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Enhanced Resolution of Hyperoxic Acute Lung Injury as a result of Aspirin Triggered Resolvin D1 Treatment.
Am J Respir Cell Mol Biol. 2015 Sep; 53(3):422-35.AJ

Abstract

Acute lung injury (ALI), which presents as acute respiratory failure, is a major clinical problem that requires aggressive care, and patients who require prolonged oxygen exposure are at risk of developing this disease. Although molecular determinants of ALI have been reported, the molecules involved in disease catabasis associated with oxygen toxicity have not been well studied. It has been reported that lung mucosa is rich in omega-3 fatty acid dicosahexanoic acid (DHA), which has antiinflammatory properties. Aspirin-triggered resolvin D1 (AT-RvD1) is a potent proresolution metabolite of DHA that can curb the inflammatory effects in various acute injuries, yet the effect of AT-RvD1 on hyperoxic acute lung injury (HALI) or in the oxygen toxicity setting in general has not been investigated. The effects of AT-RvD1 on HALI were determined for the first time in 8- to 10-week-old C57BL/6 mice that were exposed to hyperoxia (≥95% O2) for 48 hours. Mice were given AT-RvD1 (100 ng) in saline or a saline vehicle for 24 hours in normoxic (≈21% O2) conditions after hyperoxia. Lung tissue and bronchoalveolar lavage (BAL) fluid were collected for analysis associated with proinflammatory signaling and lung inflammation. AT-RvD1 treatment resulted in reduced oxidative stress, increased glutathione production, and significantly decreased tissue inflammation. AT-RvD1 treatment also significantly reduced the lung wet/dry ratio, protein in BAL fluid, and decreased apoptotic and NF-κB signaling. These results show that AT-RvD1 curbs oxygen-induced lung edema, permeability, inflammation, and apoptosis and is thus an effective therapy for prolonged hyperoxia exposure in this murine model.

Authors+Show Affiliations

Departments of 1 Internal Medicine and. 2 Molecular Medicine, Division of Allergy and Immunology, Morsani College of Medicine, University of South Florida, Tampa, Florida.Departments of 1 Internal Medicine and.Departments of 1 Internal Medicine and.Departments of 1 Internal Medicine and.Departments of 1 Internal Medicine and.Departments of 1 Internal Medicine and.Departments of 1 Internal Medicine and.Departments of 1 Internal Medicine and.Departments of 1 Internal Medicine and. 2 Molecular Medicine, Division of Allergy and Immunology, Morsani College of Medicine, University of South Florida, Tampa, Florida.

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

25647402

Citation

Cox, Ruan, et al. "Enhanced Resolution of Hyperoxic Acute Lung Injury as a Result of Aspirin Triggered Resolvin D1 Treatment." American Journal of Respiratory Cell and Molecular Biology, vol. 53, no. 3, 2015, pp. 422-35.
Cox R, Phillips O, Fukumoto J, et al. Enhanced Resolution of Hyperoxic Acute Lung Injury as a result of Aspirin Triggered Resolvin D1 Treatment. Am J Respir Cell Mol Biol. 2015;53(3):422-35.
Cox, R., Phillips, O., Fukumoto, J., Fukumoto, I., Parthasarathy, P. T., Arias, S., Cho, Y., Lockey, R. F., & Kolliputi, N. (2015). Enhanced Resolution of Hyperoxic Acute Lung Injury as a result of Aspirin Triggered Resolvin D1 Treatment. American Journal of Respiratory Cell and Molecular Biology, 53(3), 422-35. https://doi.org/10.1165/rcmb.2014-0339OC
Cox R, et al. Enhanced Resolution of Hyperoxic Acute Lung Injury as a Result of Aspirin Triggered Resolvin D1 Treatment. Am J Respir Cell Mol Biol. 2015;53(3):422-35. PubMed PMID: 25647402.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Enhanced Resolution of Hyperoxic Acute Lung Injury as a result of Aspirin Triggered Resolvin D1 Treatment. AU - Cox,Ruan,Jr AU - Phillips,Oluwakemi, AU - Fukumoto,Jutaro, AU - Fukumoto,Itsuko, AU - Parthasarathy,Prasanna Tamarapu, AU - Arias,Stephen, AU - Cho,Young, AU - Lockey,Richard F, AU - Kolliputi,Narasaiah, PY - 2015/2/4/entrez PY - 2015/2/4/pubmed PY - 2015/12/15/medline KW - acute lung injury KW - hyperoxia KW - resolvin SP - 422 EP - 35 JF - American journal of respiratory cell and molecular biology JO - Am J Respir Cell Mol Biol VL - 53 IS - 3 N2 - Acute lung injury (ALI), which presents as acute respiratory failure, is a major clinical problem that requires aggressive care, and patients who require prolonged oxygen exposure are at risk of developing this disease. Although molecular determinants of ALI have been reported, the molecules involved in disease catabasis associated with oxygen toxicity have not been well studied. It has been reported that lung mucosa is rich in omega-3 fatty acid dicosahexanoic acid (DHA), which has antiinflammatory properties. Aspirin-triggered resolvin D1 (AT-RvD1) is a potent proresolution metabolite of DHA that can curb the inflammatory effects in various acute injuries, yet the effect of AT-RvD1 on hyperoxic acute lung injury (HALI) or in the oxygen toxicity setting in general has not been investigated. The effects of AT-RvD1 on HALI were determined for the first time in 8- to 10-week-old C57BL/6 mice that were exposed to hyperoxia (≥95% O2) for 48 hours. Mice were given AT-RvD1 (100 ng) in saline or a saline vehicle for 24 hours in normoxic (≈21% O2) conditions after hyperoxia. Lung tissue and bronchoalveolar lavage (BAL) fluid were collected for analysis associated with proinflammatory signaling and lung inflammation. AT-RvD1 treatment resulted in reduced oxidative stress, increased glutathione production, and significantly decreased tissue inflammation. AT-RvD1 treatment also significantly reduced the lung wet/dry ratio, protein in BAL fluid, and decreased apoptotic and NF-κB signaling. These results show that AT-RvD1 curbs oxygen-induced lung edema, permeability, inflammation, and apoptosis and is thus an effective therapy for prolonged hyperoxia exposure in this murine model. SN - 1535-4989 UR - https://www.unboundmedicine.com/medline/citation/25647402/Enhanced_Resolution_of_Hyperoxic_Acute_Lung_Injury_as_a_result_of_Aspirin_Triggered_Resolvin_D1_Treatment_ L2 - https://www.atsjournals.org/doi/10.1165/rcmb.2014-0339OC?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -