Journal ArticleDOI
Heme protects intestinal mucosal barrier in DSS-induced colitis through regulating macrophage polarization in both HO-1-dependent and HO-1-independent way
Yanwei Wu,Bing Wu,Zongwang Zhang,Huimin Lu,Chen Fan,Qing Qi,Yuanzhuo Gao,Heng Li,Chunlan Feng,Jianping Zuo,Wei Tang +10 more
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TLDR
Results showed that the modification of colon tissue microenvironment with heme supplementation plays a protective role in DSS‐induced colitis mice through regulating the macrophage polarization in both HO‐1‐dependent and HO‐ 1‐independent way, indicating a new choice to therapeutically modulate the macophage function and prevent IBD.Abstract:
Hemoglobin-derived heme was reported to play protective roles in hemorrhagic diseases by modulating the macrophages toward recovery. Mucosal bleeding is one of the pathological features of inflammatory bowel diseases (IBD). However, whether heme provides anti-inflammatory profiles in macrophages, thus contributing to the intestinal mucosal barrier protection, is unclear. In the current study, we investigated the beneficial effects of heme on DSS-induced colitis mice and explored the underlying mechanisms. In vivo, systemic heme supplementation by hemin injection relieved intestinal inflammation and remedied intestinal mucosal barrier damage by correcting abnormal intestinal macrophage polarization. In vitro, we confirmed the reciprocally regulating effects of hemin on M1/M2 macrophage polarization in BMDM. Intriguingly, with knockdown of HO-1, the inhibiting effects of hemin on M1 polarization were maintained, while the promoting effects on M2 polarization were reversed. Further research proved that hemin repressed the inflammatory profiles in macrophages through inhibiting the translocation of NF-κB p65 by disrupting IRF5-NF-κB p65 complex formation in Spi-C-dependent way. In conclusion, these results showed that the modification of colon tissue microenvironment with heme supplementation plays a protective role in DSS-induced colitis mice through regulating the macrophage polarization in both HO-1-dependent and HO-1-independent way, indicating a new choice to therapeutically modulate the macrophage function and prevent IBD.read more
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Regulation of inflammation by the antioxidant haem oxygenase 1
TL;DR: In this paper, an overview of haem oxygenase 1 (HO-1) for immunologists, including its roles in iron metabolism and antioxidant defence, and the impact of HO-1 induction in specific immune cell populations.
Journal ArticleDOI
Gut microbiota-derived butyrate regulates gut mucus barrier repair by activating the macrophage/WNT/ERK signaling pathway
TL;DR: In this paper , butyrate-induced macrophages increased mucin production and the proportion of goblet cells in the colon crypt in a macrophage-dependent manner by using clodronate liposomes.
Journal ArticleDOI
Gut microbiota-derived butyrate regulates gut mucus barrier repair by activating the macrophage/WNT/ERK signaling pathway.
TL;DR: It is found that butyrate increased mucin production and the proportion of mucin-secreting goblet cells in the colon crypt in a macrophage-dependent manner by using clodronate liposomes, implying that the microbial metabolitebutyrate may serve as a candidate therapeutic target for UC.
Journal ArticleDOI
Excretory/Secretory Products From Trichinella spiralis Adult Worms Attenuated DSS-Induced Colitis in Mice by Driving PD-1-Mediated M2 Macrophage Polarization.
Zixia Wang,Chunyue Hao,Qinghui Zhuang,Bin Zhan,Ximeng Sun,Jingjing Huang,Yuli Cheng,Xinping Zhu +7 more
TL;DR: The protective effects of T. spiralis AES on DSS-induced colitis were found to associate with PD-1 upregulation and M2 macrophage polarization, which is a key mechanism of helminth-induced modulation of the host immune system.
Journal ArticleDOI
Macrophage immunometabolism in inflammatory bowel diseases: From pathogenesis to therapy.
Xiaohua Pan,Qing Zhu,Xiaoliang Dong,Jihong Liu,He Liu,Zhengran Ren,Binbin Li,Li-Long Pan,Jian Sun +8 more
TL;DR: In this article , metabolic alterations underlie intestinal macrophage phenotype and function during IBD, and how microenvironmental cues trigger their metabolic reprogramming processes, and also summarized potential therapeutic approaches for IBD by manipulating cellular metabolism of macrophages.
References
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Journal ArticleDOI
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Dong Im Cho,Mi Ra Kim,Hye yun Jeong,Hae Chang Jeong,Myung Ho Jeong,Sung Ho Yoon,Yong Sook Kim,Youngkeun Ahn +7 more
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