Disequilibrium of M1 and M2 Macrophages Correlates with the Development of Experimental Inflammatory Bowel Diseases

  title={Disequilibrium of M1 and M2 Macrophages Correlates with the Development of Experimental Inflammatory Bowel Diseases},
  author={Wei Zhu and Jianbo Yu and Ying Nie and Xuekui Shi and Yang Liu and Fujuan Li and Xiaoli Zhang},
  journal={Immunological Investigations},
  pages={638 - 652}
Ulcerative colitis, a major inflammatory bowel disease, is an idiopathic inflammatory disorder of the colonic mucosa, accompanied by an aberrant immune reaction to intestinal microflora. Macrophages are central mediators of intestinal immune homeostasis and inflammation. The relationship between macrophages and the pathogenesis of colitis is poorly understood. We aimed to characterize the changing populations and roles of M1/M2 macrophages in colitis. We demonstrated that M1 macrophages… 

The Role of Tissue-Resident Macrophages in the Development and Treatment of Inflammatory Bowel Disease

Light is shed on the origin and maintenance of intestinal macrophages, as well as the role of macrophage-derived exosome in the occurrence and development of IBD.

Depression Exacerbates Dextran Sulfate Sodium-Induced Colitis via IRF5-Mediated Macrophage Polarization

ITD patients with inflammatory bowel disease and concurrent depression are predisposed to severer disease activity and a worse prognosis, and IRF5-mediated macrophage polarization may likely underlie the deterioration of DSS-induced colitis caused by depression.

Sorting nexin 10 acting as a novel regulator of macrophage polarization mediates inflammatory response in experimental mouse colitis

It is shown that deficiency of SNX10 polarized macrophages derived from mouse bone marrow or human peripheral blood mononuclear cells (PBMCs) towards an anti-inflammatory M2 phenotype, which partially reversed bySNX10 plasmid transfection.

Control of Intestinal Inflammation, Colitis-Associated Tumorigenesis, and Macrophage Polarization by Fibrinogen-Like Protein 2

It is reported that Fgl2 deficiency increased susceptibility to dextran sodium sulfate-induced colitis and CAC in a mouse model and may serve as a therapeutic target in inflammatory diseases, including IBD.

M2 macrophages and their role in rheumatic diseases

The markers of human M2 macrophages, the role played by them in inflammation or progression of rheumatic diseases, their potential to act as biomarkers, and, finally, therapeutic strategies aiming at altering/enhancing the macrophage phenotype are discussed.

DA-DRD5 signaling controls colitis by regulating colonic M1/M2 macrophage polarization

These findings provide the first demonstration of DA-DRD5 signaling in colonic macrophages controlling the development of colitis by regulating M1/M2 macrophage polarization.



The key role of macrophages in the immunopathogenesis of inflammatory bowel disease.

  • Y. Mahida
  • Medicine, Biology
    Inflammatory bowel diseases
  • 2000
Macrophages play a major role in mediating the chronic mucosal inflammation seen in patients with ulcerative colitis and Crohn's disease and appear to be important during resolution of inflammation and repair of the intestinal mucosa that occurs during disease remission.

IL-23 is essential for T cell-mediated colitis and promotes inflammation via IL-17 and IL-6.

This study shows that in these models, IL-23 is essential for manifestation of chronic intestinal inflammation, whereas IL-12 is not, and a critical target of IL- 23 is a unique subset of tissue-homing memory T cells, which are specifically activated by IL-21 to produce the proinflammatory mediators IL-17 and IL-6.

Ex vivo programmed macrophages ameliorate experimental chronic inflammatory renal disease.

It is demonstrated that macrophages not only act as effectors of immune injury but can be induced to provide protection against immune injury.

In vitro-derived alternatively activated macrophages reduce colonic inflammation in mice.

The ability to derive AAMs from patients' blood suggests that adoptive transfer of these cells could be a novel approach to inflammatory bowel disease.

Epithelial-derived IL-33 and its receptor ST2 are dysregulated in ulcerative colitis and in experimental Th1/Th2 driven enteritis

The IL-33/ST2 system plays an important role in IBD and experimental colitis, is modulated by anti-TNF therapy, and may represent a specific biomarker for active UC.

Foxp3+ Regulatory T Cells, Th17 Effector Cells, and Cytokine Environment in Inflammatory Bowel Disease

IBD is associated with a reduced ratio of Treg to Th 17 cells in peripheral blood and is characterized by a proinflammatory cytokine microenvironment, which supports the continued generation of Th17 cells.

Parasitic Helminth Cystatin Inhibits DSS-Induced Intestinal Inflammation Via IL-10+F4/80+ Macrophage Recruitment

Many immune down-regulatory molecules have been isolated from parasites, including cystatin (cystain protease inhibitor). In a previous study, we isolated and characterized Type I cystatin

Lamina propria macrophages and dendritic cells differentially induce regulatory and interleukin 17–producing T cell responses

A population of CD11b+F4/80+CD11c− macrophages in the lamina propria that expressed several anti-inflammatory molecules, including interleukin 10 (IL-10), but little or no proinflammatory cytokines, even after stimulation with Toll-like receptor ligands is described.

Monoclonal anti-interleukin 23 reverses active colitis in a T cell-mediated model in mice.

Bacterial-reactive CD4(+) Th17 cells are potent effector cells in chronic colitis and IL-23 is an attractive therapeutic target for inflammatory bowel disease.

Interleukin-23 drives innate and T cell–mediated intestinal inflammation

IL-23 is newly identified as a driver of innate immune pathology in the intestine and selective targeting of IL-23 represents an attractive therapeutic approach in human IBD.