Increased GABA signaling in liver macrophage promotes HBV replication in HBV-carrier mice

• Published in: Virus research Vol. 344; p. 199366
• Main Authors: Chen, Yunling, Yin, Zhaoqing, Zhang, Xiaonan, Zhao, Yiwei, Liu, Tinghao, Lu, Wei-Yang, Wang, Shuanglian
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.06.2024; Elsevier
• Subjects: Animals; Disease Models, Animal; GABA, macrophage; gamma-Aminobutyric Acid - metabolism; HBV replication; Hepatitis B - metabolism; Hepatitis B - virology; Hepatitis B virus - genetics; Hepatitis B virus - physiology; Humans; Liver - metabolism; Liver - virology; Macrophage polarization; Macrophages - virology; Mice; Receptors, GABA-A - genetics; Receptors, GABA-A - metabolism; Signal Transduction; Virus Replication; HBV replication; Macrophage polarization; GABA, macrophage
• ISSN: 0168-1702; 1872-7492
• DOI: 10.1016/j.virusres.2024.199366

•A functional GABA signaling system exists in liver macrophages.•Activation of GABA signaling leads to the M2-like anti-inflammatory phenotype of liver macrophages.•GABA signaling activation promotes HBV replication in HBV-carrier mice. Gamma-aminobutyric acid (GABA) signals in various non-neuronal cells including hepatocytes and some immune cells. Studies, including ours, show that type A GABA receptors (GABAARs)-mediated signaling occurs in macrophages regulating tissue-specific functions. Our recent study reveals that activation of GABAARs in liver macrophages promotes their M2-like polarization and increases HBV replication in mice. This short article briefly summarizes the GABA signaling system in macrophages and discusses potential mechanisms by which GABA signaling promotes HBV replication.