Macrophage plasticity, polarization, and function in health and disease

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...

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Published inJournal of cellular physiology Vol. 233; no. 9; pp. 6425 - 6440
Main Authors Shapouri‐Moghaddam, Abbas, Mohammadian, Saeed, Vazini, Hossein, Taghadosi, Mahdi, Esmaeili, Seyed‐Alireza, Mardani, Fatemeh, Seifi, Bita, Mohammadi, Asadollah, Afshari, Jalil T., Sahebkar, Amirhossein
Format Journal Article
LanguageEnglish
Published United States Wiley Subscription Services, Inc 01.09.2018
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Abstract 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. 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.
AbstractList 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. 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.
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. This article is protected by copyright. All rights reserved.
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.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.
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.
Author Vazini, Hossein
Taghadosi, Mahdi
Mardani, Fatemeh
Shapouri‐Moghaddam, Abbas
Afshari, Jalil T.
Sahebkar, Amirhossein
Mohammadian, Saeed
Esmaeili, Seyed‐Alireza
Seifi, Bita
Mohammadi, Asadollah
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  givenname: Abbas
  surname: Shapouri‐Moghaddam
  fullname: Shapouri‐Moghaddam, Abbas
  organization: Mashhad University of Medical Sciences
– sequence: 2
  givenname: Saeed
  surname: Mohammadian
  fullname: Mohammadian, Saeed
  organization: Mashhad University of Medical Sciences
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  givenname: Hossein
  surname: Vazini
  fullname: Vazini, Hossein
  organization: Islamic Azad University
– sequence: 4
  givenname: Mahdi
  surname: Taghadosi
  fullname: Taghadosi, Mahdi
  organization: Kermanshah University of Medical Sciences
– sequence: 5
  givenname: Seyed‐Alireza
  surname: Esmaeili
  fullname: Esmaeili, Seyed‐Alireza
  organization: Mashhad University of Medical Sciences
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  givenname: Fatemeh
  surname: Mardani
  fullname: Mardani, Fatemeh
  organization: Mashhad University of Medical Sciences
– sequence: 7
  givenname: Bita
  surname: Seifi
  fullname: Seifi, Bita
  organization: Islamic Azad University
– sequence: 8
  givenname: Asadollah
  surname: Mohammadi
  fullname: Mohammadi, Asadollah
  organization: Mashhad University of Medical Sciences
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  givenname: Jalil T.
  surname: Afshari
  fullname: Afshari, Jalil T.
  organization: Mashhad University of Medical Sciences
– sequence: 10
  givenname: Amirhossein
  orcidid: 0000-0002-8656-1444
  surname: Sahebkar
  fullname: Sahebkar, Amirhossein
  email: sahebkara@mums.ac.ir, amir_saheb2000@yahoo.com
  organization: Mashhad University of Medical Sciences
BackLink https://www.ncbi.nlm.nih.gov/pubmed/29319160$$D View this record in MEDLINE/PubMed
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Keywords Polarization
Inflammation
Tissue repair
Plasticity
Macrophage
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Snippet Macrophages are heterogeneous and their phenotype and functions are regulated by the surrounding micro‐environment. Macrophages commonly exist in two distinct...
Macrophages are heterogeneous and their phenotype and functions are regulated by the surrounding micro-environment. Macrophages commonly exist in two distinct...
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SubjectTerms Allergies
Antigen presentation
Arteriosclerosis
Asthma
Atherosclerosis
Autoimmune diseases
Autoimmunity
Cell activation
Cytokines
Fibrosis
Homeostasis
IL-1β
Immunity
Immunoregulation
Inflammation
Interferon
Interleukins
Leukocyte migration
Lipopolysaccharides
Lymphocytes T
macrophage
Macrophages
Metabolic disorders
Metabolism
Microorganisms
miRNA
Phenotypes
Plastic properties
Plasticity
Polarization
Pregnancy
Repair
tissue repair
Transcription
Tumor necrosis factor
Wound healing
Title Macrophage plasticity, polarization, and function in health and disease
URI https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fjcp.26429
https://www.ncbi.nlm.nih.gov/pubmed/29319160
https://www.proquest.com/docview/2047430022
https://www.proquest.com/docview/1989580507
Volume 233
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