Skip to main content
Key Specialties
Cardiology Diabetology Endocrinology Gastroenterology Geriatrics and Gerontology Gynecology and Obstetrics Hematology Infectious Disease Internal Medicine Nephrology Neurology Oncology Pediatrics Respiratory Medicine Rheumatology Surgery
Congress Coverage
2024 ACC Congress 2023 ESMO Congress 2023 EASD Congress 2023 ERS Congress 2023 ESC Congress
Clinical Collections
Advances in Alzheimer’s

Keynote webinar | Spotlight on medication adherence

LIVE: Thursday 27th June 2024, 18:00-19:30 (CEST)
Join our expert panel to discover why you need to understand the drivers of non-adherence in your patients, and how you can optimize medication adherence in your clinics to drastically improve patient outcomes.
ADVANCED SEARCH
Log in
Top
Inflammation Research
Published in: Inflammation Research 9/2020

01-09-2020 | Acute Respiratory Distress-Syndrome | Review

Macrophage polarization and its role in the pathogenesis of acute lung injury/acute respiratory distress syndrome

Authors: Xuxin Chen, Jian Tang, Weizheng Shuai, Jiguang Meng, Jian Feng, Zhihai Han

Published in: Inflammation Research | Issue 9/2020

Login to get access

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.
Literature
1.
Nanchal RS, Truwit JD. Recent advances in understanding and treating acute respiratory distress syndrome. F1000Res. 2018;7(F1000 Faculty Rev):1322.
2.
Chen X, Wu S, Tang L, Ma L, Wang F, Feng H, et al. Mesenchymal stem cells overexpressing heme oxygenase-1 ameliorate lipopolysaccharide-induced acute lung injury in rats. J Cell Physiol. 2019;234:7301–19.PubMed
3.
Chen XX, Tang L, Han ZH, Wang WJ, Meng JG. 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 Toll-like receptor-4 signal pathway. Mol Med Rep. 2019;19:1891–902.PubMed
4.
Chen XX, Tang L, Fu YM, Wang Y, Han ZH, Meng JG. 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;40:1921–31.PubMed
5.
Gea-Sorlí S, Guillamat R, Serrano-Mollar A, Closa D. Activation of lung macrophage subpopulations in experimental acute pancreatitis. J Pathol. 2011;223:417–24.PubMed
6.
Wu DD, Pan PH, Liu B, Su XL, Zhang LM, Tan HY, et al. Inhibition of alveolar macrophage pyroptosis reduces lipopolysaccharide-induced acute lung injury in mice. Chin Med J (Engl). 2015;128:2638–45.
7.
Han J, Li C, Liu H, Fen D, Hu W, Liu Y, et al. Inhibition of lipopolysaccharide-mediated rat alveolar macrophage activation in vitro by antiflammin-1. Cell Biol Int. 2008;32:1108–15.PubMed
8.
Huang X, Xiu H, Zhang S, Zhang G. The role of macrophages in the pathogenesis of ALI/ARDS. Mediators Inflamm. 2018;2018:1264913.PubMedPubMedCentral
9.
Shapouri-Moghaddam A, Mohammadian S, Vazini H, Taghadosi M, Esmaeili SA, Mardani F, et al. Macrophage plasticity, polarization, and function in health and disease. J Cell Physiol. 2018;233:6425–40.PubMed
10.
Biswas SK, Chittezhath M, Shalova IN, Lim JY. Macrophage polarization and plasticity in health and disease. Immunol Res. 2012;53:11–24.PubMed
11.
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. 2017;22:186–93.PubMed
12.
Xiang J, Cheng S, Feng T, Wu Y, Xie W, Zhang M, et al. Neotuberostemonine attenuates bleomycin-induced pulmonary fibrosis by suppressing the recruitment and activation of macrophages. Int Immunopharmacol. 2016;36:158–64.PubMed
13.
Janssen WJ, Barthel L, Muldrow A, Oberley-Deegan RE, Kearns MT, Jakubzick C, et al. Fas determines differential fates of resident and recruited macrophages during resolution of acute lung injury. Am J Respir Crit Care Med. 2011;184:547–60.PubMedPubMedCentral
14.
Ginhoux F, Guilliams M. Tissue-resident macrophage ontogeny and homeostasis. Immunity. 2016;44:439–49.PubMed
15.
16.
Hettinger J, Richards DM, Hansson J, Barra MM, Joschko AC, Krijgsveld J, et al. Origin of monocytes and macrophages in a committed progenitor. Nat Immunol. 2013;14:821–30.PubMed
17.
18.
Yona S, Kim KW, Wolf Y, Mildner A, Varol D, Breker M, et al. Fate mapping reveals origins and dynamics of monocytes and tissue macrophages under homeostasis. Immunity. 2013;38:79–91.PubMed
19.
20.
Hashimoto D, Chow A, Noizat C, Teo P, Beasley MB, Leboeuf M, et al. Tissue-resident macrophages self-maintain locally throughout adult life with minimal contribution from circulating monocytes. Immunity. 2013;38:792–804.PubMed
21.
Sieweke MH, Allen JE. Beyond stem cells: self-renewal of differentiated macrophages. Science. 2013;342:1242974.PubMed
22.
23.
Wang N, Liang H, Zen K. Molecular mechanisms that influence the macrophage m1–m2 polarization balance. Front Immunol. 2014;5:614.PubMedPubMedCentral
24.
Chávez-Galán L, Olleros ML, Vesin D, Garcia I. Much more than M1 and M2 macrophages, there are also CD169(+) and TCR(+) macrophages. Front Immunol. 2015;6:263.PubMedPubMedCentral
25.
Aggarwal NR, King LS, D'Alessio FR. Diverse macrophage populations mediate acute lung inflammation and resolution. Am J Physiol Lung Cell Mol Physiol. 2014;306:L709–L725725.PubMedPubMedCentral
26.
Fukui S, Iwamoto N, Takatani A, Igawa T, Shimizu T, Umeda M, et al. M1 and M2 monocytes in rheumatoid arthritis: a contribution of Imbalance of M1/M2 monocytes to osteoclastogenesis. Front Immunol. 2017;8:1958.PubMed
27.
Gordon S, Martinez FO. Alternative activation of macrophages: mechanism and functions. Immunity. 2010;32:593–604.PubMed
28.
Zhang YH, He M, Wang Y, Liao AH. Modulators of the balance between M1 and M2 macrophages during pregnancy. Front Immunol. 2017;8:120.PubMedPubMedCentral
29.
Zhou D, Huang C, Lin Z, Zhan S, Kong L, Fang C, et al. Macrophage polarization and function with emphasis on the evolving roles of coordinated regulation of cellular signaling pathways. Cell Signal. 2014;26:192–7.PubMed
30.
Hoeksema MA, Stöger JL, de Winther MP. Molecular pathways regulating macrophage polarization: implications for atherosclerosis. Curr Atheroscler Rep. 2012;14:254–63.PubMedPubMedCentral
31.
Lawrence T, Natoli G. Transcriptional regulation of macrophage polarization: enabling diversity with identity. Nat Rev Immunol. 2011;11:750–61.PubMed
32.
Han MS, Jung DY, Morel C, Lakhani SA, Kim JK, Flavell RA, et al. JNK expression by macrophages promotes obesity-induced insulin resistance and inflammation. Science. 2013;339:218–22.PubMed
33.
Yang S, Wang H, Yang Y, Wang R, Wang Y, Wu C, et al. Baicalein administered in the subacute phase ameliorates ischemia-reperfusion-induced brain injury by reducing neuroinflammation and neuronal damage. Biomed Pharmacother. 2019;117:109102.PubMed
34.
Shi Q, Zhao L, Xu C, Zhang L, Zhao H. High molecular weight hyaluronan suppresses macrophage M1 polarization and enhances IL-10 production in PM2.5-induced lung inflammation. Molecules. 2019;24:1766.
35.
Yang J, Yang L, Tian L, Ji X, Yang L, Li L. Sphingosine 1-phosphate (S1P)/S1P receptor2/3 axis promotes inflammatory M1 polarization of bone marrow-derived monocyte/macrophage via G(α)i/o/PI3K/JNK pathway. Cell Physiol Biochem. 2018;49:1677–93.PubMed
36.
Mao Y, Wang B, Xu X, Du W, Li W, Wang Y. Glycyrrhizic acid promotes M1 macrophage polarization in murine bone marrow-derived macrophages associated with the activation of JNK and NF-κB. Mediators Inflamm. 2015;2015:372931.PubMedPubMedCentral
37.
Oliveira AG, Araujo TG, Carvalho BM, Guadagnini D, Rocha GZ, Bagarolli RA, et al. Acute exercise induces a phenotypic switch in adipose tissue macrophage polarization in diet-induced obese rats. Obes (Silver Spring). 2013;21:2545–56.
38.
Wan S, Sun H. Glucagon-like peptide-1 modulates RAW264.7 macrophage polarization by interfering with the JNK/STAT3 signaling pathway. Exp Ther Med. 2019;17:3573–9.PubMedPubMedCentral
39.
Zhong J, Wang H, Chen W, Sun Z, Chen J, Xu Y, et al. Correction: Ubiquitylation of MFHAS1 by the ubiquitin ligase praja2 promotes M1 macrophage polarization by activating JNK and p38 pathways. Cell Death Dis. 2018;9:782.PubMedPubMedCentral
40.
Hao J, Hu Y, Li Y, Zhou Q, Lv X. Involvement of JNK signaling in IL4-induced M2 macrophage polarization. Exp Cell Res. 2017;357:155–62.PubMed
41.
Ruse M, Knaus UG. New players in TLR-mediated innate immunity: PI3K and small Rho GTPases. Immunol Res. 2006;34:33–48.PubMed
42.
Luyendyk JP, Schabbauer GA, Tencati M, Holscher T, Pawlinski R, Mackman N. Genetic analysis of the role of the PI3K-Akt pathway in lipopolysaccharide-induced cytokine and tissue factor gene expression in monocytes/macrophages. J Immunol. 2008;180:4218–26.PubMedPubMedCentral
43.
Arranz A, Doxaki C, Vergadi E, Martinez de la Torre Y, Vaporidi K, Lagoudaki ED, et al. Akt1 and Akt2 protein kinases differentially contribute to macrophage polarization. Proc Natl Acad Sci USA. 2012;109:9517–22.PubMed
44.
Fukao T, Koyasu S. PI3K and negative regulation of TLR signaling. Trends Immunol. 2003;24:358–63.PubMed
45.
Bao L, Li X. MicroRNA-32 targeting PTEN enhances M2 macrophage polarization in the glioma microenvironment and further promotes the progression of glioma. Mol Cell Biochem. 2019;460:67-79
46.
Zhang LL, Zhang LF, Shi YB. Down-regulated paxillin suppresses cell proliferation and invasion by inhibiting M2 macrophage polarization in colon cancer. Biol Chem. 2018;399:1285–95.PubMed
47.
Xu F, Kang Y, Zhang H, Piao Z, Yin H, Diao R, et al. Akt1-mediated regulation of macrophage polarization in a murine model of Staphylococcus aureus pulmonary infection. J Infect Dis. 2013;208:528–38.PubMed
48.
Artavanis-Tsakonas S, Rand MD, Lake RJ. Notch signaling: cell fate control and signal integration in development. Science. 1999;284:770–6.PubMed
49.
50.
Rutz S, Janke M, Kassner N, Hohnstein T, Krueger M, Scheffold A. Notch regulates IL-10 production by T helper 1 cells. Proc Natl Acad Sci U S A. 2008;105:3497–502.PubMedPubMedCentral
51.
Wei W, Li ZP, Bian ZX, Han QB. Astragalus Polysaccharide RAP induces macrophage phenotype polarization to M1 via the notch signaling pathway. Molecules. 2019;24:2016.
52.
Zhang W, Xu W, Xiong S. Blockade of Notch1 signaling alleviates murine lupus via blunting macrophage activation and M2b polarization. J Immunol. 2010;184:6465–78.PubMed
53.
Pagie S, Gérard N, Charreau B. Notch signaling triggered via the ligand DLL4 impedes M2 macrophage differentiation and promotes their apoptosis. Cell Commun Signal. 2018;16:4.PubMedPubMedCentral
54.
Vieceli Dalla Sega F, Fortini F, Aquila G, Campo G, Vaccarezza M, Rizzo P. Notch signaling regulates immune responses in atherosclerosis. Front Immunol. 2019;10:1130.PubMedPubMedCentral
55.
56.
57.
Murray PJ. The JAK-STAT signaling pathway: input and output integration. J Immunol. 2007;178:2623–9.PubMed
58.
Hu X, Chen J, Wang L, Ivashkiv LB. Crosstalk among Jak-STAT, Toll-like receptor, and ITAM-dependent pathways in macrophage activation. J Leukoc Biol. 2007;82:237–43.PubMed
59.
Hall CJ, Boyle RH, Astin JW, Flores MV, Oehlers SH, Sanderson LE, et al. Immunoresponsive gene 1 augments bactericidal activity of macrophage-lineage cells by regulating β-oxidation-dependent mitochondrial ROS production. Cell Metab. 2013;18:265–78.PubMed
60.
Oh H, Park SH, Kang MK, Kim YH, Lee EJ, Kim DY, et al. Asaronic acid attenuates macrophage activation toward M1 phenotype through inhibition of NF-κB pathway and JAK-STAT signaling in glucose-loaded murine macrophages. J Agric Food Chem. 2019;67:10069–78.PubMed
61.
Liang YB, Tang H, Chen ZB, Zeng LJ, Wu JG, Yang W, et al. Downregulated SOCS1 expression activates the JAK1/STAT1 pathway and promotes polarization of macrophages into M1 type. Mol Med Rep. 2017;16:6405–11.PubMed
62.
Zhao J, Yu H, Liu Y, Gibson SA, Yan Z, Xu X, et al. Protective effect of suppressing STAT3 activity in LPS-induced acute lung injury. Am J Physiol Lung Cell Mol Physiol. 2016;311:L868–L880880.PubMedPubMedCentral
63.
64.
Whyte CS, Bishop ET, Rückerl D, Gaspar-Pereira S, Barker RN, Allen JE, et al. Suppressor of cytokine signaling (SOCS)1 is a key determinant of differential macrophage activation and function. J Leukoc Biol. 2011;90:845–54.PubMed
65.
Liu Y, Stewart KN, Bishop E, Marek CJ, Kluth DC, Rees AJ, et al. Unique expression of suppressor of cytokine signaling 3 is essential for classical macrophage activation in rodents in vitro and in vivo. J Immunol. 2008;180:6270–8.PubMed
66.
Molteni M, Gemma S, Rossetti C. The role of toll-like receptor 4 in infectious and noninfectious inflammation. Mediators Inflamm. 2016;2016:6978936.PubMedPubMedCentral
67.
Travis MA, Sheppard D. TGF-β activation and function in immunity. Annu Rev Immunol. 2014;32:51–82.PubMed
68.
Hata A, Chen YG. TGF-β signaling from receptors to smads. Cold Spring Harb Perspect Biol. 2016;8:a022061.
69.
Malyshev I, Malyshev Y. Current concept and update of the macrophage plasticity concept: intracellular mechanisms of reprogramming and m3 macrophage “switch” phenotype. Biomed Res Int. 2015;2015:341308.PubMedPubMedCentral
70.
Zhang F, Wang H, Wang X, Jiang G, Liu H, Zhang G, et al. TGF-β induces M2-like macrophage polarization via SNAIL-mediated suppression of a pro-inflammatory phenotype. Oncotarget. 2016;7:52294–30606.PubMedPubMedCentral
71.
Imtiyaz HZ, Simon MC. Hypoxia-inducible factors as essential regulators of inflammation. Curr Top Microbiol Immunol. 2010;345:105–20.PubMedPubMedCentral
72.
Takeda N, O'Dea EL, Doedens A, Kim JW, Weidemann A, Stockmann C, et al. Differential activation and antagonistic function of HIF-{alpha} isoforms in macrophages are essential for NO homeostasis. Genes Dev. 2010;24:491–501.PubMedPubMedCentral
73.
Xuan D, Han Q, Tu Q, Zhang L, Yu L, Murry D, et al. Epigenetic modulation in periodontitis: interaction of adiponectin and JMJD3-IRF4 axis in macrophages. J Cell Physiol. 2016;231:1090–6.PubMed
74.
Satoh T, Takeuchi O, Vandenbon A, Yasuda K, Tanaka Y, Kumagai Y, et al. The Jmjd3-Irf4 axis regulates M2 macrophage polarization and host responses against helminth infection. Nat Immunol. 2010;11:936–44.PubMed
75.
De Santa F, Totaro MG, Prosperini E, Notarbartolo S, Testa G, Natoli G. The histone H3 lysine-27 demethylase Jmjd3 links inflammation to inhibition of polycomb-mediated gene silencing. Cell. 2007;130:1083–94.PubMed
76.
Krausgruber T, Blazek K, Smallie T, Alzabin S, Lockstone H, Sahgal N, et al. IRF5 promotes inflammatory macrophage polarization and TH1-TH17 responses. Nat Immunol. 2011;12:231–8.PubMed
77.
Bouhlel MA, Derudas B, Rigamonti E, Dièvart R, Brozek J, Haulon S, et al. PPARgamma activation primes human monocytes into alternative M2 macrophages with anti-inflammatory properties. Cell Metab. 2007;6:137–43.PubMed
78.
Huang JT, Welch JS, Ricote M, Binder CJ, Willson TM, Kelly C, et al. Interleukin-4-dependent production of PPAR-gamma ligands in macrophages by 12/15-lipoxygenase. Nature. 1999;400:378–82.PubMed
79.
Szanto A, Balint BL, Nagy ZS, Barta E, Dezso B, Pap A, et al. STAT6 transcription factor is a facilitator of the nuclear receptor PPARγ-regulated gene expression in macrophages and dendritic cells. Immunity. 2010;33:699–712.PubMedPubMedCentral
80.
Pello OM, De Pizzol M, Mirolo M, Soucek L, Zammataro L, Amabile A, et al. Role of c-MYC in alternative activation of human macrophages and tumor-associated macrophage biology. Blood. 2012;119:411–21.PubMed
81.
Andreoli V, Gehrau RC, Bocco JL. Biology of Krüppel-like factor 6 transcriptional regulator in cell life and death. IUBMB Life. 2010;62:896–905.
82.
Liao X, Sharma N, Kapadia F, Zhou G, Lu Y, Hong H, et al. Krüppel-like factor 4 regulates macrophage polarization. J Clin Invest. 2011;121:2736–49.PubMedPubMedCentral
83.
Date D, Das R, Narla G, Simon DI, Jain MK, Mahabeleshwar GH. Kruppel-like transcription factor 6 regulates inflammatory macrophage polarization. J Biol Chem. 2014;289:10318–29.PubMedPubMedCentral
84.
Martinez-Nunez RT, Louafi F, Sanchez-Elsner T. The interleukin 13 (IL-13) pathway in human macrophages is modulated by microRNA-155 via direct targeting of interleukin 13 receptor alpha1 (IL13Ralpha1). J Biol Chem. 2011;286:1786–94.PubMed
85.
Cai X, Yin Y, Li N, Zhu D, Zhang J, Zhang CY, et al. Re-polarization of tumor-associated macrophages to pro-inflammatory M1 macrophages by microRNA-155. J Mol Cell Biol. 2012;4:341–3.PubMed
86.
Ponomarev ED, Veremeyko T, Barteneva N, Krichevsky AM, Weiner HL. MicroRNA-124 promotes microglia quiescence and suppresses EAE by deactivating macrophages via the C/EBP-α-PU.1 pathway. Nat Med. 2011;17:64–70.PubMed
87.
Zhuang G, Meng C, Guo X, Cheruku PS, Shi L, Xu H, et al. A novel regulator of macrophage activation: miR-223 in obesity-associated adipose tissue inflammation. Circulation. 2012;125:2892–903.PubMed
88.
Banerjee S, Xie N, Cui H, Tan Z, Yang S, Icyuz M, et al. MicroRNA let-7c regulates macrophage polarization. J Immunol. 2013;190:6542–9.PubMedPubMedCentral
89.
90.
Shibata Y, Berclaz PY, Chroneos ZC, Yoshida M, Whitsett JA, Trapnell BC. GM-CSF regulates alveolar macrophage differentiation and innate immunity in the lung through PU.1. Immunity. 2001;15:557–67.PubMed
91.
92.
Duan M, Li WC, Vlahos R, Maxwell MJ, Anderson GP, Hibbs ML. Distinct macrophage subpopulations characterize acute infection and chronic inflammatory lung disease. J Immunol. 2012;189:946–55.PubMed
93.
Short KR, Kroeze E, Fouchier R, Kuiken T. Pathogenesis of influenza-induced acute respiratory distress syndrome. Lancet Infect Dis. 2014;14:57–69.
94.
Higgins DM, Sanchez-Campillo J, Rosas-Taraco AG, Higgins JR, Lee EJ, Orme IM, et al. Relative levels of M-CSF and GM-CSF influence the specific generation of macrophage populations during infection with Mycobacterium tuberculosis. J Immunol. 2008;180:4892–900.PubMed
95.
Laskin DL, Malaviya R, Laskin JD. Role of macrophages in acute lung injury and chronic fibrosis induced by pulmonary toxicants. Toxicol Sci. 2019;168:287–301.PubMed
96.
Wang J, Li R, Peng Z, Zhou W, Hu B, Rao X, et al. GTS-21 reduces inflammation in acute lung injury by regulating M1 polarization and function of alveolar macrophages. Shock. 2019;51:389–400.PubMed
97.
Zhuo Y, Li D, Cui L, Li C, Zhang S, Zhang Q, et al. Treatment with 3,4-dihydroxyphenylethyl alcohol glycoside ameliorates sepsis-induced ALI in mice by reducing inflammation and regulating M1 polarization. Biomed Pharmacother. 2019;116:109012.PubMed
98.
Wang Y, Xu Y, Zhang P, Ruan W, Zhang L, Yuan S, et al. Smiglaside A ameliorates LPS-induced acute lung injury by modulating macrophage polarization via AMPK-PPARγ pathway. Biochem Pharmacol. 2018;156:385–95.PubMed
99.
Bittencourt-Mernak MI, Pinheiro NM, Santana FP, Guerreiro MP, Saraiva-Romanholo BM, Grecco SS, et al. Prophylactic and therapeutic treatment with the flavonone sakuranetin ameliorates LPS-induced acute lung injury. Am J Physiol Lung Cell Mol Physiol. 2017;312:L217–L230230.PubMed
100.
Pinheiro NM, Santana FP, Almeida RR, Guerreiro M, Martins MA, Caperuto LC, et al. Acute lung injury is reduced by the α7nAChR agonist PNU-282987 through changes in the macrophage profile. FASEB J. 2017;31:320–32.PubMed
101.
Dolinay T, Kaminski N, Felgendreher M, Kim HP, Reynolds P, Watkins SC, et al. Gene expression profiling of target genes in ventilator-induced lung injury. Physiol Genomics. 2006;26:68–75.PubMed
102.
Johnston LK, Rims CR, Gill SE, McGuire JK, Manicone AM. Pulmonary macrophage subpopulations in the induction and resolution of acute lung injury. Am J Respir Cell Mol Biol. 2012;47:417–26.PubMedPubMedCentral
103.
Herold S, Mayer K, Lohmeyer J. Acute lung injury: how macrophages orchestrate resolution of inflammation and tissue repair. Front Immunol. 2011;2:65.PubMedPubMedCentral
104.
Shirey KA, Pletneva LM, Puche AC, Keegan AD, Prince GA, Blanco JC, et al. Control of RSV-induced lung injury by alternatively activated macrophages is IL-4R alpha-, TLR4-, and IFN-beta-dependent. Mucosal Immunol. 2010;3:291–300.PubMedPubMedCentral
105.
Tu GW, Shi Y, Zheng YJ, Ju MJ, He HY, Ma GG, et al. Glucocorticoid attenuates acute lung injury through induction of type 2 macrophage. J Transl Med. 2017;15:181.PubMedPubMedCentral
106.
Thompson BT, Chambers RC, Liu KD. Acute respiratory distress syndrome. N Engl J Med. 2017;377:562–72.PubMed
107.
Strieter RM. What differentiates normal lung repair and fibrosis? Inflammation, resolution of repair, and fibrosis. Proc Am Thorac Soc. 2008;5:305–10.PubMedPubMedCentral
108.
Lupher ML Jr, Gallatin WM. Regulation of fibrosis by the immune system. Adv Immunol. 2006;89:245–88.PubMed
109.
Sinha P, Clements VK, Ostrand-Rosenberg S. Interleukin-13-regulated M2 macrophages in combination with myeloid suppressor cells block immune surveillance against metastasis. Cancer Res. 2005;65:11743–51.PubMed
110.
Tsoutsou PG, Gourgoulianis KI, Petinaki E, Germenis A, Tsoutsou AG, Mpaka M, et al. Cytokine levels in the sera of patients with idiopathic pulmonary fibrosis. Respir Med. 2006;100:938–45.PubMed
111.
Meneghin A, Hogaboam CM. Infectious disease, the innate immune response, and fibrosis. J Clin Invest. 2007;117:530–8.PubMedPubMedCentral
112.
D'Alessio FR, Craig JM, Singer BD, Files DC, Mock JR, Garibaldi BT, et al. Enhanced resolution of experimental ARDS through IL-4-mediated lung macrophage reprogramming. Am J Physiol Lung Cell Mol Physiol. 2016;310:L733–L746746.PubMedPubMedCentral
113.
Wakayama H, Hashimoto N, Matsushita Y, Matsubara K, Yamamoto N, Hasegawa Y, et al. Factors secreted from dental pulp stem cells show multifaceted benefits for treating acute lung injury in mice. Cytotherapy. 2015;17:1119–29.PubMed
Metadata
Title
Macrophage polarization and its role in the pathogenesis of acute lung injury/acute respiratory distress syndrome
Authors
Xuxin Chen
Jian Tang
Weizheng Shuai
Jiguang Meng
Jian Feng
Zhihai Han
Publication date
01-09-2020
Publisher
Springer International Publishing
Published in
Inflammation Research / Issue 9/2020
Print ISSN: 1023-3830
Electronic ISSN: 1420-908X
DOI
https://doi.org/10.1007/s00011-020-01378-2

Other articles of this Issue 9/2020

Inflammation Research 9/2020 Go to the issue

Original Research Article

Anti-inflammatory latex proteins of the medicinal plant Calotropis procera: a promising alternative for oral mucositis treatment

Original Research Article

Simple, sensitive and specific quantification of diamine oxidase activity in complex matrices using newly discovered fluorophores derived from natural substrates

Review

Changes of lipoxin levels during pregnancy and the monthly-cycle, condition the normal course of pregnancy or pathology

Original Research Paper

The expression levels of CHI3L1 and IL15Rα correlate with TGM2 in duodenum biopsies of patients with celiac disease

Review

Intercellular communication and ion channels in neuropathic pain chronicization

Short Communication

SARS-CoV-2 will constantly sweep its tracks: a vaccine containing CpG motifs in ‘lasso’ for the multi-faced virus
Live Webinar | 27-06-2024 | 18:00 (CEST)

Keynote webinar | Spotlight on medication adherence

Reserve your place

Live: Thursday 27th June 2024, 18:00-19:30 (CEST)

WHO estimates that half of all patients worldwide are non-adherent to their prescribed medication. The consequences of poor adherence can be catastrophic, on both the individual and population level.

Join our expert panel to discover why you need to understand the drivers of non-adherence in your patients, and how you can optimize medication adherence in your clinics to drastically improve patient outcomes.

Prof. Kevin Dolgin
Prof. Florian Limbourg
Prof. Anoop Chauhan
Developed by: Springer Medicine
Obesity Clinical Trial Summary

At a glance: The STEP trials

Read more

A round-up of the STEP phase 3 clinical trials evaluating semaglutide for weight loss in people with overweight or obesity.

Developed by: Springer Medicine
Image Credits