tolerance in lung transplantation.The Journal of clinical investigation · 2014Article
- Complement-mediated microvascular injury leads to chronic rejection.Advances in experimental medicine and biology · 2013Review
- Ecto-5'-nucleotidase (CD73) attenuates allograft airway rejection through adenosine 2A receptor stimulation.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
- Suppression of nitrosative and oxidative stress to reduce cardiac allograft vasculopathy.American journal of physiology. Heart and circulatory physiology · 2009Article
- The complex role of iNOS in acutely rejecting cardiac transplants.Free radical biology & medicine · 2008Review
- Human and murine obliterative bronchiolitis in transplant.Proceedings of the American Thoracic Society · 2007Review
- Obligatory role for interleukin-13 in obstructive lesion development in airway allografts.The American journal of pathology · 2006Article
- Reciprocal regulation of airway rejection by the inducible gas-forming enzymes heme oxygenase and nitric oxide synthase.The Journal of experimental medicine · 2005Article
- BLT1-mediated T cell trafficking is critical for rejection and obliterative bronchiolitis after lung transplantation.The Journal of experimental medicine · 2005Article
- Chemokine-mediated angiogenesis: an essential link in the evolution of airway fibrosis?The Journal of clinical investigation · 2005Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Chronic airway rejection is characterized by prolonged inflammation, epithelial damage, and eventual luminal obliterative bronchiolitis (OB). In cardiac allografts, the inducible nitric oxide synthase (iNOS) promotes acute rejection but paradoxically reduces neointimal formation, the hallmark of chronic rejection. The specific roles of NOS isoforms in modulating lymphocyte traffic and airway rejection are not known. Using a double lumen mouse tracheal transplant model, tracheal grafts from B10.A (allo) or C57BL/6J (iso) mice were transplanted into cyclosporine-treated wild-type (WT) iNOS(-/-) or endothelial NOS (eNOS)(-/-) recipients. OB was observed in WT tracheal allografts at 3 weeks (53 +/- 2% luminal occlusion vs. 17 +/- 1% for isografts, P < 0.05) with sites of obstructive lesion formation coinciding with areas of CD3(+) CD8(+) T cell-rich lymphocytic bronchitis. In contrast, allografts in iNOS(-/-) recipients exhibited reductions in local expression of proinflammatory chemokines and cytokines, graft T cell recruitment and apoptosis, and luminal obliteration (29 +/- 2%, P < 0.05 vs. WT allografts). Recipient eNOS deficiency, however, suppressed neither chemokine expression, lymphocyte infiltration, nor airway occlusion (54 +/- 2%). These data demonstrate that iNOS exacerbates luminal obliteration of airway allografts in contrast with the known suppression by iNOS of cardiac allograft vasculopathy. Because iNOS(-/-) airways transplanted into WT allograft hosts are not protected from rejection, these data suggest that iNOS expressed by graft-infiltrating leukocytes exerts the dominant influence on airway rejection.
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Registered trials
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