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Aspirin-triggered resolvin D1 reduces mucosal inflammation and promotes resolution in a murine model of acute lung injury.
Mucosal Immunol. 2013 Mar; 6(2):256-66.MI

Abstract

Acute lung injury (ALI) is a severe illness with excess mortality and no specific therapy. Protective actions were recently uncovered for docosahexaenoic acid-derived mediators, including D-series resolvins. Here, we used a murine self-limited model of hydrochloric acid-induced ALI to determine the effects of aspirin-triggered resolvin D1 (AT-RvD1; 7S,8R,17R-trihydroxy-4Z,9E,11E,13Z,15E,19Z-docosahexaenoic acid) on mucosal injury. RvD1 and its receptor ALX/FPR2 were identified in murine lung after ALI. AT-RvD1 (~0.5-5 μg kg(-1)) decreased peak inflammation, including bronchoalveolar lavage fluid (BALF) neutrophils by ~75%. Animals treated with AT-RvD1 had improved epithelial and endothelial barrier integrity and decreased airway resistance concomitant with increased BALF epinephrine levels. AT-RvD1 inhibited neutrophil-platelet heterotypic interactions by downregulating both P-selectin and its ligand CD24. AT-RvD1 also significantly decreased levels of BALF pro-inflammatory cytokines, including interleukin (IL)-1β, IL-6, Kupffer cells, and tumor necrosis factor-α, and decreased nuclear factor-κB-phosphorylated p65 nuclear translocation. Taken together, these findings indicate that AT-RvD1 displays potent mucosal protection and promotes catabasis after ALI.

Authors+Show Affiliations

Pulmonary and Critical Care Medicine, Department of Internal Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

22785226

Citation

Eickmeier, O, et al. "Aspirin-triggered Resolvin D1 Reduces Mucosal Inflammation and Promotes Resolution in a Murine Model of Acute Lung Injury." Mucosal Immunology, vol. 6, no. 2, 2013, pp. 256-66.
Eickmeier O, Seki H, Haworth O, et al. Aspirin-triggered resolvin D1 reduces mucosal inflammation and promotes resolution in a murine model of acute lung injury. Mucosal Immunol. 2013;6(2):256-66.
Eickmeier, O., Seki, H., Haworth, O., Hilberath, J. N., Gao, F., Uddin, M., Croze, R. H., Carlo, T., Pfeffer, M. A., & Levy, B. D. (2013). Aspirin-triggered resolvin D1 reduces mucosal inflammation and promotes resolution in a murine model of acute lung injury. Mucosal Immunology, 6(2), 256-66. https://doi.org/10.1038/mi.2012.66
Eickmeier O, et al. Aspirin-triggered Resolvin D1 Reduces Mucosal Inflammation and Promotes Resolution in a Murine Model of Acute Lung Injury. Mucosal Immunol. 2013;6(2):256-66. PubMed PMID: 22785226.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Aspirin-triggered resolvin D1 reduces mucosal inflammation and promotes resolution in a murine model of acute lung injury. AU - Eickmeier,O, AU - Seki,H, AU - Haworth,O, AU - Hilberath,J N, AU - Gao,F, AU - Uddin,M, AU - Croze,R H, AU - Carlo,T, AU - Pfeffer,M A, AU - Levy,B D, Y1 - 2012/07/11/ PY - 2012/7/13/entrez PY - 2012/7/13/pubmed PY - 2013/7/24/medline SP - 256 EP - 66 JF - Mucosal immunology JO - Mucosal Immunol VL - 6 IS - 2 N2 - Acute lung injury (ALI) is a severe illness with excess mortality and no specific therapy. Protective actions were recently uncovered for docosahexaenoic acid-derived mediators, including D-series resolvins. Here, we used a murine self-limited model of hydrochloric acid-induced ALI to determine the effects of aspirin-triggered resolvin D1 (AT-RvD1; 7S,8R,17R-trihydroxy-4Z,9E,11E,13Z,15E,19Z-docosahexaenoic acid) on mucosal injury. RvD1 and its receptor ALX/FPR2 were identified in murine lung after ALI. AT-RvD1 (~0.5-5 μg kg(-1)) decreased peak inflammation, including bronchoalveolar lavage fluid (BALF) neutrophils by ~75%. Animals treated with AT-RvD1 had improved epithelial and endothelial barrier integrity and decreased airway resistance concomitant with increased BALF epinephrine levels. AT-RvD1 inhibited neutrophil-platelet heterotypic interactions by downregulating both P-selectin and its ligand CD24. AT-RvD1 also significantly decreased levels of BALF pro-inflammatory cytokines, including interleukin (IL)-1β, IL-6, Kupffer cells, and tumor necrosis factor-α, and decreased nuclear factor-κB-phosphorylated p65 nuclear translocation. Taken together, these findings indicate that AT-RvD1 displays potent mucosal protection and promotes catabasis after ALI. SN - 1935-3456 UR - https://www.unboundmedicine.com/medline/citation/22785226/Aspirin_triggered_resolvin_D1_reduces_mucosal_inflammation_and_promotes_resolution_in_a_murine_model_of_acute_lung_injury_ L2 - https://doi.org/10.1038/mi.2012.66 DB - PRIME DP - Unbound Medicine ER -