Loss of Bcl‐3 regulates macrophage polarization by promoting macrophage glycolysis

Author:

Liu Shengnan12,Wang Hao3,Li Jiaoyang12,Gao Jingtao4,Yu Li12,Wei Xiaofei12,Cui Mengchao12,Zhao Yuxin4,Liang Yinming12,Wang Hui124ORCID

Affiliation:

1. Henan Key Laboratory of Immunology and Targeted Drug, School of Laboratory Medicine Xinxiang Medical University Xinxiang China

2. Henan Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine Xinxiang Medical University Xinxiang China

3. The Third Affiliated Hospital, Xinxiang Medical University Xinxiang China

4. Department of Immunology, School of Basic Medical Sciences Xinjiang Medical University Urumqi China

Abstract

AbstractM1/M2 macrophage polarization plays an important role in regulating the balance of the microenvironment within tissues. Moreover, macrophage polarization involves the reprogramming of metabolism, such as glucose and lipid metabolism. Transcriptional coactivator B‐cell lymphoma‐3 (Bcl‐3) is an atypical member of the IκB family that controls inflammatory factor levels in macrophages by regulating nuclear factor kappa B pathway activation. However, the relationship between Bcl‐3 and macrophage polarization and metabolism remains unclear. In this study, we show that the knockdown of Bcl‐3 in macrophages can regulate glycolysis‐related gene expression by promoting the activation of the nuclear factor kappa B pathway. Furthermore, the loss of Bcl‐3 was able to promote the interferon gamma/lipopolysaccharide‐induced M1 macrophage polarization by accelerating glycolysis. Taken together, these results suggest that Bcl‐3 may be a candidate gene for regulating M1 polarization in macrophages.

Funder

National Natural Science Foundation of China

Publisher

Wiley

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