## 4 Discussion
Similarly, the current study shows a significant increase in the OVA-slg E content within the serum, representing a hallmark of the allergic inflammation triggered by OVA sensitization and subsequent nasal re-exposure. In contrast, the groups treated with various doses of IAP extract exhibited a significant decrease in the serum OVA-slg E content in a dose-dependent manner when compared with the OVA control group. This outcomeunderscores the anti-allergic inflammatory potential of IAP extract, as evidenced by its ability to suppress the OVA-induced increase in the serum OVA-slg E content. Th2 cells and the corresponding inflammatory cytokines play pivotal roles in the pathogenesis of allergic asthma [58; 59]. In particular, IL-4 promotes the differentiation of IgE-producing B lymphocytes, thereby fostering the development of allergic inflammation and airway remodeling [11; 12]. IL-5 is specifically associated with eosinophilic leukocytes, contributing to their proliferation, differentiation, migration, activity, replenishment, and survival. The differentiation of eosinophilic leukocytes within tissues is associated with the induction of various allergic reactions, including asthma [14]. This study employed an enzyme-linked immunosorbent assay (ELISA) and real-time RT-PCR analyses to ascertain the levels of IL-4 and IL-5 both in the BALF and lung tissue. The results indicate noteworthy increases in the IL-4 and IL-5 contents, alongside increased IL-4 and IL-5 mRNA expressions, following OVA sensitization and topical re-exposure through nasal administration. Conversely, the administration of various doses of IAP extract led to significant reductions in the IL-4 and IL-5 contents and in the mRNA expressions within both the BALF and lung tissue, demonstrating a dose-dependent pattern. These findings collectively provide compelling evidence that the oral administration of IAP extract effectively mitigates OVA-induced allergic asthma in a dose-dependent manner by modulating the activity of Th2-cell-associated inflammatory cytokines, especially IL-4 and IL-5. The pathological manifestations of asthma have been primarily centered around excessive mucus production, airway obstruction, and the infiltration of various inflammatory cells including lymphocytes, eosinophilic leukocytes, and mast cells [20; 21; 60]. Histopathological examinations have consistently revealed significant alterations, such as the thickening of the alveolar septa due to the presence of inflammatory cells, and the infiltration of various inflammatory cells including mast cells and eosinophilic leukocytes around the alveoli and bronchioles in the lungs of allergic asthma mouse models induced by OVA sensitization and local re-exposure through nasal administration [20; 21; 24; 56]. The assessment of the ASA (\(\%\)/mm\({}^{2}\)) serves as a critical indicator of indirect lung gas exchange capacity. A reduction in the ASA corresponds to a decline in the gas exchange surface area within the lung, resulting in diminished lung function. A decreased ASA has been histopathologically reported in different lung diseases [20; 21; 39; 43; 44; 61]. In line with previous findings from drug efficacy experiments conducted on OVA-induced allergic asthma models [20; 21; 24; 56], the current study observed significant sarcomatus lesions characterized by the thickening of the alveolar septum due to the infiltration of inflammatory cells around the alveoli and bronchioles in response to OVA sensitization and local re-exposure through nasal administration. Furthermore, a histomorphometric analysis demonstrated significant increases in the thickness of the mean alveolar septum, as well as the presence of infiltrating inflammatory cells within the alveoli and peribronchiolar regions, including eosinophilic leukocytes and mast cells. These changes were associated with a reduction in the ASA compared to the intact vehicle control group.