Acute and subacute oral toxicity of deoxynivalenol exposure in a Dermatophagoides farinae induced murine asthma model.

Previously, researchers have demonstrated that mycotoxin deoxynivalenol significantly enhances immunocyte activation. However, the interaction between deoxynivalenol exposure and immune disorders remains unclear. In this study, we aimed to investigate whether acute and subacute oral exposure to deoxynivalenol exacerbates the development of respiratory allergy using a mite allergen (Dermatophagoides farina, Derf)-induced mouse model of asthma. The direct relationship between deoxynivalenol exposure and asthma development was examined following acute oral deoxynivalenol administration (0, 0.1, or 0.3 mg/kg body weight), immediately before the final mite allergen challenge. Simultaneously, the influence of subacute oral exposure via low dose deoxynivalenol contaminated wheat (0.33 ppm) was evaluated using the same settings. To detect the pro-inflammatory effects of deoxynivalenol exposure, we examined the total and Derf-specific serum IgE levels, histology, number of immunocytes, and cytokine and chemokine secretion. Acute oral deoxynivalenol significantly enhanced the inflammatory responses, including cellular infiltration into bronchoalveolar lavage fluid, infiltration of immunocytes and cytokine production in local lymph nodes, and cytokine levels in lung tissues. Corresponding pro-inflammatory responses were observed in a mouse group exposed to subacute oral deoxynivalenol. In vivo results were validated by in vitro experiments using the human bronchial epithelial (BEAS-2B) and human eosinophilic leukemia (EOL-1) cell lines. Following exposure to deoxynivalenol, the secretion of interleukin (IL)-1β, IL-6, IL-8, and/or tumor necrosis factor (TNF)-α in BEAS-2B cells, as well as EoL-1 cells, increased significantly. Our findings indicate that deoxynivalenol exposure is significantly involved in the pro-inflammatory response observed in respiratory allergy.