Macrophage Polarization and Its Role in the Pathogenesis of Acute Lung Injury/acute Respiratory Distress Syndrome

Overview

Journal Inflamm Res

Specialties Allergy & Immunology
Pathology

Date 2020 Jul 11

PMID 32647933

Citations 139

Authors

Xuxin Chen

Jian Tang

Weizheng Shuai

Jiguang Meng

Jian Feng

Zhihai Han

Affiliations

Soon will be listed here.

Abstract

Purpose: Macrophages are highly plastic cells. Under different stimuli, macrophages can be polarized into several different subsets. Two main macrophage subsets have been suggested: classically activated or inflammatory (M1) macrophages and alternatively activated or anti-inflammatory (M2) macrophages. Macrophage polarization is governed by a highly complex set of regulatory networks. Many recent studies have shown that macrophages are key orchestrators in the pathogenesis of acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) and that regulation of macrophage polarization may improve the prognosis of ALI/ARDS. A further understanding of the mechanisms of macrophage polarization is expected to be helpful in the development of novel therapeutic targets to treat ALI/ARDS. Therefore, we performed a literature review to summarize the regulatory mechanisms of macrophage polarization and its role in the pathogenesis of ALI/ARDS.

Methods: A computer-based online search was performed using the PubMed database and Web of Science database for published articles concerning macrophages, macrophage polarization, and ALI/ARDS.

Results: In this review, we discuss the origin, polarization, and polarization regulation of macrophages as well as the role of macrophage polarization in various stages of ARDS. According to the current literature, regulating the polarized state of macrophages might be a potential therapeutic strategy against ALI/ARDS.

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References

Chen X, Wu S, Tang L, Ma L, Wang F, Feng H . Mesenchymal stem cells overexpressing heme oxygenase-1 ameliorate lipopolysaccharide-induced acute lung injury in rats. J Cell Physiol. 2018; 234(5):7301-7319. DOI: 10.1002/jcp.27488. View

Chen X, Tang L, Han Z, Wang W, Meng J . Coculture with bone marrow‑derived mesenchymal stem cells attenuates inflammation and apoptosis in lipopolysaccharide‑stimulated alveolar epithelial cells via enhanced secretion of keratinocyte growth factor and angiopoietin‑1 modulating the.... Mol Med Rep. 2019; 19(3):1891-1902. DOI: 10.3892/mmr.2019.9836. View

Chen X, Tang L, Fu Y, Wang Y, Han Z, Meng J . Paralemmin-3 contributes to lipopolysaccharide-induced inflammatory response and is involved in lipopolysaccharide-Toll-like receptor-4 signaling in alveolar macrophages. Int J Mol Med. 2017; 40(6):1921-1931. DOI: 10.3892/ijmm.2017.3161. View

Gea-Sorli S, Guillamat R, Serrano-Mollar A, Closa D . Activation of lung macrophage subpopulations in experimental acute pancreatitis. J Pathol. 2010; 223(3):417-24. DOI: 10.1002/path.2814. View

Han J, Li C, Liu H, Fen D, Hu W, Liu Y . Inhibition of lipopolysaccharide-mediated rat alveolar macrophage activation in vitro by antiflammin-1. Cell Biol Int. 2008; 32(9):1108-15. DOI: 10.1016/j.cellbi.2008.04.023. View

Huang X, Xiu H, Zhang S, Zhang G . The Role of Macrophages in the Pathogenesis of ALI/ARDS. Mediators Inflamm. 2018; 2018:1264913. PMC: 5989173. DOI: 10.1155/2018/1264913. View

Shapouri-Moghaddam A, Mohammadian S, Vazini H, Taghadosi M, Esmaeili S, Mardani F . Macrophage plasticity, polarization, and function in health and disease. J Cell Physiol. 2018; 233(9):6425-6440. DOI: 10.1002/jcp.26429. View

Biswas S, Chittezhath M, Shalova I, Lim J . Macrophage polarization and plasticity in health and disease. Immunol Res. 2012; 53(1-3):11-24. DOI: 10.1007/s12026-012-8291-9. View

Patel U, Rajasingh S, Samanta S, Cao T, Dawn B, Rajasingh J . Macrophage polarization in response to epigenetic modifiers during infection and inflammation. Drug Discov Today. 2016; 22(1):186-193. PMC: 5226865. DOI: 10.1016/j.drudis.2016.08.006. View

10.

Xiang J, Cheng S, Feng T, Wu Y, Xie W, Zhang M . Neotuberostemonine attenuates bleomycin-induced pulmonary fibrosis by suppressing the recruitment and activation of macrophages. Int Immunopharmacol. 2016; 36:158-164. DOI: 10.1016/j.intimp.2016.04.016. View

11.

Janssen W, Barthel L, Muldrow A, Oberley-Deegan R, Kearns M, Jakubzick C . Fas determines differential fates of resident and recruited macrophages during resolution of acute lung injury. Am J Respir Crit Care Med. 2011; 184(5):547-60. PMC: 3175550. DOI: 10.1164/rccm.201011-1891OC. View

12.

Ginhoux F, Guilliams M . Tissue-Resident Macrophage Ontogeny and Homeostasis. Immunity. 2016; 44(3):439-449. DOI: 10.1016/j.immuni.2016.02.024. View

13.

Davies L, Taylor P . Tissue-resident macrophages: then and now. Immunology. 2015; 144(4):541-8. PMC: 4368161. DOI: 10.1111/imm.12451. View

14.

Hettinger J, Richards D, Hansson J, Barra M, Joschko A, Krijgsveld J . Origin of monocytes and macrophages in a committed progenitor. Nat Immunol. 2013; 14(8):821-30. DOI: 10.1038/ni.2638. View

15.

Pittet M, Nahrendorf M, Swirski F . The journey from stem cell to macrophage. Ann N Y Acad Sci. 2014; 1319:1-18. PMC: 4074243. DOI: 10.1111/nyas.12393. View

16.

Yona S, Kim K, Wolf Y, Mildner A, Varol D, Breker M . Fate mapping reveals origins and dynamics of monocytes and tissue macrophages under homeostasis. Immunity. 2013; 38(1):79-91. PMC: 3908543. DOI: 10.1016/j.immuni.2012.12.001. View

17.

Davies L, Jenkins S, Allen J, Taylor P . Tissue-resident macrophages. Nat Immunol. 2013; 14(10):986-95. PMC: 4045180. DOI: 10.1038/ni.2705. View

18.

Hashimoto D, Chow A, Noizat C, Teo P, Beasley M, Leboeuf M . Tissue-resident macrophages self-maintain locally throughout adult life with minimal contribution from circulating monocytes. Immunity. 2013; 38(4):792-804. PMC: 3853406. DOI: 10.1016/j.immuni.2013.04.004. View

19.

Sieweke M, Allen J . Beyond stem cells: self-renewal of differentiated macrophages. Science. 2013; 342(6161):1242974. DOI: 10.1126/science.1242974. View

20.

Gordon S, Pluddemann A . Tissue macrophages: heterogeneity and functions. BMC Biol. 2017; 15(1):53. PMC: 5492929. DOI: 10.1186/s12915-017-0392-4. View