LXA4 Inhibits Lipopolysaccharide-Induced Inflammatory Cell Accumulation by Resident Macrophages in Mice

Hong-Xia Mei, Yang Ye, Hao-Ran Xu, Shu-Yang Xiang, Qian Yang, Hong-Yu Ma, Sheng-Wei Jin, Qian Wang Department of Anesthesia and Critical Care, The Second Afﬁliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 325027, People’s Republic...

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Autores principales:	Mei HX, Ye Y, Xu HR, Xiang SY, Yang Q, Ma HY, Jin SW, Wang Q
Formato:	article
Lenguaje:	EN
Publicado:	Dove Medical Press 2021
Materias:	resident macrophage recruited macrophage neutrophil lipoxin a4 lipopolysaccharide Pathology RB1-214 Therapeutics. Pharmacology RM1-950
Acceso en línea:	https://doaj.org/article/fa63d4c6674b42a4a6f2844b65334c63
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spelling	oai:doaj.org-article:fa63d4c6674b42a4a6f2844b65334c632021-12-02T14:15:10ZLXA4 Inhibits Lipopolysaccharide-Induced Inflammatory Cell Accumulation by Resident Macrophages in Mice1178-7031https://doaj.org/article/fa63d4c6674b42a4a6f2844b65334c632021-04-01T00:00:00Zhttps://www.dovepress.com/lxa4-inhibits-lipopolysaccharide-induced-inflammatory-cell-accumulatio-peer-reviewed-article-JIRhttps://doaj.org/toc/1178-7031Hong-Xia Mei, Yang Ye, Hao-Ran Xu, Shu-Yang Xiang, Qian Yang, Hong-Yu Ma, Sheng-Wei Jin, Qian Wang Department of Anesthesia and Critical Care, The Second Afﬁliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 325027, People’s Republic of ChinaCorrespondence: Sheng-Wei Jin; Qian WangDepartment of Anesthesia and Critical Care, The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, 109 Xueyuan Road, Wenzhou, Zhejiang Province, 325027, People’s Republic of ChinaTel +86-577-88002806Fax +86-577-88832693Email jinshengwei69@163.com; wqian84@163.comIntroduction: Alveolar macrophages that regulate the inflammatory response in lungs are the main target cell for the treatment of inflammatory pulmonary pathologies, such as acute respiratory distress syndrome (ARDS). Yolk sac derived alveolar resident macrophages play an important role in the pulmonary inflammatory response. With regards to anti-inflammatory actions, lipoxin A4 (LXA4) has been identified as an inflammatory “braking signal”.Methods: In vivo, LXA4 (0.1 μg/mouse) was injected intraperitoneally after intratracheal (1 mg/kg) lipopolysaccharide (LPS) administration; flow cytometry was used to measure peripheral blood monocyte derived recruited macrophage and neutrophil numbers; resident alveolar macrophage was depleted by liposome clodronate; CXCL2, CCL2, MMP9 level was detected by RT-PCR and ELISA. In vitro, sorted resident macrophages (1× 106) were cultured with LPS (1 μg/mL) and LXA4 (100 nmol/mL) with or without BOC-2 (10 μM) for 24 h to gain a better understanding of the mechanisms of LXA4.Results: LXA4 inhibited tumor necrosis factor-a (TNF-a) and interleukin-1β (IL-1β) production induced by LPS. LXA4 also mediated LPS-induced macrophage recruitment and showed that this was dependent on CCL2 secretion and release by resident macrophages. LXA4 protects lung tissue by inhibiting neutrophil recruitment, partly through the CXCL2/MMP-9 signaling pathway. CXCL2 and MMP-9 are mainly expressed by resident macrophages and neutrophils, respectively. Finally, LXA4’s beneficial effects were abrogated by BOC-2, an LXA4 receptor inhibitor.Conclusion: These results suggest that LXA4 may be a promising therapy for preventing and treating ARDS.Keywords: resident macrophage, recruited macrophage, neutrophil, lipoxin A4, lipopolysaccharideMei HXYe YXu HRXiang SYYang QMa HYJin SWWang QDove Medical Pressarticleresident macrophagerecruited macrophageneutrophillipoxin a4lipopolysaccharidePathologyRB1-214Therapeutics. PharmacologyRM1-950ENJournal of Inflammation Research, Vol Volume 14, Pp 1375-1385 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	resident macrophage recruited macrophage neutrophil lipoxin a4 lipopolysaccharide Pathology RB1-214 Therapeutics. Pharmacology RM1-950
spellingShingle	resident macrophage recruited macrophage neutrophil lipoxin a4 lipopolysaccharide Pathology RB1-214 Therapeutics. Pharmacology RM1-950 Mei HX Ye Y Xu HR Xiang SY Yang Q Ma HY Jin SW Wang Q LXA4 Inhibits Lipopolysaccharide-Induced Inflammatory Cell Accumulation by Resident Macrophages in Mice
description	Hong-Xia Mei, Yang Ye, Hao-Ran Xu, Shu-Yang Xiang, Qian Yang, Hong-Yu Ma, Sheng-Wei Jin, Qian Wang Department of Anesthesia and Critical Care, The Second Afﬁliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 325027, People’s Republic of ChinaCorrespondence: Sheng-Wei Jin; Qian WangDepartment of Anesthesia and Critical Care, The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, 109 Xueyuan Road, Wenzhou, Zhejiang Province, 325027, People’s Republic of ChinaTel +86-577-88002806Fax +86-577-88832693Email jinshengwei69@163.com; wqian84@163.comIntroduction: Alveolar macrophages that regulate the inflammatory response in lungs are the main target cell for the treatment of inflammatory pulmonary pathologies, such as acute respiratory distress syndrome (ARDS). Yolk sac derived alveolar resident macrophages play an important role in the pulmonary inflammatory response. With regards to anti-inflammatory actions, lipoxin A4 (LXA4) has been identified as an inflammatory “braking signal”.Methods: In vivo, LXA4 (0.1 μg/mouse) was injected intraperitoneally after intratracheal (1 mg/kg) lipopolysaccharide (LPS) administration; flow cytometry was used to measure peripheral blood monocyte derived recruited macrophage and neutrophil numbers; resident alveolar macrophage was depleted by liposome clodronate; CXCL2, CCL2, MMP9 level was detected by RT-PCR and ELISA. In vitro, sorted resident macrophages (1× 106) were cultured with LPS (1 μg/mL) and LXA4 (100 nmol/mL) with or without BOC-2 (10 μM) for 24 h to gain a better understanding of the mechanisms of LXA4.Results: LXA4 inhibited tumor necrosis factor-a (TNF-a) and interleukin-1β (IL-1β) production induced by LPS. LXA4 also mediated LPS-induced macrophage recruitment and showed that this was dependent on CCL2 secretion and release by resident macrophages. LXA4 protects lung tissue by inhibiting neutrophil recruitment, partly through the CXCL2/MMP-9 signaling pathway. CXCL2 and MMP-9 are mainly expressed by resident macrophages and neutrophils, respectively. Finally, LXA4’s beneficial effects were abrogated by BOC-2, an LXA4 receptor inhibitor.Conclusion: These results suggest that LXA4 may be a promising therapy for preventing and treating ARDS.Keywords: resident macrophage, recruited macrophage, neutrophil, lipoxin A4, lipopolysaccharide
format	article
author	Mei HX Ye Y Xu HR Xiang SY Yang Q Ma HY Jin SW Wang Q
author_facet	Mei HX Ye Y Xu HR Xiang SY Yang Q Ma HY Jin SW Wang Q
author_sort	Mei HX
title	LXA4 Inhibits Lipopolysaccharide-Induced Inflammatory Cell Accumulation by Resident Macrophages in Mice
title_short	LXA4 Inhibits Lipopolysaccharide-Induced Inflammatory Cell Accumulation by Resident Macrophages in Mice
title_full	LXA4 Inhibits Lipopolysaccharide-Induced Inflammatory Cell Accumulation by Resident Macrophages in Mice
title_fullStr	LXA4 Inhibits Lipopolysaccharide-Induced Inflammatory Cell Accumulation by Resident Macrophages in Mice
title_full_unstemmed	LXA4 Inhibits Lipopolysaccharide-Induced Inflammatory Cell Accumulation by Resident Macrophages in Mice
title_sort	lxa4 inhibits lipopolysaccharide-induced inflammatory cell accumulation by resident macrophages in mice
publisher	Dove Medical Press
publishDate	2021
url	https://doaj.org/article/fa63d4c6674b42a4a6f2844b65334c63
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LXA4 Inhibits Lipopolysaccharide-Induced Inflammatory Cell Accumulation by Resident Macrophages in Mice

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