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Macrophage Heterogeneity in Respiratory Diseases

Boorsma, Carian E., Draijer, Christina, Melgert, Barbro N.·2013·Mediators of Inflammation
DOI 10.1155/2013/769214PMC PMC3600198
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Abstract

Macrophages are among the most abundant cells in the respiratory tract, and they can have strikingly different phenotypes within this environment. Our knowledge of the different phenotypes and their functions in the lung is sketchy at best, but they appear to be linked to the protection of gas exchange against microbial threats and excessive tissue responses. Phenotypical changes of macrophages within the lung are found in many respiratory diseases including asthma, chronic obstructive pulmonary disease (COPD), and pulmonary fibrosis. This paper will give an overview of what macrophage phenotypes have been described, what their known functions are, what is known about their presence in the different obstructive and restrictive respiratory diseases (asthma, COPD, pulmonary fibrosis), and how they are thought to contribute to the etiology and resolution of these diseases.

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Figure 1 Schematic representation of the three macrophage phenotypes and their characteristics. IFNγ: interferon gamma; TNFα: tumor necrosis factor alpha; LPS: lipopolysaccharide; MHC class II: major histocompatibility complex class II; IL: interleukin; NO: nitric oxide; IRF5: interferon regulatory factor 5; Fe: iron; TGM2: transglutaminase 2; YM1: chitinase-3-like protein-3; FIZZ1/Relmα: resistin-like molecule-α; Arg-1: arginase-1; TGFβ: transforming growth factor beta; TLR: Toll-like receptor; PGE2: prostaglandin E2; PPARγ: peroxisome proliferator-activated receptor gamma.
Figure 1 Schematic representation of the three macrophage phenotypes and their characteristics. IFNγ: interferon gamma; TNFα: tumor necrosis factor alpha; LPS: lipopolysaccharide; MHC class II: major histocompatibility complex class II; IL: interleukin; NO: nitric oxide; IRF5: interferon regulatory factor 5; Fe: iron; TGM2: transglutaminase 2; YM1: chitinase-3-like protein-3; FIZZ1/Relmα: resistin-like molecule-α; Arg-1: arginase-1; TGFβ: transforming growth factor beta; TLR: Toll-like receptor; PGE2: prostaglandin E2; PPARγ: peroxisome proliferator-activated receptor gamma.CC BY · PubMed Central
Figure 2 Schematic representation of the presence of M1, M2, and M2-like macrophages in lung tissue during homeostatic conditions, induction of asthma, and during moderate and severe asthma.
Figure 2 Schematic representation of the presence of M1, M2, and M2-like macrophages in lung tissue during homeostatic conditions, induction of asthma, and during moderate and severe asthma.CC BY · PubMed Central
Figure 3 Schematic representation of the presence of M1, M2, and M2-like macrophages in lung tissue during homeostatic conditions, during healthy smoking, and in COPD. Please note the dysfunctional state of macrophages during COPD.
Figure 3 Schematic representation of the presence of M1, M2, and M2-like macrophages in lung tissue during homeostatic conditions, during healthy smoking, and in COPD. Please note the dysfunctional state of macrophages during COPD.CC BY · PubMed Central
Figure 4 Schematic representation of the presence of M1, M2, and M2-like macrophages in lung tissue during homeostatic conditions and after injury to the lung. Normally after lung injury a process of tissue repair is initiated with four distinct phases leading to homeostatic conditions again. In lung fibrosis this normal tissue repair response is dysregulated leading to deposition of excess extracellular matrix and little resolution of scar tissue.
Figure 4 Schematic representation of the presence of M1, M2, and M2-like macrophages in lung tissue during homeostatic conditions and after injury to the lung. Normally after lung injury a process of tissue repair is initiated with four distinct phases leading to homeostatic conditions again. In lung fibrosis this normal tissue repair response is dysregulated leading to deposition of excess extracellular matrix and little resolution of scar tissue.CC BY · PubMed Central

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Metadata

Authors
Boorsma, C. E., Draijer, C., & Melgert, B. N.
Affiliations
Department of Pharmacokinetics, Toxicology and Targeting, Groningen Research Institute for Pharmacy, University of Groningen, Antonius Deusinglaan 1, 9713 AV Groningen, The Netherlands
Venue
Mediators of Inflammation
Publisher
Hindawi Limited
Published
2013
Volume
2013
Pages
1-19
ISSN
  • 0962-9351
  • 1466-1861
DOI
10.1155/2013/769214
PMC
PMC3600198
Cited by
126
References
16
Language
en
Licence
creativecommons.org/licenses/by/3.0/ (unspecified)

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