For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
71
views
70
references
 Top references
cited by
143
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      193
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: not found

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

      review-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          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.

          Related collections

          Most cited references70

          • Record: found
          • Abstract: found
          • Article: not found

          Macrophage plasticity, polarization, and function in health and disease.

          Fatemeh Mardani, Abbas Shapouri-Moghaddam, Saeed Mohammadian … (2018)
          Macrophages are heterogeneous and their phenotype and functions are regulated by the surrounding micro-environment. Macrophages commonly exist in two distinct subsets: 1) Classically activated or M1 macrophages, which are pro-inflammatory and polarized by lipopolysaccharide (LPS) either alone or in association with Th1 cytokines such as IFN-γ, GM-CSF, and produce pro-inflammatory cytokines such as interleukin-1β (IL-1β), IL-6, IL-12, IL-23, and TNF-α; and 2) Alternatively activated or M2 macrophages, which are anti-inflammatory and immunoregulatory and polarized by Th2 cytokines such as IL-4 and IL-13 and produce anti-inflammatory cytokines such as IL-10 and TGF-β. M1 and M2 macrophages have different functions and transcriptional profiles. They have unique abilities by destroying pathogens or repair the inflammation-associated injury. It is known that M1/M2 macrophage balance polarization governs the fate of an organ in inflammation or injury. When the infection or inflammation is severe enough to affect an organ, macrophages first exhibit the M1 phenotype to release TNF-α, IL-1β, IL-12, and IL-23 against the stimulus. But, if M1 phase continues, it can cause tissue damage. Therefore, M2 macrophages secrete high amounts of IL-10 and TGF-β to suppress the inflammation, contribute to tissue repair, remodeling, vasculogenesis, and retain homeostasis. In this review, we first discuss the basic biology of macrophages including origin, differentiation and activation, tissue distribution, plasticity and polarization, migration, antigen presentation capacity, cytokine and chemokine production, metabolism, and involvement of microRNAs in macrophage polarization and function. Secondly, we discuss the protective and pathogenic role of the macrophage subsets in normal and pathological pregnancy, anti-microbial defense, anti-tumor immunity, metabolic disease and obesity, asthma and allergy, atherosclerosis, fibrosis, wound healing, and autoimmunity.
          Article 0 comments Cited 1876 times – based on 0 reviews     Review now
          Article has an altmetric score of 23
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Tissue-Resident Macrophage Ontogeny and Homeostasis.

            Florent Ginhoux, Martin Guilliams (2016)
            Defining the origins and developmental pathways of tissue-resident macrophages should help refine our understanding of the role of these cells in various disease settings and enable the design of novel macrophage-targeted therapies. In recent years the long-held belief that macrophage populations in the adult are continuously replenished by monocytes from the bone marrow (BM) has been overturned with the advent of new techniques to dissect cellular ontogeny. The new paradigm suggests that several tissue-resident macrophage populations are seeded during waves of embryonic hematopoiesis and self-maintain independently of BM contribution during adulthood. However, the exact nature of the embryonic progenitors that give rise to adult tissue-resident macrophages is still debated, and the mechanisms enabling macrophage population maintenance in the adult are undefined. Here, we review the emergence of these concepts and discuss current controversies and future directions in macrophage biology.
            Article 0 comments Cited 788 times – based on 0 reviews     Review now
            Article has an altmetric score of 71
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              IRF5 promotes inflammatory macrophage polarization and TH1-TH17 responses.

              Thomas Krausgruber, Katrina Blazek, Tim Smallie … (2011)
              Polymorphisms in the gene encoding the transcription factor IRF5 that lead to higher mRNA expression are associated with many autoimmune diseases. Here we show that IRF5 expression in macrophages was reversibly induced by inflammatory stimuli and contributed to the plasticity of macrophage polarization. High expression of IRF5 was characteristic of M1 macrophages, in which it directly activated transcription of the genes encoding interleukin 12 subunit p40 (IL-12p40), IL-12p35 and IL-23p19 and repressed the gene encoding IL-10. Consequently, those macrophages set up the environment for a potent T helper type 1 (T(H)1)-T(H)17 response. Global gene expression analysis demonstrated that exogenous IRF5 upregulated or downregulated expression of established phenotypic markers of M1 or M2 macrophages, respectively. Our data suggest a critical role for IRF5 in M1 macrophage polarization and define a previously unknown function for IRF5 as a transcriptional repressor.
              Article 0 comments Cited 496 times – based on 0 reviews     Review now
              Article has an altmetric score of 23
                Bookmark
                All references

                Author and article information

                Contributors
                Jian Feng: fg5001@foxmail.com
                Zhihai Han:
                ORCID: http://orcid.org/0000-0002-2167-2258
                zhihaihandoctor@163.com
                Journal
                Journal ID (nlm-ta): Inflamm Res
                Journal ID (iso-abbrev): Inflamm. Res
                Title: Inflammation Research
                Publisher: Springer International Publishing (Cham )
                ISSN (Print): 1023-3830
                ISSN (Electronic): 1420-908X
                Publication date (Electronic): 10 July 2020
                Pages: 1-13
                Affiliations
                [1 ]GRID grid.414252.4, ISNI 0000 0004 1761 8894, Department of Pulmonary and Critical Care Medicine, The Sixth Medical Center of Chinese, , PLA General Hospital, ; No. 6 Fucheng Road, Beijing, 100037 China
                [2 ]GRID grid.414252.4, ISNI 0000 0004 1761 8894, Department of ICU, The Sixth Medical Center of Chinese, , PLA General Hospital, ; Beijing, 100037 China
                [3 ]GRID grid.488387.8, Department of Cardiology, , The Affiliated Hospital of Southwest Medical University, ; No. 25 Taiping Street, Luzhou, 646000 China
                Author notes

                Responsible Editor: John Di Battista.

                Author information
                http://orcid.org/0000-0002-2167-2258
                Article
                Publisher ID: 1378
                DOI: 10.1007/s00011-020-01378-2
                PMC ID: 7347666
                PubMed ID: 32647933
                SO-VID: fdd82e68-8799-4489-801a-4507b0e57d46
                Copyright © © Springer Nature Switzerland AG 2020
                License:

                This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.

                History
                Date received : 30 May 2020
                Date revision received : 30 May 2020
                Date accepted : 6 July 2020
                Funding
                Funded by: Innovative Cultivation Foundation of The Sixth Medical Center of PLA General Hospital
                Award ID: CXPY201902
                Award Recipient :
                Funded by: FundRef http://dx.doi.org/10.13039/501100001809, National Natural Science Foundation of China;
                Award ID: 81300050
                Award ID: 31300946
                Award Recipient :
                Funded by: FundRef http://dx.doi.org/10.13039/501100004826, Natural Science Foundation of Beijing Municipality;
                Award ID: 7182163
                Award Recipient :
                Categories
                Subject: Review

                ScienceOpen disciplines: Immunology
                Keywords: acute lung injury,acute respiratory distress syndrome,macrophage,macrophage polarization
                Data availability:
                ScienceOpen disciplines: Immunology
                Keywords: acute lung injury, acute respiratory distress syndrome, macrophage, macrophage polarization

                Comments

                Comment on this article

                scite_
                0
                0
                0
                0
                Smart Citations
                0
                0
                0
                0
                Citing PublicationsSupportingMentioningContrasting
                View Citations

                See how this article has been cited at scite.ai

                scite shows how a scientific paper has been cited by providing the context of the citation, a classification describing whether it supports, mentions, or contrasts the cited claim, and a label indicating in which section the citation was made.

                Similar content193

                See all similar

                Cited by142

                See all cited by

                Most referenced authors1,658

                See all reference authors