TMEM16F Expressed in Kupffer Cells Regulates Liver Inflammation and Metabolism to Protect Against Listeria Monocytogenes

Abstract Infection by bacteria leads to tissue damage and inflammation, which need to be tightly controlled by host mechanisms to avoid deleterious consequences. It is previously reported that TMEM16F, a calcium‐activated lipid scramblase expressed in various immune cell types including T cells and...

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Main Authors: Jianlong Tang, Hua Song, Shimin Li, Sin Man Lam, Jieming Ping, Mengyun Yang, Na Li, Teding Chang, Ze Yu, Weixiang Liu, Yan Lu, Min Zhu, Zhaohui Tang, Zheng Liu, Yusong R. Guo, Guanghou Shui, André Veillette, Zhutian Zeng, Ning Wu
Format: Article
Language:English
Published: Wiley 2024-10-01
Series:Advanced Science
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Online Access:https://doi.org/10.1002/advs.202402693
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author Jianlong Tang
Hua Song
Shimin Li
Sin Man Lam
Jieming Ping
Mengyun Yang
Na Li
Teding Chang
Ze Yu
Weixiang Liu
Yan Lu
Min Zhu
Zhaohui Tang
Zheng Liu
Yusong R. Guo
Guanghou Shui
André Veillette
Zhutian Zeng
Ning Wu
author_facet Jianlong Tang
Hua Song
Shimin Li
Sin Man Lam
Jieming Ping
Mengyun Yang
Na Li
Teding Chang
Ze Yu
Weixiang Liu
Yan Lu
Min Zhu
Zhaohui Tang
Zheng Liu
Yusong R. Guo
Guanghou Shui
André Veillette
Zhutian Zeng
Ning Wu
author_sort Jianlong Tang
collection DOAJ
description Abstract Infection by bacteria leads to tissue damage and inflammation, which need to be tightly controlled by host mechanisms to avoid deleterious consequences. It is previously reported that TMEM16F, a calcium‐activated lipid scramblase expressed in various immune cell types including T cells and neutrophils, is critical for the control of infection by bacterium Listeria monocytogenes (Lm) in vivo. This function correlated with the capacity of TMEM16F to repair the plasma membrane (PM) damage induced in T cells in vitro, by the Lm toxin listeriolysin O (LLO). However, whether the protective effect of TMEM16F on Lm infection in vivo is mediated by an impact in T cells, or in other cell types, is not determined. Herein, the immune cell types and mechanisms implicated in the protective effect of TMEM16F against Lm in vivo are elucidated. Cellular protective effects of TMEM16F correlated with its capacity of lipid scrambling and augment PM fluidity. Using cell type‐specific TMEM16F‐deficient mice, the indication is obtained that TMEM16F expressed in liver Kupffer cells (KCs), but not in T cells or B cells, is key for protection against Listeria in vivo. In the absence of TMEM16F, Listeria induced PM rupture and fragmentation of KCs in vivo. KC death associated with greater liver damage, inflammatory changes, and dysregulated liver metabolism. Overall, the results uncovered that TMEM16F expressed in Kupffer cells is crucial to protect the host against Listeria infection. This influence is associated with the capacity of Kupffer cell‐expressed TMEM16F to prevent excessive inflammation and abnormal liver metabolism.
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spelling doaj-art-450c2d021b794d45ad4d02b1ca5d99ce2025-08-20T02:10:42ZengWileyAdvanced Science2198-38442024-10-011139n/an/a10.1002/advs.202402693TMEM16F Expressed in Kupffer Cells Regulates Liver Inflammation and Metabolism to Protect Against Listeria MonocytogenesJianlong Tang0Hua Song1Shimin Li2Sin Man Lam3Jieming Ping4Mengyun Yang5Na Li6Teding Chang7Ze Yu8Weixiang Liu9Yan Lu10Min Zhu11Zhaohui Tang12Zheng Liu13Yusong R. Guo14Guanghou Shui15André Veillette16Zhutian Zeng17Ning Wu18Department of Immunology School of Basic Medicine Tongji Medical College Huazhong University of Science and Technology (HUST) Wuhan 430030 ChinaDepartment of Immunology School of Basic Medicine Tongji Medical College Huazhong University of Science and Technology (HUST) Wuhan 430030 ChinaThe CAS Key Laboratory of Innate Immunity and Chronic Disease School of Basic Medical Sciences Division of Life Sciences and Medicine University of Science and Technology of China Hefei 230001 ChinaState Key Laboratory of Molecular Developmental Biology Institute of Genetics and Developmental Biology Chinese Academy of Sciences Beijing 100101 ChinaDepartment of Immunology School of Basic Medicine Tongji Medical College Huazhong University of Science and Technology (HUST) Wuhan 430030 ChinaDepartment of Immunology School of Basic Medicine Tongji Medical College Huazhong University of Science and Technology (HUST) Wuhan 430030 ChinaDepartment of biochemistry and molecular biology School of Basic Medicine Tongji Medical College Huazhong University of Science and Technology Wuhan 430030 ChinaDepartment of Traumatic Surgery Tongji Trauma Center Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430030 ChinaDepartment of Otolaryngology‐Head and Neck Surgery Tongji Hospital Tongji Medical College Huazhong University of Science and Technology No. 1095 Jiefang Avenue Wuhan 430030 ChinaDepartment of Immunology School of Basic Medicine Tongji Medical College Huazhong University of Science and Technology (HUST) Wuhan 430030 ChinaDepartment of Clinical Immunology The Third Affiliated Hospital of Sun Yat‐sen University Guangzhou 510630 ChinaDepartment of Thoracic Surgery Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430030 ChinaDepartment of Traumatic Surgery Tongji Trauma Center Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430030 ChinaDepartment of Otolaryngology‐Head and Neck Surgery Tongji Hospital Tongji Medical College Huazhong University of Science and Technology No. 1095 Jiefang Avenue Wuhan 430030 ChinaDepartment of biochemistry and molecular biology School of Basic Medicine Tongji Medical College Huazhong University of Science and Technology Wuhan 430030 ChinaState Key Laboratory of Molecular Developmental Biology Institute of Genetics and Developmental Biology Chinese Academy of Sciences Beijing 100101 ChinaLaboratory of Molecular Oncology Institut de recherches cliniques de Montréal (IRCM) Montréal Québec H2W1R7 CanadaThe CAS Key Laboratory of Innate Immunity and Chronic Disease School of Basic Medical Sciences Division of Life Sciences and Medicine University of Science and Technology of China Hefei 230001 ChinaDepartment of Immunology School of Basic Medicine Tongji Medical College Huazhong University of Science and Technology (HUST) Wuhan 430030 ChinaAbstract Infection by bacteria leads to tissue damage and inflammation, which need to be tightly controlled by host mechanisms to avoid deleterious consequences. It is previously reported that TMEM16F, a calcium‐activated lipid scramblase expressed in various immune cell types including T cells and neutrophils, is critical for the control of infection by bacterium Listeria monocytogenes (Lm) in vivo. This function correlated with the capacity of TMEM16F to repair the plasma membrane (PM) damage induced in T cells in vitro, by the Lm toxin listeriolysin O (LLO). However, whether the protective effect of TMEM16F on Lm infection in vivo is mediated by an impact in T cells, or in other cell types, is not determined. Herein, the immune cell types and mechanisms implicated in the protective effect of TMEM16F against Lm in vivo are elucidated. Cellular protective effects of TMEM16F correlated with its capacity of lipid scrambling and augment PM fluidity. Using cell type‐specific TMEM16F‐deficient mice, the indication is obtained that TMEM16F expressed in liver Kupffer cells (KCs), but not in T cells or B cells, is key for protection against Listeria in vivo. In the absence of TMEM16F, Listeria induced PM rupture and fragmentation of KCs in vivo. KC death associated with greater liver damage, inflammatory changes, and dysregulated liver metabolism. Overall, the results uncovered that TMEM16F expressed in Kupffer cells is crucial to protect the host against Listeria infection. This influence is associated with the capacity of Kupffer cell‐expressed TMEM16F to prevent excessive inflammation and abnormal liver metabolism.https://doi.org/10.1002/advs.202402693inflammationkupffer celllipid scramblinglisteria monocytogenesmacrophageplasma membrane integrity
spellingShingle Jianlong Tang
Hua Song
Shimin Li
Sin Man Lam
Jieming Ping
Mengyun Yang
Na Li
Teding Chang
Ze Yu
Weixiang Liu
Yan Lu
Min Zhu
Zhaohui Tang
Zheng Liu
Yusong R. Guo
Guanghou Shui
André Veillette
Zhutian Zeng
Ning Wu
TMEM16F Expressed in Kupffer Cells Regulates Liver Inflammation and Metabolism to Protect Against Listeria Monocytogenes
Advanced Science
inflammation
kupffer cell
lipid scrambling
listeria monocytogenes
macrophage
plasma membrane integrity
title TMEM16F Expressed in Kupffer Cells Regulates Liver Inflammation and Metabolism to Protect Against Listeria Monocytogenes
title_full TMEM16F Expressed in Kupffer Cells Regulates Liver Inflammation and Metabolism to Protect Against Listeria Monocytogenes
title_fullStr TMEM16F Expressed in Kupffer Cells Regulates Liver Inflammation and Metabolism to Protect Against Listeria Monocytogenes
title_full_unstemmed TMEM16F Expressed in Kupffer Cells Regulates Liver Inflammation and Metabolism to Protect Against Listeria Monocytogenes
title_short TMEM16F Expressed in Kupffer Cells Regulates Liver Inflammation and Metabolism to Protect Against Listeria Monocytogenes
title_sort tmem16f expressed in kupffer cells regulates liver inflammation and metabolism to protect against listeria monocytogenes
topic inflammation
kupffer cell
lipid scrambling
listeria monocytogenes
macrophage
plasma membrane integrity
url https://doi.org/10.1002/advs.202402693
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