Resveratrol pretreatment mitigates LPS-induced acute lung injury by regulating conventional dendritic cells’ maturation and function

Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is a severe syndrome lacking efficient therapy and resulting in high morbidity and mortality. Although resveratrol (RES), a natural phytoalexin, has been reported to protect the ALI by suppressing the inflammatory response, the detai...

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Autores principales: Guo Bingnan, Peng Yigen, Gu Yuting, Zhong Yi, Su Chenglei, Liu Lin, Chai Dafei, Song Tengfei, Zhao Ningjun, Yan Xianliang, Xu Tie
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Lenguaje:EN
Publicado: De Gruyter 2021
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spelling oai:doaj.org-article:06c8703fa96745fda282f063da7e69402021-12-05T14:10:42ZResveratrol pretreatment mitigates LPS-induced acute lung injury by regulating conventional dendritic cells’ maturation and function2391-541210.1515/biol-2021-0110https://doaj.org/article/06c8703fa96745fda282f063da7e69402021-09-01T00:00:00Zhttps://doi.org/10.1515/biol-2021-0110https://doaj.org/toc/2391-5412Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is a severe syndrome lacking efficient therapy and resulting in high morbidity and mortality. Although resveratrol (RES), a natural phytoalexin, has been reported to protect the ALI by suppressing the inflammatory response, the detailed mechanism of how RES affected the immune system is poorly studied. Pulmonary conventional dendritic cells (cDCs) are critically involved in the pathogenesis of inflammatory lung diseases including ALI. In this study, we aimed to investigate the protective role of RES via pulmonary cDCs in lipopolysaccharide (LPS)-induced ALI mice. Murine ALI model was established by intratracheally challenging with 5 mg/kg LPS. We found that RES pretreatment could mitigate LPS-induced ALI. Additionally, proinflammatory-skewed cytokines decreased whereas anti-inflammatory-related cytokines increased in bronchoalveolar lavage fluid by RES pretreatment. Mechanistically, RES regulated pulmonary cDCs’ maturation and function, exhibiting lower level of CD80, CD86, major histocompatibility complex (MHC) II expression, and IL-10 secretion in ALI mice. Furthermore, RES modulated the balance between proinflammation and anti-inflammation of cDCs. Moreover, in vitro RES pretreatment regulated the maturation and function of bone marrow derived dendritic cells (BMDCs). Finally, the adoptive transfer of RES-pretreated BMDCs enhanced recovery of ALI. Thus, these data might further extend our understanding of a protective role of RES in regulating pulmonary cDCs against ALI.Guo BingnanPeng YigenGu YutingZhong YiSu ChengleiLiu LinChai DafeiSong TengfeiZhao NingjunYan XianliangXu TieDe Gruyterarticleresveratrollpsacute lung injuryconventional dendritic cellsBiology (General)QH301-705.5ENOpen Life Sciences, Vol 16, Iss 1, Pp 1064-1081 (2021)
institution DOAJ
collection DOAJ
language EN
topic resveratrol
lps
acute lung injury
conventional dendritic cells
Biology (General)
QH301-705.5
spellingShingle resveratrol
lps
acute lung injury
conventional dendritic cells
Biology (General)
QH301-705.5
Guo Bingnan
Peng Yigen
Gu Yuting
Zhong Yi
Su Chenglei
Liu Lin
Chai Dafei
Song Tengfei
Zhao Ningjun
Yan Xianliang
Xu Tie
Resveratrol pretreatment mitigates LPS-induced acute lung injury by regulating conventional dendritic cells’ maturation and function
description Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is a severe syndrome lacking efficient therapy and resulting in high morbidity and mortality. Although resveratrol (RES), a natural phytoalexin, has been reported to protect the ALI by suppressing the inflammatory response, the detailed mechanism of how RES affected the immune system is poorly studied. Pulmonary conventional dendritic cells (cDCs) are critically involved in the pathogenesis of inflammatory lung diseases including ALI. In this study, we aimed to investigate the protective role of RES via pulmonary cDCs in lipopolysaccharide (LPS)-induced ALI mice. Murine ALI model was established by intratracheally challenging with 5 mg/kg LPS. We found that RES pretreatment could mitigate LPS-induced ALI. Additionally, proinflammatory-skewed cytokines decreased whereas anti-inflammatory-related cytokines increased in bronchoalveolar lavage fluid by RES pretreatment. Mechanistically, RES regulated pulmonary cDCs’ maturation and function, exhibiting lower level of CD80, CD86, major histocompatibility complex (MHC) II expression, and IL-10 secretion in ALI mice. Furthermore, RES modulated the balance between proinflammation and anti-inflammation of cDCs. Moreover, in vitro RES pretreatment regulated the maturation and function of bone marrow derived dendritic cells (BMDCs). Finally, the adoptive transfer of RES-pretreated BMDCs enhanced recovery of ALI. Thus, these data might further extend our understanding of a protective role of RES in regulating pulmonary cDCs against ALI.
format article
author Guo Bingnan
Peng Yigen
Gu Yuting
Zhong Yi
Su Chenglei
Liu Lin
Chai Dafei
Song Tengfei
Zhao Ningjun
Yan Xianliang
Xu Tie
author_facet Guo Bingnan
Peng Yigen
Gu Yuting
Zhong Yi
Su Chenglei
Liu Lin
Chai Dafei
Song Tengfei
Zhao Ningjun
Yan Xianliang
Xu Tie
author_sort Guo Bingnan
title Resveratrol pretreatment mitigates LPS-induced acute lung injury by regulating conventional dendritic cells’ maturation and function
title_short Resveratrol pretreatment mitigates LPS-induced acute lung injury by regulating conventional dendritic cells’ maturation and function
title_full Resveratrol pretreatment mitigates LPS-induced acute lung injury by regulating conventional dendritic cells’ maturation and function
title_fullStr Resveratrol pretreatment mitigates LPS-induced acute lung injury by regulating conventional dendritic cells’ maturation and function
title_full_unstemmed Resveratrol pretreatment mitigates LPS-induced acute lung injury by regulating conventional dendritic cells’ maturation and function
title_sort resveratrol pretreatment mitigates lps-induced acute lung injury by regulating conventional dendritic cells’ maturation and function
publisher De Gruyter
publishDate 2021
url https://doaj.org/article/06c8703fa96745fda282f063da7e6940
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