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Early tumor necrosis factor-alpha release from the pulmonary macrophage in lung ischemia-reperfusion injury.
J Thorac Cardiovasc Surg. 2004 May; 127(5):1502-8.JT

Abstract

OBJECTIVE

Tumor necrosis factor-alpha is a proinflammatory mediator required for the development of experimental lung ischemia-reperfusion injury. The alveolar macrophage is a rich source of tumor necrosis factor-alpha in multiple models of acute lung injury. The present study was undertaken to determine whether the alveolar macrophage is an important source of tumor necrosis factor-alpha in lung ischemia-reperfusion injury and whether suppression of its function protects against injury.

METHODS

Left lungs of Long-Evans rats underwent normothermic ischemia for 90 minutes and reperfusion for up to 4 hours. Treated animals received gadolinium chloride, a rare earth metal that inhibits macrophage function. Injury was quantitated via lung tissue neutrophil accumulation (myeloperoxidase content), lung vascular permeability, and bronchoalveolar lavage fluid leukocyte, cytokine, and chemokine content. Separate samples were generated for immunohistochemistry.

RESULTS

Tumor necrosis factor-alpha secretion occurred at 15 minutes of reperfusion and was localized to the alveolar macrophage by immunohistochemistry. In gadolinium-treated animals, lung vascular permeability was reduced by 66% at 15 minutes (P <.03) of reperfusion and by 34% at 4 hours (P <.02) of reperfusion. Suppression of macrophage function resulted in a 35% reduction in lung myeloperoxidase content (P <.03) and similar reductions in bronchoalveolar lavage leukocyte accumulation. Tumor necrosis factor-alpha and microphage inflammatory protein-1alpha protein levels were markedly reduced in the bronchoalveolar lavage of gadolinium-treated animals by enzyme-linked immunosorbent assay.

CONCLUSIONS

The alveolar macrophage secretes tumor necrosis factor-alpha protein by 15 minutes of reperfusion, which orchestrates the early events that eventually result in lung ischemia-reperfusion injury at 4 hours. Gadolinium pretreatment markedly reduces tumor necrosis factor-alpha elaboration, resulting in significant protection against lung ischemia-reperfusion injury.

Authors+Show Affiliations

Division of Cardiothoracic Surgery, Department of Surgery, University of Washington Medical Center, Seattle 98195, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

15116014

Citation

Naidu, Babu V., et al. "Early Tumor Necrosis Factor-alpha Release From the Pulmonary Macrophage in Lung Ischemia-reperfusion Injury." The Journal of Thoracic and Cardiovascular Surgery, vol. 127, no. 5, 2004, pp. 1502-8.
Naidu BV, Woolley SM, Farivar AS, et al. Early tumor necrosis factor-alpha release from the pulmonary macrophage in lung ischemia-reperfusion injury. J Thorac Cardiovasc Surg. 2004;127(5):1502-8.
Naidu, B. V., Woolley, S. M., Farivar, A. S., Thomas, R., Fraga, C. H., Goss, C. H., & Mulligan, M. S. (2004). Early tumor necrosis factor-alpha release from the pulmonary macrophage in lung ischemia-reperfusion injury. The Journal of Thoracic and Cardiovascular Surgery, 127(5), 1502-8.
Naidu BV, et al. Early Tumor Necrosis Factor-alpha Release From the Pulmonary Macrophage in Lung Ischemia-reperfusion Injury. J Thorac Cardiovasc Surg. 2004;127(5):1502-8. PubMed PMID: 15116014.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Early tumor necrosis factor-alpha release from the pulmonary macrophage in lung ischemia-reperfusion injury. AU - Naidu,Babu V, AU - Woolley,Steven M, AU - Farivar,Alexander S, AU - Thomas,Robert, AU - Fraga,Charles H, AU - Goss,Christopher H, AU - Mulligan,Michael S, PY - 2004/4/30/pubmed PY - 2004/6/2/medline PY - 2004/4/30/entrez SP - 1502 EP - 8 JF - The Journal of thoracic and cardiovascular surgery JO - J Thorac Cardiovasc Surg VL - 127 IS - 5 N2 - OBJECTIVE: Tumor necrosis factor-alpha is a proinflammatory mediator required for the development of experimental lung ischemia-reperfusion injury. The alveolar macrophage is a rich source of tumor necrosis factor-alpha in multiple models of acute lung injury. The present study was undertaken to determine whether the alveolar macrophage is an important source of tumor necrosis factor-alpha in lung ischemia-reperfusion injury and whether suppression of its function protects against injury. METHODS: Left lungs of Long-Evans rats underwent normothermic ischemia for 90 minutes and reperfusion for up to 4 hours. Treated animals received gadolinium chloride, a rare earth metal that inhibits macrophage function. Injury was quantitated via lung tissue neutrophil accumulation (myeloperoxidase content), lung vascular permeability, and bronchoalveolar lavage fluid leukocyte, cytokine, and chemokine content. Separate samples were generated for immunohistochemistry. RESULTS: Tumor necrosis factor-alpha secretion occurred at 15 minutes of reperfusion and was localized to the alveolar macrophage by immunohistochemistry. In gadolinium-treated animals, lung vascular permeability was reduced by 66% at 15 minutes (P <.03) of reperfusion and by 34% at 4 hours (P <.02) of reperfusion. Suppression of macrophage function resulted in a 35% reduction in lung myeloperoxidase content (P <.03) and similar reductions in bronchoalveolar lavage leukocyte accumulation. Tumor necrosis factor-alpha and microphage inflammatory protein-1alpha protein levels were markedly reduced in the bronchoalveolar lavage of gadolinium-treated animals by enzyme-linked immunosorbent assay. CONCLUSIONS: The alveolar macrophage secretes tumor necrosis factor-alpha protein by 15 minutes of reperfusion, which orchestrates the early events that eventually result in lung ischemia-reperfusion injury at 4 hours. Gadolinium pretreatment markedly reduces tumor necrosis factor-alpha elaboration, resulting in significant protection against lung ischemia-reperfusion injury. SN - 0022-5223 UR - https://www.unboundmedicine.com/medline/citation/15116014/Early_tumor_necrosis_factor_alpha_release_from_the_pulmonary_macrophage_in_lung_ischemia_reperfusion_injury_ DB - PRIME DP - Unbound Medicine ER -