Summary
Introduction:
This text is a research article that investigates the effects of vegetable glycerin (VG), a main e-cigarette constituent, on endotoxin-induced acute lung injury (aLI) in mice. The study aims to analyze lung histopathology, expression of chemokine receptors, and regulatory signaling after administering VG and lipopolysaccharide (LPS) to mice.
Key Points:
* The study found that VG significantly increased aLI-associated histopathological and fibrotic changes in both the VG group and LPS-induced aLI mice (VG + LPS group).
* Immunohistochemistry (IhC) and western blot analyses revealed that VG administration resulted in upregulation of neutrophil markers (Ly6G and MPO) and the expression of transforming growth factor-β (TGF-β), a central mediator of fibrogenesis, in the lungs of both VG and VG + LPS groups.
* VG enhanced the expression of adhesion molecules (VLa-4 and VCaM-1) and increased activation of p38 mitogen-activated protein kinase (p38 MaPK) to prompt neutrophil recruitment in the lungs of mice with aLI.
* Intraperitoneal administration of a p38 inhibitor attenuated these histopathological changes significantly as well as VG-induced upregulation in expression of Ly6G, MPO, VLa-4, VCaM-1, TGF-β, and collagen-1 in mice with aLI.
Main Message:
The study suggests that VG enhances neutrophil chemotaxis and fibrosis and amplifies the inflammatory response associated with LPS-induced aLI in the lungs via enhancement of p38 MaPK activity. These findings highlight the potential risks associated with e-cigarette use and the need for further research to establish clear public policy guidance and regulation.
Citation
Su VYF, Chen WC, Yu WK, Wu hh, Chen h, Yang KY. The main e-cigarette component vegetable glycerin enhances neutrophil migration and fibrosis in endotoxin-induced lung injury via p38 MaPK activation. Respiratory research. 2023;24(1):9. doi:10.1186/s12931-022-02307-z
