scholarly journals YAP Aggravates Inflammatory Bowel Disease by Regulating M1/M2 Macrophage Polarization and Gut Microbial Homeostasis

Cell Reports ◽  
2019 ◽  
Vol 27 (4) ◽  
pp. 1176-1189.e5 ◽  
Author(s):  
Xin Zhou ◽  
Weiyun Li ◽  
Shuang Wang ◽  
Panli Zhang ◽  
Qiong Wang ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Macrophage Polarization ◽  
M2 Macrophage ◽  
Inflammatory Bowel ◽  
M2 Macrophage Polarization

scholarly journals MiR-98-5p expression inhibits polarization of macrophages to an M2 phenotype by targeting Trib1 in inflammatory bowel disease

2020 ◽  
Author(s):  
Yunhua Peng ◽  
Qingyuan Wang ◽  
Wei Yang ◽  
Qiqi Yang ◽  
Ynani Pei ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Macrophage Polarization ◽  
Luciferase Reporter ◽  
Marker Genes ◽  
M2 Macrophage ◽  
M1 Macrophage ◽  
Inflammatory Bowel ◽  
M2 Macrophage Polarization ◽  
M2 Phenotype

Herein, we unfolded miR-98-5p mechanism in inflammatory bowel disease (IBD). IBD mouse model was established. The severity of colitis was assessed daily using the disease activity index (DAI). Murine peritoneal macrophages were stimulated by lipopolysaccharide (LPS). MiR-98-5p, tribbles homolog 1 (Trib1), M1 and M2 macrophage marker genes mRNA expression was analyzed. The relationship between miR-98-5p and Trib1 was explored using a luciferase reporter assay. The strategy of loss-of-function was used to explore the mechanism of miR-98-5p in macrophage polarization, inflammation and IBD. The results revealed that IBD mice had higher DAI index and miR-98-5p expression when compared to the Sham group. MiR-98-5p and Trib1 displayed a targeted regulation relationship. Knockdown of miR-98-5p transformed LPS-induced M1 macrophage polarization into M2 macrophage polarization and inhibited inflammation via up-regulating Trib1. However, shTrib1 reversed the effects. In vivo experiment, silencing of miR-98-5p, diminished the DAI and promoted M2 macrophage polarization. In conclusion, knockdown of miR-98-5p changed macrophage polarization to the M2 phenotype by increasing Trib1 expression, thereby alleviating IBD symptoms.

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

2021 ◽  
Vol 12 (6) ◽  
Author(s):  
Lu Liu ◽  
Yuqing Wu ◽  
Bingwei Wang ◽  
Yuying Jiang ◽  
Lin Lin ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Macrophage Polarization ◽  
Experimental Colitis ◽  
M2 Macrophage ◽  
M1 Macrophages ◽  
Inflammatory Bowel ◽  
M2 Macrophage Polarization ◽  
Mechanistic Basis ◽  
Functional Relevance ◽  
Creb Pathway

AbstractThe decrease of neurotransmitter dopamine (DA) levels in the intestine is closely related to the development of inflammatory bowel disease (IBD). However, the functional relevance and underlying mechanistic basis of the effects of DA signaling on IBD remains unclear. Here, we observed that the DRD5 receptor is highly expressed in colonic macrophages, and the deficiency of DA-DRD5 signaling exacerbated experimental colitis. Moreover, DA-DRD5 signaling can inhibit M1 by negatively regulating NF-κB signaling but promote M2 macrophage polarization through activation of the CREB pathway, respectively. The deficiency of DRD5 signaling increased colonic M1 macrophages but reduced M2 cells during colitis. Additionally, the administration of a D1-like agonist that has a higher affinity to DRD5 can attenuate the colitogenic phenotype of mice. Collectively, these findings provide the first demonstration of DA-DRD5 signaling in colonic macrophages controlling the development of colitis by regulating M1/M2 macrophage polarization.

scholarly journals Colonic macrophage polarization in homeostasis, inflammation, and cancer

2016 ◽  
Vol 311 (1) ◽  
pp. G59-G73 ◽  
Author(s):  
Raymond A. Isidro ◽  
Caroline B. Appleyard
Keyword(s):  
Inflammatory Bowel Disease ◽  
Tumor Growth ◽  
Bowel Disease ◽  
Macrophage Polarization ◽  
Inflammatory Conditions ◽  
Inflammatory Phenotype ◽  
Cancer Tumor ◽  
Colon And Rectum ◽  
Inflammatory Bowel ◽  
Anti Inflammatory

Our review focuses on the colonic macrophage, a monocyte-derived, tissue-resident macrophage, and the role it plays in health and disease, specifically in inflammatory conditions such as inflammatory bowel disease and cancer of the colon and rectum. We give special emphasis to macrophage polarization, or phenotype, in these different states. We focus on macrophages because they are one of the most numerous leukocytes in the colon, and because they normally contribute to homeostasis through an anti-inflammatory phenotype. However, in conditions such as inflammatory bowel disease, proinflammatory macrophages are increased in the colon and have been linked to disease severity and progression. In colorectal cancer, tumor cells may employ anti-inflammatory macrophages to promote tumor growth and dissemination, whereas proinflammatory macrophages may antagonize tumor growth. Given the key roles that this cell type plays in homeostasis, inflammation, and cancer, the colonic macrophage is an intriguing therapeutic target. As such, potential macrophage-targeting strategies are discussed.

Sign in / Sign up

Export Citation Format

Share Document