LPCAT1 reduces inflammatory response, apoptosis and barrier damage of nasal mucosal epithelial cells caused by allergic rhinitis through endoplasmic reticulum stress

Allergic rhinitis (AR), common in children and adolescents, involves Lysophosphatidylcholine Acyltransferase 1 (LPCAT1) catalyzing surfactant lipid biosynthesis and suppressing endoplasmic reticulum expression. However, the precise mechanism underlying the impact of LPCAT1 on epithelial cell damage in AR remains elusive. Hence, the present investigation elucidated the potential effect of LPCAT1 on epithelial cell damage in AR by inhibiting endoplasmic reticulum stress. To assess cell viability, CCK8 assay was employed. Additionally, western blotting was utilized to evaluate the expression of endoplasmic reticulum stress-associated proteins ATF6, CHOP, p-eIF2α, p-IRE1, and LPCAT1. Subsequently, an interference plasmid targeting LPCAT1 was constructed, and western blot analysis was conducted to determine interference level of LPCAT1. An ELISA assay was employed to quantify the concentrations of TNFα, IL-1β, IL-6, GM-CSF, and eotaxin. Additionally, flow cytometry and western blotting techniques were utilized to evaluate cellular Apoptosis, whereas immunofluorescence staining was applied to detect the expression levels of ZO-1. Our findings indicated that IL-13 stimulation resulted in an elevated expression of ER stress proteins and LPCAT1 in nasal mucosal epithelial cells. Furthermore, LPCAT1 interference diminished the expression of inflammatory mediators, Apoptosis markers, barrier disruption indicators, and ER stress proteins in IL-13-stimulated nasal mucosal epithelial cells. Further, by inhibiting ER stress, LPCAT1 interference diminished the expression of inflammatory factors, Apoptosis, and barrier damage in nasal mucosal epithelial cells stimulated by IL-13. Concisely, LPCAT1 ameliorates AR-induced inflammation, Apoptosis, and barrier impairment in nasal mucosal epithelial cells by modulating ER stress, implying its potential as a novel therapeutic target for AR.

AR; ER stress; Inflammatory responseamage; LPCAT1.