Functions of Macrophages in the Maintenance of Intestinal Homeostasis

Wang, Shuai; Ye, Qianhong; Zeng, Xiangfang; Qiao, Shiyan

doi:10.1155/2019/1512969

Cited by 65 publications

(53 citation statements)

References 78 publications

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“…In addition, other innate effector cells such as eosinophils are produced by Ly6C hi monocytes through secretion of CCL11 (eotaxin). More importantly, Ly6C hi monocytes are reported to directly regulate the pathogenic effects of neutrophils and the production of TNF-α and reactive oxygen species (ROS) by neutrophils in a PGE2-dependent manner [88]. Excessive accumulation of lipid-laden foam cells in endothelium signifies the earliest manifestation of an atherosclerotic lesion ( Figure 5).…”

Section: Mcp-1: a Biochemical Marker Associated With Endothelial Dysfmentioning

confidence: 99%

Endothelial Dysfunction in Obesity-Induced Inflammation: Molecular Mechanisms and Clinical Implications

et al. 2020

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Obesity is characterized by the excessive deposition of fat that may interfere with the normal metabolic process of the body. It is a chronic condition associated with various metabolic syndromes, whose prevalence is grossly increasing, and affects both children and adults. Accumulation of excessive macronutrients on the adipose tissues promotes the secretion and release of inflammatory mediators, including interleukin-6 (IL-6), interleukin 1β, tumor necrotic factor-α (TNF-α), leptin, and stimulation of monocyte chemoattractant protein-1 (MCP-1), which subsequently reduce the production of adiponectin thereby initiating a proinflammatory state. During obesity, adipose tissue synthesizes and releases a large number of hormones and cytokines that alter the metabolic processes, with a profound influence on endothelial dysfunction, a situation associated with the formation of atherosclerotic plaque. Endothelial cells respond to inflammation and stimulation of MCP-1, which is described as the activation of adhesion molecules leading to proliferation and transmigration of leukocytes, which facilitates their increase in atherogenic and thromboembolic potentials. Endothelial dysfunction forms the cornerstone of this discussion, as it has been considered as the initiator in the progression of cardiovascular diseases in obesity. Overexpression of proinflammatory cytokines with subsequent reduction of anti-inflammatory markers in obesity, is considered to be the link between obesity-induced inflammation and endothelial dysfunction. Inhibition of inflammatory mechanisms and management and control of obesity can assist in reducing the risks associated with cardiovascular complications.

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Section: Mcp-1: a Biochemical Marker Associated With Endothelial Dysfmentioning

confidence: 99%

Endothelial Dysfunction in Obesity-Induced Inflammation: Molecular Mechanisms and Clinical Implications

et al. 2020

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“…Dysregulated homeostasis of immune cells is associated with intestinal inflammation [8]. Of the several immune cells that regulate inflammatory responses, macrophages are important during the development of intestinal inflammation [9][10][11]. Inflammatory bowel diseases (IBD), including Crohn's disease (CD) and ulcerative colitis (UC), are inflammatory disorders that affect the gastrointestinal tract.…”

Section: Introductionmentioning

confidence: 99%

Detrimental Role of Nerve Injury-Induced Protein 1 in Myeloid Cells under Intestinal Inflammatory Conditions

Jung

Kang

Pak

et al. 2020

IJMS

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Nerve injury-induced protein 1 (Ninjurin1, Ninj1) is a cell-surface adhesion molecule that regulates cell migration and attachment. This study demonstrates the increase in Ninj1 protein expression during development of intestinal inflammation. Ninj1-deficient mice exhibited significantly attenuated bodyweight loss, shortening of colon length, intestinal inflammation, and lesser pathological lesions than wild-type mice. Although more severe inflammation and serious lesions are observed in wild-type mice than Ninj1-deficient mice, there were no changes in the numbers of infiltrating macrophages in the inflamed tissues obtained from WT and Ninj1-deficient mice. Ninj1 expression results in activation of macrophages, and these activated macrophages secrete more cytokines and chemokines than Ninj1-deficient macrophages. Moreover, mice with conditional deletion of Ninj1 in myeloid cells (Ninj1fl/fl; Lyz-Cre+) alleviated experimental colitis compared with wild-type mice. In summary, we propose that the Ninj1 in myeloid cells play a pivotal function in intestinal inflammatory conditions.

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“…Intestinal macrophages are considered to be the main participants in establishing and maintaining gut homeostasis 4 , 70 and are important scavengers of dead and dying cells 70 . An increasing number of studies have shown that macrophages are novel potential targets for the development of new treatment approaches for IBD 4 , 6 . Thus, it is believed that understanding how apoptotic cell-engulfing macrophages promote the proliferation of epithelial cells (and thus contribute to tissue homeostasis) during IBD is believed to be critical for developing therapeutic strategies to cure such diseases 9 .…”

Section: Discussionmentioning

confidence: 99%

“…Inflammatory bowel disease (IBD) is a chronic inflammatory condition of the gastrointestinal tract caused by impairment of the intestinal epithelial cell (IEC) layers 1 – 3 . Increasing evidence suggests that macrophages have protective functions in intestinal health and disease 4 – 6 . Macrophages engulf apoptotic cells that were produced by tissue damage.…”

Section: Introductionmentioning

confidence: 99%

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Activation of mTORC1 by LSECtin in macrophages directs intestinal repair in inflammatory bowel disease

Cheng

Liu

et al. 2020

Cell Death Dis

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Damage to intestinal epithelial cells and the induction of cellular apoptosis are characteristics of inflammatory bowel disease. The C-type lectin receptor family member LSECtin promotes apoptotic cell clearance by macrophages and induces the production of anti-inflammatory/tissue growth factors, which direct intestinal repair in experimental colitis. However, the mechanisms by which the phagocytosis of apoptotic cells triggers the pro-repair function of macrophages remain largely undefined. Here, using immunoprecipitation in combination with mass spectrometry to identify LSECtin-interacting proteins, we found that LSECtin interacted with mTOR, exhibiting a role in activating mTORC1. Mechanistically, apoptotic cells enhance the interaction between LSECtin and mTOR, and increase the activation of mTORC1 induced by LSECtin in macrophages. Elevated mTORC1 signaling triggers macrophages to produce anti-inflammatory/tissue growth factors that contribute to the proliferation of epithelial cells and promote the reestablishment of tissue homeostasis. Collectively, our findings suggest that LSECtin-dependent apoptotic cell clearance by macrophages activates mTORC1, and thus contributes to intestinal regeneration and the remission of colitis.

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Functions of Macrophages in the Maintenance of Intestinal Homeostasis

Cited by 65 publications

References 78 publications

Endothelial Dysfunction in Obesity-Induced Inflammation: Molecular Mechanisms and Clinical Implications

Endothelial Dysfunction in Obesity-Induced Inflammation: Molecular Mechanisms and Clinical Implications

Detrimental Role of Nerve Injury-Induced Protein 1 in Myeloid Cells under Intestinal Inflammatory Conditions

Activation of mTORC1 by LSECtin in macrophages directs intestinal repair in inflammatory bowel disease

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