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16 pages, 11886 KiB

Open AccessArticle

Phenotypic Alteration of BMDM In Vitro Using Small Interfering RNA

by Noreen Halimani, Mikhail Nesterchuk, Irina N. Andreichenko, Alexandra A. Tsitrina, Andrey Elchaninov, Anastasia Lokhonina, Timur Fatkhudinov, Nataliya O. Dashenkova, Vera Brezgina, Timofei S. Zatsepin, Arsen S. Mikaelyan and Yuri V. Kotelevtsev

Cells 2022, 11(16), 2498; https://doi.org/10.3390/cells11162498 - 11 Aug 2022

Cited by 2 | Viewed by 2789

Abstract

Autologous macrophage transfer is an emerging platform for cell therapy. It is anticipated that conventional macrophage reprogramming based on ex vivo polarization using cytokines and ligands of TLRs may enhance the therapeutic effect. We describe an alternative approach based on small interfering RNA [...] Read more.

Autologous macrophage transfer is an emerging platform for cell therapy. It is anticipated that conventional macrophage reprogramming based on ex vivo polarization using cytokines and ligands of TLRs may enhance the therapeutic effect. We describe an alternative approach based on small interfering RNA (siRNA) knockdown of selected molecular cues of macrophage polarization, namely EGR2, IRF3, IRF5, and TLR4 in Raw264.7 monocyte/macrophage cell line and mouse-bone-marrow-derived macrophages (BMDMs). The impact of IRF5 knockdown was most pronounced, curtailing the expression of other inflammatory mediators such as IL-6 and NOS2, especially in M1-polarized macrophages. Contrary to IRF5, EGR2 knockdown potentiated M1-associated markers while altogether abolishing M2 marker expression, which is indicative of the principal role of EGR2 in the maintenance of alternative phenotypes. IRF3 knockdown suppressed M1 polarization but upregulated Arg 1, a canonical marker of alternative polarization in M1 macrophages. As anticipated, the knockdown of TLR4 also attenuated the M1 phenotype but, akin to IRF3, significantly induced Arginase 1 in M0 and M1, driving the phenotype towards M2. This study validates RNAi as a viable option for the alteration and maintenance of macrophage phenotypes. Full article

(This article belongs to the Special Issue Macrophages in Tissue Repair, Regeneration, and Fibrosis)

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16 pages, 2381 KiB

Open AccessArticle

CD200R1 Contributes to Successful Functional Reinnervation after a Sciatic Nerve Injury

by Bruno Pannunzio, Jesús Amo-Aparicio, Camila Julián, Rubèn López-Vales, Hugo Peluffo and Natalia Lago

Cells 2022, 11(11), 1786; https://doi.org/10.3390/cells11111786 - 30 May 2022

Cited by 1 | Viewed by 2137

Abstract

Activating and inhibitory immune receptors play a critical role in regulating systemic and central nervous system (CNS) immune and inflammatory processes. The CD200R1 immunoreceptor induces a restraining signal modulating inflammation and phagocytosis in the CNS under different inflammatory conditions. However, it remains unknown [...] Read more.

Activating and inhibitory immune receptors play a critical role in regulating systemic and central nervous system (CNS) immune and inflammatory processes. The CD200R1 immunoreceptor induces a restraining signal modulating inflammation and phagocytosis in the CNS under different inflammatory conditions. However, it remains unknown whether CD200R1 has a role in modulating the inflammatory response after a peripheral nerve injury, an essential component of the successful regeneration. Expression of CD200R1 and its ligand CD200 was analyzed during homeostasis and after a sciatic nerve crush injury in C57Bl/6 mice. The role of CD200R1 in Wallerian Degeneration (WD) and nerve regeneration was studied using a specific antibody against CD200R1 injected into the nerve at the time of injury. We found an upregulation of CD200R1 mRNA after injury whereas CD200 was downregulated acutely after nerve injury. Blockade of CD200R1 significantly reduced the acute entrance of both neutrophils and monocytes from blood after nerve injury. When long term regeneration and functional recovery were evaluated, we found that blockade of CD200R1 had a significant effect impairing the spontaneous functional recovery. Taken together, these results show that CD200R1 has a role in mounting a successful acute inflammatory reaction after injury, and contributes to an effective functional recovery. Full article

(This article belongs to the Special Issue Macrophages in Tissue Repair, Regeneration, and Fibrosis)

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21 pages, 3834 KiB

Open AccessArticle

Asymptomatic Hyperuricemia Promotes Recovery from Ischemic Organ Injury by Modulating the Phenotype of Macrophages

by Viviane Gnemmi, Qiubo Li, Qiuyue Ma, Letizia De Chiara, Giulia Carangelo, Chenyu Li, Mireia Molina-Van den Bosch, Paola Romagnani, Hans-Joachim Anders and Stefanie Steiger

Cells 2022, 11(4), 626; https://doi.org/10.3390/cells11040626 - 11 Feb 2022

Cited by 7 | Viewed by 2742

Abstract

Acute organ injury, such as acute kidney injury (AKI) and disease (AKD), are major causes of morbidity and mortality worldwide. Hyperuricemia (HU) is common in patients with impaired kidney function but the impact of asymptomatic HU on the different phases of AKI/AKD is [...] Read more.

Acute organ injury, such as acute kidney injury (AKI) and disease (AKD), are major causes of morbidity and mortality worldwide. Hyperuricemia (HU) is common in patients with impaired kidney function but the impact of asymptomatic HU on the different phases of AKI/AKD is incompletely understood. We hypothesized that asymptomatic HU would attenuate AKD because soluble, in contrast to crystalline, uric acid (sUA) can attenuate sterile inflammation. In vitro, 10 mg/dL sUA decreased reactive oxygen species and interleukin-6 production in macrophages, while enhancing fatty acid oxidation as compared with a physiological concentration of 5 mg/dL sUA or medium. In transgenic mice, asymptomatic HU of 7–10 mg/dL did not affect post-ischemic AKI/AKD but accelerated the recovery of kidney excretory function on day 14. Improved functional outcome was associated with better tubular integrity, less peritubular inflammation, and interstitial fibrosis. Mechanistic studies suggested that HU shifted macrophage polarization towards an anti-inflammatory M2-like phenotype characterized by expression of anti-oxidative and metabolic genes as compared with post-ischemic AKI-chronic kidney disease transition in mice without HU. Our data imply that asymptomatic HU acts as anti-oxidant on macrophages and tubular epithelial cells, which endorses the recovery of kidney function and structure upon AKI. Full article

(This article belongs to the Special Issue Macrophages in Tissue Repair, Regeneration, and Fibrosis)

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16 pages, 3730 KiB

Open AccessFeature PaperArticle

Macrophage-Specific MCPIP1/Regnase-1 Attenuates Kidney Ischemia-Reperfusion Injury by Shaping the Local Inflammatory Response and Tissue Regeneration

by Andrea Ribeiro, Ewelina Dobosz, Moritz Krill, Paulina Köhler, Marta Wadowska, Stefanie Steiger, Christoph Schmaderer, Joanna Koziel and Maciej Lech

Cells 2022, 11(3), 397; https://doi.org/10.3390/cells11030397 - 24 Jan 2022

Cited by 5 | Viewed by 3362

Abstract

Sterile inflammation either resolves the initial insult or leads to tissue damage. Kidney ischemia/reperfusion injury (IRI) is associated with neutrophilic infiltration, enhanced production of inflammatory mediators, accumulation of necrotic cells and tissue remodeling. Macrophage-dependent microenvironmental changes orchestrate many features of the immune response [...] Read more.

Sterile inflammation either resolves the initial insult or leads to tissue damage. Kidney ischemia/reperfusion injury (IRI) is associated with neutrophilic infiltration, enhanced production of inflammatory mediators, accumulation of necrotic cells and tissue remodeling. Macrophage-dependent microenvironmental changes orchestrate many features of the immune response and tissue regeneration. The activation status of macrophages is influenced by extracellular signals, the duration and intensity of the stimulation, as well as various regulatory molecules. The role of macrophage-derived monocyte chemoattractant protein-induced protein 1 (MCPIP1), also known as Regnase-1, in kidney ischemia-reperfusion injury (IRI) and recovery from sterile inflammation remains unresolved. In this study, we showed that macrophage-specific Mcpip1 deletion significantly affects the kidney phenotype. Macrophage-specific Mcpip1 transgenic mice displayed enhanced inflammation and loss of the tubular compartment upon IRI. We showed that MCPIP1 modulates sterile inflammation by negative regulation of Irf4 expression and accumulation of IRF4+ cells in the tissue and, consequently, suppresses the post-ischemic kidney immune response. Thus, we identified MCPIP1 as an important molecular sentinel of immune homeostasis in experimental acute kidney injury (AKI) and renal fibrosis. Full article

(This article belongs to the Special Issue Macrophages in Tissue Repair, Regeneration, and Fibrosis)

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20 pages, 2851 KiB

Open AccessArticle

Differences in Cell-Intrinsic Inflammatory Programs of Yolk Sac and Bone Marrow Macrophages

by Sara Elhag, Christopher Stremmel, Annette Zehrer, Josefine Plocke, Roman Hennel, Michaela Keuper, Clarissa Knabe, Julia Winterhalter, Vanessa Gölling, Lukas Tomas, Tobias Weinberger, Maximilian Fischer, Lulu Liu, Franziska Wagner, Michael Lorenz, Konstantin Stark, Hans Häcker, Marc Schmidt-Supprian, Uwe Völker, Martin Jastroch, Kirsten Lauber, Tobias Straub, Barbara Walzog, Elke Hammer and Christian Schulz Show full author list Hide full author list

Cells 2021, 10(12), 3564; https://doi.org/10.3390/cells10123564 - 17 Dec 2021

Cited by 4 | Viewed by 3525

Abstract

Background: Tissue-resident macrophages have mixed developmental origins. They derive in variable extent from yolk sac (YS) hematopoiesis during embryonic development. Bone marrow (BM) hematopoietic progenitors give rise to tissue macrophages in postnatal life, and their contribution increases upon organ injury. Since the phenotype [...] Read more.

Background: Tissue-resident macrophages have mixed developmental origins. They derive in variable extent from yolk sac (YS) hematopoiesis during embryonic development. Bone marrow (BM) hematopoietic progenitors give rise to tissue macrophages in postnatal life, and their contribution increases upon organ injury. Since the phenotype and functions of macrophages are modulated by the tissue of residence, the impact of their origin and developmental paths has remained incompletely understood. Methods: In order to decipher cell-intrinsic macrophage programs, we immortalized hematopoietic progenitors from YS and BM using conditional HoxB8, and carried out an in-depth functional and molecular analysis of differentiated macrophages. Results: While YS and BM macrophages demonstrate close similarities in terms of cellular growth, differentiation, cell death susceptibility and phagocytic properties, they display differences in cell metabolism, expression of inflammatory markers and inflammasome activation. Reduced abundance of PYCARD (ASC) and CASPASE-1 proteins in YS macrophages abrogated interleukin-1β production in response to canonical and non-canonical inflammasome activation. Conclusions: Macrophage ontogeny is associated with distinct cellular programs and immune response. Our findings contribute to the understanding of the regulation and programming of macrophage functions. Full article

(This article belongs to the Special Issue Macrophages in Tissue Repair, Regeneration, and Fibrosis)

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15 pages, 2828 KiB

Open AccessArticle

Infusion of Phagocytic Macrophages Overexpressing CPT1a Ameliorates Kidney Fibrosis in the UUO Model

by Priscila Calle, Soraya Játiva, Selene Torrico, Angeles Muñoz, Miriam García, Anna Sola, Dolors Serra, Paula Mera, Laura Herrero and Georgina Hotter

Cells 2021, 10(7), 1650; https://doi.org/10.3390/cells10071650 - 30 Jun 2021

Cited by 7 | Viewed by 2974

Abstract

Phagocytosis is an inherent function of tissue macrophages for the removal of apoptotic cells and cellular debris during acute and chronic injury; however, the dynamics of this event during fibrosis development is unknown. We aim to prove that during the development of kidney [...] Read more.

Phagocytosis is an inherent function of tissue macrophages for the removal of apoptotic cells and cellular debris during acute and chronic injury; however, the dynamics of this event during fibrosis development is unknown. We aim to prove that during the development of kidney fibrosis in the unilateral ureteral obstruction (UUO) model, there are some populations of macrophage with a reduced ability to phagocytose, and whether the infusion of a population of phagocytic macrophages could reduce fibrosis in the murine model UUO. For this purpose, we have identified the macrophage populations during the development of fibrosis and have characterized their phagocytic ability and their expression of CPT1a. Furthermore, we have evaluated the therapeutic effect of macrophages overexpressing CPT1a with high phagocytic skills. We evidenced that the macrophage population which exhibits high phagocytic ability (F4/80low-CD11b) in fibrotic animals decreases during the progression of fibrosis while the macrophage population with lower phagocytic ability (F4/80high-CD11b) in fibrotic conditions, conversely, increases and CPT1a macrophage cell therapy with a strengthening phagocytic ability is associated with a therapeutic effect on kidney fibrosis. We have developed a therapeutic approach to reduce fibrosis in the UUO model by enrichment of the kidney resident macrophage population with a higher proportion of exogenous phagocytic macrophages overexpressing CPT1a. Full article

(This article belongs to the Special Issue Macrophages in Tissue Repair, Regeneration, and Fibrosis)

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Review

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14 pages, 1042 KiB

Open AccessReview

Macrophages and Wnts in Tissue Injury and Repair

by Min Hee Park, Eun D. Lee and Wook-Jin Chae

Cells 2022, 11(22), 3592; https://doi.org/10.3390/cells11223592 - 14 Nov 2022

Cited by 7 | Viewed by 2047

Abstract

Macrophages are important players in the immune system that sense various tissue challenges and trigger inflammation. Tissue injuries are followed by inflammation, which is tightly coordinated with tissue repair processes. Dysregulation of these processes leads to chronic inflammation or tissue fibrosis. Wnt ligands [...] Read more.

Macrophages are important players in the immune system that sense various tissue challenges and trigger inflammation. Tissue injuries are followed by inflammation, which is tightly coordinated with tissue repair processes. Dysregulation of these processes leads to chronic inflammation or tissue fibrosis. Wnt ligands are present both in homeostatic and pathological conditions. However, their roles and mechanisms regulating inflammation and tissue repair are being investigated. Here we aim to provide an overview of overarching themes regarding Wnt and macrophages by reviewing the previous literature. We aim to gain future insights into how tissue inflammation, repair, regeneration, and fibrosis events are regulated by macrophages. Full article

(This article belongs to the Special Issue Macrophages in Tissue Repair, Regeneration, and Fibrosis)

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17 pages, 2191 KiB

Open AccessReview

Protein Lipidation by Palmitate Controls Macrophage Function

by Jeroen Guns, Sam Vanherle, Jerome J. A. Hendriks and Jeroen F. J. Bogie

Cells 2022, 11(3), 565; https://doi.org/10.3390/cells11030565 - 06 Feb 2022

Cited by 5 | Viewed by 4172

Abstract

Macrophages are present in all tissues within our body, where they promote tissue homeostasis by responding to microenvironmental triggers, not only through clearance of pathogens and apoptotic cells but also via trophic, regulatory, and repair functions. To accomplish these divergent functions, tremendous dynamic [...] Read more.

Macrophages are present in all tissues within our body, where they promote tissue homeostasis by responding to microenvironmental triggers, not only through clearance of pathogens and apoptotic cells but also via trophic, regulatory, and repair functions. To accomplish these divergent functions, tremendous dynamic fine-tuning of their physiology is needed. Emerging evidence indicates that S-palmitoylation, a reversible post-translational modification that involves the linkage of the saturated fatty acid palmitate to protein cysteine residues, directs many aspects of macrophage physiology in health and disease. By controlling protein activity, stability, trafficking, and protein–protein interactions, studies identified a key role of S-palmitoylation in endocytosis, inflammatory signaling, chemotaxis, and lysosomal function. Here, we provide an in-depth overview of the impact of S-palmitoylation on these cellular processes in macrophages in health and disease. Findings discussed in this review highlight the therapeutic potential of modulators of S-palmitoylation in immunopathologies, ranging from infectious and chronic inflammatory disorders to metabolic conditions. Full article

(This article belongs to the Special Issue Macrophages in Tissue Repair, Regeneration, and Fibrosis)

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18 pages, 3060 KiB

Open AccessReview

Macrophages and Immune Responses in Uterine Fibroids

by Alessandro Zannotti, Stefania Greco, Pamela Pellegrino, Federica Giantomassi, Giovanni Delli Carpini, Gaia Goteri, Andrea Ciavattini and Pasquapina Ciarmela

Cells 2021, 10(5), 982; https://doi.org/10.3390/cells10050982 - 22 Apr 2021

Cited by 24 | Viewed by 7847

Abstract

Uterine fibroids represent the most common benign tumors of the uterus. They are considered a typical fibrotic disorder. In fact, the extracellular matrix (ECM) proteins—above all, collagen 1A1, fibronectin and versican—are upregulated in this pathology. The uterine fibroids etiology has not yet been [...] Read more.

Uterine fibroids represent the most common benign tumors of the uterus. They are considered a typical fibrotic disorder. In fact, the extracellular matrix (ECM) proteins—above all, collagen 1A1, fibronectin and versican—are upregulated in this pathology. The uterine fibroids etiology has not yet been clarified, and this represents an important matter about their resolution. A model has been proposed according to which the formation of an altered ECM could be the result of an excessive wound healing, in turn driven by a dysregulated inflammation process. A lot of molecules act in the complex inflammatory response. Macrophages have a great flexibility since they can assume different phenotypes leading to the tissue repair process. The dysregulation of macrophage proliferation, accumulation and infiltration could lead to an uncontrolled tissue repair and to the consequent pathological fibrosis. In addition, molecules such as monocyte chemoattractant protein-1 (MCP-1), granulocyte macrophage-colony-stimulating factor (GM-CSF), transforming growth factor-beta (TGF-β), activin A and tumor necrosis factor-alfa (TNF-α) were demonstrated to play an important role in the macrophage action within the uncontrolled tissue repair that contributes to the pathological fibrosis that represents a typical feature of the uterine fibroids. Full article

(This article belongs to the Special Issue Macrophages in Tissue Repair, Regeneration, and Fibrosis)

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21 pages, 1620 KiB

Open AccessReview

Chronic Diabetic Wounds and Their Treatment with Skin Substitutes

by Jordan Holl, Cezary Kowalewski, Zbigniew Zimek, Piotr Fiedor, Artur Kaminski, Tomasz Oldak, Marcin Moniuszko and Andrzej Eljaszewicz

Cells 2021, 10(3), 655; https://doi.org/10.3390/cells10030655 - 15 Mar 2021

Cited by 99 | Viewed by 8322

Abstract

With the global prevalence of type 2 diabetes mellitus steeply rising, instances of chronic, hard-healing, or non-healing diabetic wounds and ulcers are predicted to increase. The growing understanding of healing and regenerative mechanisms has elucidated critical regulators of this process, including key cellular [...] Read more.

With the global prevalence of type 2 diabetes mellitus steeply rising, instances of chronic, hard-healing, or non-healing diabetic wounds and ulcers are predicted to increase. The growing understanding of healing and regenerative mechanisms has elucidated critical regulators of this process, including key cellular and humoral components. Despite this, the management and successful treatment of diabetic wounds represents a significant therapeutic challenge. To this end, the development of novel therapies and biological dressings has gained increased interest. Here we review key differences between normal and chronic non-healing diabetic wounds, and elaborate on recent advances in wound healing treatments with a particular focus on biological dressings and their effect on key wound healing pathways. Full article

(This article belongs to the Special Issue Macrophages in Tissue Repair, Regeneration, and Fibrosis)

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19 pages, 2173 KiB

Open AccessReview

Glomerular Macrophages in Human Auto- and Allo-Immune Nephritis

by Solange Moll, Andrea Angeletti, Leonardo Scapozza, Andrea Cavalli, Gian Marco Ghiggeri and Marco Prunotto

Cells 2021, 10(3), 603; https://doi.org/10.3390/cells10030603 - 09 Mar 2021

Cited by 5 | Viewed by 3064

Abstract

Macrophages are involved in tissue homeostasis. They participate in inflammatory episodes and are involved in tissue repair. Macrophages are characterized by a phenotypic heterogeneity and a profound cell plasticity. In the kidney, and more particularly within glomeruli, macrophages are thought to play a [...] Read more.

Macrophages are involved in tissue homeostasis. They participate in inflammatory episodes and are involved in tissue repair. Macrophages are characterized by a phenotypic heterogeneity and a profound cell plasticity. In the kidney, and more particularly within glomeruli, macrophages are thought to play a maintenance role that is potentially critical for preserving a normal glomerular structure. Literature on the glomerular macrophage role in human crescentic glomerulonephritis and renal transplantation rejection with glomerulitis, is sparse. Evidence from preclinical models indicates that macrophages profoundly modulate disease progression, both in terms of number—where depletion has resulted in a reduced glomerular lesion—and sub-phenotype—M1 being more profoundly detrimental than M2. This evidence is corroborated by better outcomes in patients with a lower number of glomerular macrophages. However, due to the very limited biopsy sample size, the type and role of macrophage subpopulations involved in human proliferative lesions is more difficult to precisely define and synthesize. Therefore, specific biomarkers of macrophage activation may enhance our ability to assess their role, potentially enabling improved monitoring of drug activity and ultimately allowing the development of novel therapeutic strategies to target these elusive cellular players. Full article

(This article belongs to the Special Issue Macrophages in Tissue Repair, Regeneration, and Fibrosis)

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17 pages, 2157 KiB

Open AccessReview

Macrophages in Lung Injury, Repair, and Fibrosis

by Peiyong Cheng, Shuangyan Li and Huaiyong Chen

Cells 2021, 10(2), 436; https://doi.org/10.3390/cells10020436 - 18 Feb 2021

Cited by 158 | Viewed by 11565

Abstract

Fibrosis progression in the lung commonly results in impaired functional gas exchange, respiratory failure, or even death. In addition to the aberrant activation and differentiation of lung fibroblasts, persistent alveolar injury and incomplete repair are the driving factors of lung fibrotic response. Macrophages [...] Read more.

Fibrosis progression in the lung commonly results in impaired functional gas exchange, respiratory failure, or even death. In addition to the aberrant activation and differentiation of lung fibroblasts, persistent alveolar injury and incomplete repair are the driving factors of lung fibrotic response. Macrophages are activated and polarized in response to lipopolysaccharide- or bleomycin-induced lung injury. The classically activated macrophage (M1) and alternatively activated macrophage (M2) have been extensively investigated in lung injury, repair, and fibrosis. In the present review, we summarized the current data on monocyte-derived macrophages that are recruited to the lung, as well as alveolar resident macrophages and their polarization, pyroptosis, and phagocytosis in acute lung injury (ALI). Additionally, we described how macrophages interact with lung epithelial cells during lung repair. Finally, we emphasized the role of macrophage polarization in the pulmonary fibrotic response, and elucidated the potential benefits of targeting macrophage in alleviating pulmonary fibrosis. Full article

(This article belongs to the Special Issue Macrophages in Tissue Repair, Regeneration, and Fibrosis)

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27 pages, 1665 KiB

Open AccessReview

Role of Cardiac Macrophages on Cardiac Inflammation, Fibrosis and Tissue Repair

by William P. Lafuse, Daniel J. Wozniak and Murugesan V. S. Rajaram

Cells 2021, 10(1), 51; https://doi.org/10.3390/cells10010051 - 31 Dec 2020

Cited by 166 | Viewed by 16580

Abstract

The immune system plays a pivotal role in the initiation, development and resolution of inflammation following insult or damage to organs. The heart is a vital organ which supplies nutrients and oxygen to all parts of the body. Heart failure (HF) has been [...] Read more.

The immune system plays a pivotal role in the initiation, development and resolution of inflammation following insult or damage to organs. The heart is a vital organ which supplies nutrients and oxygen to all parts of the body. Heart failure (HF) has been conventionally described as a disease associated with cardiac tissue damage caused by systemic inflammation, arrhythmia and conduction defects. Cardiac inflammation and subsequent tissue damage is orchestrated by the infiltration and activation of various immune cells including neutrophils, monocytes, macrophages, eosinophils, mast cells, natural killer cells, and T and B cells into the myocardium. After tissue injury, monocytes and tissue-resident macrophages undergo marked phenotypic and functional changes, and function as key regulators of tissue repair, regeneration and fibrosis. Disturbance in resident macrophage functions such as uncontrolled production of inflammatory cytokines, growth factors and inefficient generation of an anti-inflammatory response or unsuccessful communication between macrophages and epithelial and endothelial cells and fibroblasts can lead to aberrant repair, persistent injury, and HF. Therefore, in this review, we discuss the role of cardiac macrophages on cardiac inflammation, tissue repair, regeneration and fibrosis. Full article

(This article belongs to the Special Issue Macrophages in Tissue Repair, Regeneration, and Fibrosis)

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21 pages, 1362 KiB

Open AccessReview

At the Forefront of the Mucosal Barrier: The Role of Macrophages in the Intestine

by Barbara Ruder and Christoph Becker

Cells 2020, 9(10), 2162; https://doi.org/10.3390/cells9102162 - 24 Sep 2020

Cited by 33 | Viewed by 4764

Abstract

Macrophages are part of the innate immunity and are key players for the maintenance of intestinal homeostasis. They belong to the group of mononuclear phagocytes, which exert bactericidal functions and help to clear apoptotic cells. Moreover, they play essential roles for the maintenance [...] Read more.

Macrophages are part of the innate immunity and are key players for the maintenance of intestinal homeostasis. They belong to the group of mononuclear phagocytes, which exert bactericidal functions and help to clear apoptotic cells. Moreover, they play essential roles for the maintenance of epithelial integrity and tissue remodeling during wound healing processes and might be implicated in intestinal tumor development. Macrophages are antigen-presenting cells and secrete immune-modulatory factors, like chemokines and cytokines, which are necessary to activate other intestinal immune cells and therefore to shape immune responses in the gut. However, overwhelming activation or increased secretion of pro-inflammatory cytokines might also contribute to the pathogenesis of inflammatory bowel disease. Presently, intestinal macrophages are in the center of intense studies, which might help to develop new therapeutic strategies to counteract the development or treat already existing inflammatory diseases in the gut. In this review, we focus on the origin of intestinal macrophages and, based on current knowledge, discuss their role in the gut during homeostasis and inflammation, as well as during intestinal wound healing and tumor development. Full article

(This article belongs to the Special Issue Macrophages in Tissue Repair, Regeneration, and Fibrosis)

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