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- Title
Role of brain‐derived neurotrophic factor in endotoxaemia‐induced acute lung injury.
- Authors
Shi, Jinye; Song, Shuang; Wu, Kaixuan; Liang, Gui; Wang, Aizhong; Xu, Xiaotao
- Abstract
Acute lung injury (ALI) or acute respiratory distress syndrome (ARDS), which is a pulmonary manifestation of a systemic reactive inflammatory syndrome, is a serious disease with high mortality, and sepsis is an important risk factor in the development of ALI. Brain‐derived neurotrophic factor (BDNF) is a member of the nerve growth factor family. It plays an essential role in the regulation of the modification of synaptic efficacy and brain metabolic activity and enhances neuronal survival. However, the role and underlying mechanism of BDNF in sepsis‐induced ALI remain unclear. Here, we sought to observe the expression of BDNF in the lung tissues of mice. C57BL/6J mice were divided randomly into two groups: saline (n = 4) and lipopolysaccharide (LPS) (n = 4). We found that BDNF expression was elevated in the lung tissues of septic mice. Furthermore, we found that BDNF colocalized with aquaporin 5, a marker for type I alveolar epithelial cells, by immunofluorescence staining. In addition, we also found that tropomyosin‐related kinase B, the specific receptor of BDNF, colocalized with surfactant protein C, a marker for type II alveolar epithelial cells, by immunofluorescence staining. Finally, the present study indicated that BDNF may alleviate excessive LPS‐induced autophagy in alveolar epithelial cells. Overall, we hypothesize that BDNF expression increases in the lung tissues of septic mice as a compensatory mechanism to ameliorate sepsis‐induced ALI by inhibiting excessive alveolar epithelial cell autophagy. What is the central question of this study?Does brain‐derived neurotrophic factor (BDNF) expressed in type I alveolar epithelial cells exert a protective effect in sepsis‐induced acute lung injury (ALI)?What is the main finding and its importance?BDNF was mainly coexpressed with aquaporin 5 (expressed in type I alveolar epithelial cells). In contrast, BDNF was less colocalized with F4/80 (expressed in alveolar macrophages) or surfactant protein C (expressed in type II alveolar epithelial cells). The increased expression of BDNF protein in the lung tissues of septic mice as a compensatory mechanism may alleviate sepsis‐induced ALI by inhibiting excessive cellular autophagy.
- Subjects
BRAIN-derived neurotrophic factor; PULMONARY alveolar proteinosis; LUNG injuries; NERVE growth factor; ADULT respiratory distress syndrome; AQUAPORINS; PROTEIN C
- Publication
Experimental Physiology, 2023, Vol 108, Issue 12, p1456
- ISSN
0958-0670
- Publication type
Article
- DOI
10.1113/EP091228