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Ann Thorac Surg 2006;82:2017-2023
© 2006 The Society of Thoracic Surgeons
a Department of Thoracic and Cardiovascular Surgery, Mie University Graduate School of Medicine, Tsu, Japan
b Department of Surgery, Indiana University School of Medicine, Indianapolis, Indiana
Accepted for publication June 19, 2006.
* Address correspondence to Dr Shimamoto, Department of Thoracic and Cardiovascular Surgery, Mie University Graduate School of Medicine, 2-174, Edobashi, Tsu, Mie 514-8507, Japan (Email: jj6jdv{at}clin.medic.mie-u.ac.jp).
Presented at the Poster Session of the Forty-second Annual Meeting of The Society of Thoracic Surgeons, Chicago, IL, Jan 30–Feb 1, 2006.
BACKGROUND: We have previously reported that nuclear factor (NF)-
B activation and inflammatory cytokine expression were involved in the development of lung ischemia-reperfusion injury (LIRI). Because Toll-like receptor 4 (TLR4) activates NF-B-dependent transcription of inflammatory cytokine genes during myocardial ischemia-reperfusion injury, we examined whether absence of TLR4 in TLR4-deficient mice protects against LIRI.
METHODS: Left lungs of wild-type (C57BL/6J) mice or TLR4-null (TLR4–/–) mice were made ischemic for 60 minutes and then reperfused for 180 minutes. Response to injury was quantified by tissue myeloperoxidase activity, vascular permeability ([125I]-bovine serum albumin extravasation), and leukocyte and inflammatory mediator accumulation in bronchoalveolar lavage expression. Lung homogenates were also analyzed for activation of mitogen-activated protein kinases and nuclear translocation of the transcription factors NF-B and activator protein-1.
RESULTS: After LIRI, lungs from TLR4–/– mice demonstrated a 52.4% reduction in vascular permeability (p = 0.001), a 52.6% reduction in lung myeloperoxidase activity (p = 0.006), and a marked reduction in bronchoalveolar lavage leukocyte accumulation when compared with lungs from wild-type mice. The TLR4–/– mice lungs, subjected to LIRI, also demonstrated marked reductions in amounts of several proinflammatory cytokines/chemokines in bronchoalveolar lavage samples. Phosporylation of c-Jun NH2-terminal kinase, and activation of NF-B and activator protein-1 were also significantly reduced in homogenates of lungs from TLR4–/– mice injured by ischemia and reperfusion (p < 0.05).
CONCLUSIONS: These data suggest that TLR4 plays a role in LIRI. Thus, TLR4 may be a potential therapeutic target to minimize ischemic-reperfusion–induced tissue damage and organ dysfunction.
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Ann. Thorac. Surg. 2006 82: 2023.
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