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Protective actions of aspirin-triggered (17R) resolvin D1 and its analogue, 17R-hydroxy-19-para-fluorophenoxy-resolvin D1 methyl ester, in C5a-dependent IgG immune complex-induced inflammation and lung injury.
J Immunol. 2014 Oct 01; 193(7):3769-78.JI

Abstract

Increasing evidence suggests that the novel anti-inflammatory and proresolving mediators such as the resolvins play an important role during inflammation. However, the functions of these lipid mediators in immune complex-induced lung injury remain unknown. In this study, we determined the role of aspirin-triggered resolvin D1 (AT-RvD1) and its metabolically stable analog, 17R-hydroxy-19-para-fluorophenoxy-resolvin D1 methyl ester (p-RvD1), in IgG immune complex-induced inflammatory responses in myeloid cells and injury in the lung. We show that lung vascular permeability in the AT-RvD1- or p-RvD1-treated mice was significantly reduced when compared with values in mice receiving control vesicle during the injury. Furthermore, i.v. administration of either AT-RvD1 or p-RvD1 caused significant decreases in the bronchoalveolar lavage fluid contents of neutrophils, inflammatory cytokines, and chemokines. Of interest, AT-RvD1 or p-RvD1 significantly reduced bronchoalveolar lavage fluid complement C5a level. By EMSA, we demonstrate that IgG immune complex-induced activation of NF-κB and C/EBPβ transcription factors in the lung was significantly inhibited by AT-RvD1 and p-RvD1. Moreover, AT-RvD1 dramatically mitigates IgG immune complex-induced NF-κB and C/EBP activity in alveolar macrophages. Also, secretion of TNF-α, IL-6, keratinocyte cell-derived chemokine, and MIP-1α from IgG immune complex-stimulated alveolar macrophages or neutrophils was significantly decreased by AT-RvD1. These results suggest a new approach to the blocking of immune complex-induced inflammation.

Authors+Show Affiliations

Department of Anesthesiology, Perioperative, and Pain Medicine, Center for Experimental Therapeutics and Reperfusion Injury, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115; Zhejiang Respiratory Drugs Research Laboratory of the State Food and Drug Administration of China, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310058, China;Department of Anesthesiology, Perioperative, and Pain Medicine, Center for Experimental Therapeutics and Reperfusion Injury, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115;Department of Anesthesiology, Perioperative, and Pain Medicine, Center for Experimental Therapeutics and Reperfusion Injury, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115;Department of Chemistry, University of Southern California, Los Angeles, CA 90089; and Loker Hydrocarbon Research Institute, University of Southern California, Los Angeles, CA 90089.Department of Anesthesiology, Perioperative, and Pain Medicine, Center for Experimental Therapeutics and Reperfusion Injury, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115; hgao@zeus.bwh.harvard.edu cnserhan@zeus.bwh.harvard.edu.Department of Anesthesiology, Perioperative, and Pain Medicine, Center for Experimental Therapeutics and Reperfusion Injury, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115; hgao@zeus.bwh.harvard.edu cnserhan@zeus.bwh.harvard.edu.

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

25172497

Citation

Tang, Huifang, et al. "Protective Actions of Aspirin-triggered (17R) Resolvin D1 and Its Analogue, 17R-hydroxy-19-para-fluorophenoxy-resolvin D1 Methyl Ester, in C5a-dependent IgG Immune Complex-induced Inflammation and Lung Injury." Journal of Immunology (Baltimore, Md. : 1950), vol. 193, no. 7, 2014, pp. 3769-78.
Tang H, Liu Y, Yan C, et al. Protective actions of aspirin-triggered (17R) resolvin D1 and its analogue, 17R-hydroxy-19-para-fluorophenoxy-resolvin D1 methyl ester, in C5a-dependent IgG immune complex-induced inflammation and lung injury. J Immunol. 2014;193(7):3769-78.
Tang, H., Liu, Y., Yan, C., Petasis, N. A., Serhan, C. N., & Gao, H. (2014). Protective actions of aspirin-triggered (17R) resolvin D1 and its analogue, 17R-hydroxy-19-para-fluorophenoxy-resolvin D1 methyl ester, in C5a-dependent IgG immune complex-induced inflammation and lung injury. Journal of Immunology (Baltimore, Md. : 1950), 193(7), 3769-78. https://doi.org/10.4049/jimmunol.1400942
Tang H, et al. Protective Actions of Aspirin-triggered (17R) Resolvin D1 and Its Analogue, 17R-hydroxy-19-para-fluorophenoxy-resolvin D1 Methyl Ester, in C5a-dependent IgG Immune Complex-induced Inflammation and Lung Injury. J Immunol. 2014 Oct 1;193(7):3769-78. PubMed PMID: 25172497.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Protective actions of aspirin-triggered (17R) resolvin D1 and its analogue, 17R-hydroxy-19-para-fluorophenoxy-resolvin D1 methyl ester, in C5a-dependent IgG immune complex-induced inflammation and lung injury. AU - Tang,Huifang, AU - Liu,Yanlan, AU - Yan,Chunguang, AU - Petasis,Nicos A, AU - Serhan,Charles N, AU - Gao,Hongwei, Y1 - 2014/08/29/ PY - 2014/8/31/entrez PY - 2014/8/31/pubmed PY - 2014/11/15/medline SP - 3769 EP - 78 JF - Journal of immunology (Baltimore, Md. : 1950) JO - J Immunol VL - 193 IS - 7 N2 - Increasing evidence suggests that the novel anti-inflammatory and proresolving mediators such as the resolvins play an important role during inflammation. However, the functions of these lipid mediators in immune complex-induced lung injury remain unknown. In this study, we determined the role of aspirin-triggered resolvin D1 (AT-RvD1) and its metabolically stable analog, 17R-hydroxy-19-para-fluorophenoxy-resolvin D1 methyl ester (p-RvD1), in IgG immune complex-induced inflammatory responses in myeloid cells and injury in the lung. We show that lung vascular permeability in the AT-RvD1- or p-RvD1-treated mice was significantly reduced when compared with values in mice receiving control vesicle during the injury. Furthermore, i.v. administration of either AT-RvD1 or p-RvD1 caused significant decreases in the bronchoalveolar lavage fluid contents of neutrophils, inflammatory cytokines, and chemokines. Of interest, AT-RvD1 or p-RvD1 significantly reduced bronchoalveolar lavage fluid complement C5a level. By EMSA, we demonstrate that IgG immune complex-induced activation of NF-κB and C/EBPβ transcription factors in the lung was significantly inhibited by AT-RvD1 and p-RvD1. Moreover, AT-RvD1 dramatically mitigates IgG immune complex-induced NF-κB and C/EBP activity in alveolar macrophages. Also, secretion of TNF-α, IL-6, keratinocyte cell-derived chemokine, and MIP-1α from IgG immune complex-stimulated alveolar macrophages or neutrophils was significantly decreased by AT-RvD1. These results suggest a new approach to the blocking of immune complex-induced inflammation. SN - 1550-6606 UR - https://www.unboundmedicine.com/medline/citation/25172497/Protective_actions_of_aspirin_triggered__17R__resolvin_D1_and_its_analogue_17R_hydroxy_19_para_fluorophenoxy_resolvin_D1_methyl_ester_in_C5a_dependent_IgG_immune_complex_induced_inflammation_and_lung_injury_ L2 - http://www.jimmunol.org/cgi/pmidlookup?view=long&pmid=25172497 DB - PRIME DP - Unbound Medicine ER -