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

被引:11
作者
Guo, Bingnan [1 ,2 ]
Peng, Yigen [3 ]
Gu, Yuting [1 ,2 ]
Zhong, Yi [1 ,2 ]
Su, Chenglei [1 ,2 ]
Liu, Lin [1 ,2 ]
Chai, Dafei [4 ]
Song, Tengfei [5 ]
Zhao, Ningjun [1 ,2 ]
Yan, Xianliang [1 ,2 ]
Xu, Tie [1 ,2 ,3 ]
机构
[1] Xuzhou Med Univ, Jiangsu Inst Hlth Emergency, Xuzhou 221004, Jiangsu, Peoples R China
[2] Xuzhou Med Univ, Dept Emergency Med, Affiliated Hosp, Xuzhou 221000, Jiangsu, Peoples R China
[3] Nanjing Med Univ, Dept Emergency Med, Affiliated Jiangning Hosp, Nanjing 211100, Jiangsu, Peoples R China
[4] Xuzhou Med Univ, Canc Inst, Xuzhou 221004, Jiangsu, Peoples R China
[5] Feinstein Inst Med Res, Manhasset, NY 11030 USA
来源
OPEN LIFE SCIENCES | 2021年 / 16卷 / 01期
基金
中国国家自然科学基金;
关键词
resveratrol; LPS; acute lung injury; conventional dendritic cells; ACUTE RESPIRATORY-DISTRESS; OXIDATIVE STRESS; T-CELLS; INFLAMMATION; MECHANISMS; SEPSIS; APOPTOSIS; RESPONSES; OUTCOMES;
D O I
10.1515/biol-2021-0110
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
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.
引用
收藏
页码:1064 / 1081
页数:18
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