Altered lung inflammation and expression of endoplasmic reticulum stress markers in male mice aged-asthma model.

Although there is a strong correlation between aging and asthma pathophysiology, the underlying mechanism has not been fully elucidated. The endoplasmic reticulum (ER) has been demonstrated to be a crucial intracellular organelle involved in the pathogenesis of numerous diseases. The aim of the current study was to investigate ER stress markers in the lung tissue of aged ovalbumin (OVA)-sensitized mice. Male BALB/C mice were randomly divided into the following four groups (10 in each): 1) control, 2) OVA-sensitized (OVA), 3) D-galactose-induced aging (D-gal), and 4) OVA-sensitized associated with D-galactose-induced aging (OVA+D-gal). Total WBCs and differential cells were counted using the bronchoalveolar lavage (BAL) fluid. Lung tissue was analyzed for ER stress markers (ATF4, ATF6, GRP78, CHOP, and XBP1) through Real Time-PCR technique as well as histopathological assessment. The data indicated a significant increase in both total WBCs and differential cells within the OVA, D-gal, and OVA+D-gal groups when compared to the control group, particularly evident in the OVA+D-gal group. Also, the results showed that the increased expression of ER stress markers (ATF4, ATF6, GRP78, CHOP, and XBP1) was significantly higher in the OVA, D-gal, and OVA+D-gal groups than in the control group. Interestingly, the increased expression of CHOP, ATF4, and XBP1 was observed in the OVA+D-gal group more than in other groups. In aged OVA-sensitized mice, the findings revealed a maladaptive ER stress response in their lung tissue, characterized by elevated levels of CHOP, ATF4, and XBP1 expression.