Tissue-Specific Role of Macrophages in Noninfectious Inflammatory Disorders - PubMed (original) (raw)
Review
Tissue-Specific Role of Macrophages in Noninfectious Inflammatory Disorders
Daria Skuratovskaia et al. Biomedicines. 2020.
Abstract
Chronic inflammation may not begin with local tissue disorders, such as hypoxia, but with the accumulation of critically activated macrophages in one site. The purpose of this review is to analyze the data reported in the scientific literature on the features of the functions of macrophages and their contributions to the development of pathology in various tissues during aseptic inflammation in obese subjects. In individuals with obesity, increased migration of monocytes from the peripheral blood to various tissues, the proliferation of resident macrophages and a change in the balance between alternatively activated anti-inflammatory macrophages (M2) and pro-inflammatory classically activated macrophages (M1) towards the latter have been observed. The primary cause of some metabolic pathologies has been precisely identified as the recruitment of macrophages with an altered phenotype, which is probably typical for many other pathologies. Recent studies have identified phenotypes, such as metabolically activated M (MMe), oxidized (Mox), hemoglobin-related macrophages (Mhem and MHb), M4 and neuroimmunological macrophages (NAM, SAM), which directly and indirectly affect energy metabolism. The high heterogeneity of macrophages in tissues contributes to the involvement of these cells in the development of a wide range of immune responses, including pathological ones. The replenishment of tissue-specific macrophages occurs at the expense of infiltrating monocyte-derived macrophages (MoMFs) in the pathological process. The origin of MoMFs from a general precursor retains their common regulatory mechanisms and similar sensitivity to regulatory stimuli. This makes it possible to find universal approaches to the effect on these cells and, as a consequence, universal approaches for the treatment of various pathological conditions.
Keywords: NAFLD; adipose tissue; atherosclerosis; endothelial dysfunction; inflammation; liver; macrophage; nervous tissue; obesity.
Conflict of interest statement
The authors declare no conflict of interest. “The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, or in the decision to publish the results”.
Figures
Figure 1
Tissue distribution of macrophages in non-infectious metabolic disorders. M1—inflammatory classically activated macrophages; M2—alternatively activated anti-inflammatory macrophages; M4—M4 macrophage; Mhem—hemoglobin-related macrophages; KC—Kupffer cells; LCM—liver capsular macrophages; LPM—large peritoneal macrophages; MoMF—monocyte-derived macrophages; Mox—oxidized macrophages; NAM—neuro-associated macrophages; SAM—sympathetic neuron-associated macrophages; MMe—metabolically activated macrophages; oxoLDL—oxidized low-density lipoprotein; ApoB—Apolipoprotein B. This figure has been created by modifying the templates from Servier Medical Art (
).
Figure 2
Inductors, markers and functions of macrophages subtypes in tissues. All macrophage subtypes may take a pro- or anti-inflammatory phenotype in obesity. MoMFs are a common precursor for subtypes of migrating macrophages in tissue. When damaged, MoMFs can assume a tissue-specific phenotype. Determining the exact origin of macrophages (resident or migratory) is a task in modern science. The plasticity of macrophages between M1 and M2 is also present in the resident forms and is shown by an arrow. The arrow indicates the stimuli, markers and functions that characterize both types of polarization. ABCA1—ATP binding cassette subfamily a member 1; AP—atherosclerosis plaque; AT—adipose tissue; DAMPS—damage-associated molecular patterns; GCLM—glutamate–cysteine ligase modifier subunit; GST—glutathione S-transferase; Hb/Hp—hemoglobin/haptoglobin; HO-1—heme oxygenase 1; IL—Interleukin; KC—Kupffer cells; LCM—liver capsular macrophages; LPM— large peritoneal macrophages; LPS—lipopolysaccharide; MAOA—monoamine oxidase A; MoMF—monocyte-derived macrophage; Mox—oxidized macrophages; MR—mannose receptor; NAM—neuro-associated macrophages; NE—norepinephrine; Nox2—NADPH oxidase-2; OxPL—oxidized phospholipids; PLIN2—Perilipin 2; PPARγ—peroxisome proliferator-activated receptor gamma; ROS—reactive oxygen species; SAM—sympathetic neuron-associated macrophages; SLC6A2—carrier family 6 member 2; SNS—sympathetic nervous system; Srnx-1—sulfiredoxin-1; TH—tyrosine hydroxylase; TLR—Toll-like receptor; Txnrd1—thioredoxin reductase 1; MMe—metabolically activated macrophages; *—mouse-specific markers; #—cannot be M1 and M2. This figure has been created by modifying the templates from Servier Medical Art (
).
References
- Obesity. [(accessed on 25 September 2020)]; Available online: https://www.who.int/westernpacific/health-topics/obesity.
- Litvinova L.S., Kiriyenkova Y.V., Aksyonova N.N., Gazatova N.D., Zatolokin P.A. Features of cellular immunity and cytokine repertoire in patients with metabolic syndrome. Bull. Sib. Med. 2012;11:53–57. doi: 10.20538/1682-0363-2012-3-53-57. - DOI
- Litvinova L.S., Vasilenko M.A., Zatolokin P.A., Aksenova N.N., Fattakhov N.S. Adipokines in metabolic processes regulating during obesity treatment. Diabetes Mellit. 2014;17:51–59. doi: 10.14341/DM2014351-59. - DOI
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- No. 18-015-00084-a/Russian Foundation for Basic Research
- No.19-415-393004/Russian Foundation for Basic Research
- No.19-44-390005/Russian Foundation for Basic Research
- No. 2495.2020.7/State support of leading scientific schools of the Russian Federation
- No. 075-03-2020-080/State Assignment
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