PD-L1 Blockade Attenuated Sepsis-Induced Liver Injury in a Mouse Cecal Ligation and Puncture Model

Liver plays a major role in hypermetabolism and produces acute phase proteins during systemic inflammatory response syndrome and it is of vital importance in host defense and bacteria clearance. Our previous studies indicated that programmed death-1 (PD-1) and its ligand programmed death ligand-1 (P...

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Main Authors: Weimin Zhu, Rui Bao, Xiaohua Fan, Tianzhu Tao, Jiali Zhu, Jiafeng Wang, Jinbao Li, Lulong Bo, Xiaoming Deng
Format: Article
Language:English
Published: Wiley 2013-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/2013/361501
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author Weimin Zhu
Rui Bao
Xiaohua Fan
Tianzhu Tao
Jiali Zhu
Jiafeng Wang
Jinbao Li
Lulong Bo
Xiaoming Deng
author_facet Weimin Zhu
Rui Bao
Xiaohua Fan
Tianzhu Tao
Jiali Zhu
Jiafeng Wang
Jinbao Li
Lulong Bo
Xiaoming Deng
author_sort Weimin Zhu
collection DOAJ
description Liver plays a major role in hypermetabolism and produces acute phase proteins during systemic inflammatory response syndrome and it is of vital importance in host defense and bacteria clearance. Our previous studies indicated that programmed death-1 (PD-1) and its ligand programmed death ligand-1 (PD-L1) are crucial modulators of host immune responses during sepsis. Our current study was designed to investigate the role of PD-L1 in sepsis-induced liver injury by a mouse cecal ligation and puncture (CLP) model. Our results indicated that there was a significant increase of PD-L1 expression in liver after CLP challenge compared to sham-operated controls, in terms of levels of mRNA transcription and immunohistochemistry. Anti-PD-L1 antibody significantly alleviated the morphology of liver injury in CLP mice. Anti-PD-L1 antibody administration decreased ALT and AST release in CLP mice, decreased the levels of tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-10 mRNA in liver after sepsis challenge. Thus, anti-PD-L1 antibody might have a therapeutic potential in attenuating liver injury in sepsis.
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institution Kabale University
issn 0962-9351
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language English
publishDate 2013-01-01
publisher Wiley
record_format Article
series Mediators of Inflammation
spelling doaj-art-6eefb01753024222891a2acd7cde508a2025-02-03T01:01:51ZengWileyMediators of Inflammation0962-93511466-18612013-01-01201310.1155/2013/361501361501PD-L1 Blockade Attenuated Sepsis-Induced Liver Injury in a Mouse Cecal Ligation and Puncture ModelWeimin Zhu0Rui Bao1Xiaohua Fan2Tianzhu Tao3Jiali Zhu4Jiafeng Wang5Jinbao Li6Lulong Bo7Xiaoming Deng8Department of Anesthesiology, Changhai Hospital, Second Military Medical University, 168 Changhai Road, Shanghai 200433, ChinaDepartment of Anesthesiology, Changhai Hospital, Second Military Medical University, 168 Changhai Road, Shanghai 200433, ChinaDepartment of Anesthesiology, Changhai Hospital, Second Military Medical University, 168 Changhai Road, Shanghai 200433, ChinaDepartment of Anesthesiology, Changhai Hospital, Second Military Medical University, 168 Changhai Road, Shanghai 200433, ChinaDepartment of Anesthesiology, Changhai Hospital, Second Military Medical University, 168 Changhai Road, Shanghai 200433, ChinaDepartment of Anesthesiology, Changhai Hospital, Second Military Medical University, 168 Changhai Road, Shanghai 200433, ChinaDepartment of Anesthesiology, Changhai Hospital, Second Military Medical University, 168 Changhai Road, Shanghai 200433, ChinaDepartment of Anesthesiology, Changhai Hospital, Second Military Medical University, 168 Changhai Road, Shanghai 200433, ChinaDepartment of Anesthesiology, Changhai Hospital, Second Military Medical University, 168 Changhai Road, Shanghai 200433, ChinaLiver plays a major role in hypermetabolism and produces acute phase proteins during systemic inflammatory response syndrome and it is of vital importance in host defense and bacteria clearance. Our previous studies indicated that programmed death-1 (PD-1) and its ligand programmed death ligand-1 (PD-L1) are crucial modulators of host immune responses during sepsis. Our current study was designed to investigate the role of PD-L1 in sepsis-induced liver injury by a mouse cecal ligation and puncture (CLP) model. Our results indicated that there was a significant increase of PD-L1 expression in liver after CLP challenge compared to sham-operated controls, in terms of levels of mRNA transcription and immunohistochemistry. Anti-PD-L1 antibody significantly alleviated the morphology of liver injury in CLP mice. Anti-PD-L1 antibody administration decreased ALT and AST release in CLP mice, decreased the levels of tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-10 mRNA in liver after sepsis challenge. Thus, anti-PD-L1 antibody might have a therapeutic potential in attenuating liver injury in sepsis.http://dx.doi.org/10.1155/2013/361501
spellingShingle Weimin Zhu
Rui Bao
Xiaohua Fan
Tianzhu Tao
Jiali Zhu
Jiafeng Wang
Jinbao Li
Lulong Bo
Xiaoming Deng
PD-L1 Blockade Attenuated Sepsis-Induced Liver Injury in a Mouse Cecal Ligation and Puncture Model
Mediators of Inflammation
title PD-L1 Blockade Attenuated Sepsis-Induced Liver Injury in a Mouse Cecal Ligation and Puncture Model
title_full PD-L1 Blockade Attenuated Sepsis-Induced Liver Injury in a Mouse Cecal Ligation and Puncture Model
title_fullStr PD-L1 Blockade Attenuated Sepsis-Induced Liver Injury in a Mouse Cecal Ligation and Puncture Model
title_full_unstemmed PD-L1 Blockade Attenuated Sepsis-Induced Liver Injury in a Mouse Cecal Ligation and Puncture Model
title_short PD-L1 Blockade Attenuated Sepsis-Induced Liver Injury in a Mouse Cecal Ligation and Puncture Model
title_sort pd l1 blockade attenuated sepsis induced liver injury in a mouse cecal ligation and puncture model
url http://dx.doi.org/10.1155/2013/361501
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