Chlorella sorokiniana attenuates deoxynivalenol-exacerbated allergic dermatitis and type 2 immune responses in mice.

Chronic dietary exposure to low concentrations of deoxynivalenol (DON), a trichothecene mycotoxin found in cereal products, disrupts immune homeostasis and exacerbates allergic inflammation. Chlorella sorokiniana (CS) can adsorb DON and reduce its systemic absorption. However, whether this DON-binding activity protects against DON-induced immune dysregulation remains unclear. Here, we investigated the effects of CS on DON-induced toxicity and DON-exacerbated allergic dermatitis. In vitro, murine DC2.4 dendritic cells were exposed to DON in the presence or absence of CS-treated DON preparations. DON reduced cell viability and ATP-dependent luminescence while increasing IL-1β and TNFα production in a concentration-dependent manner. Pretreatment with CS attenuated these cytotoxic and pro-inflammatory effects. In vivo, chronic low-dose DON exposure aggravated toluene diisocyanate-induced allergic dermatitis, as demonstrated by increased ear swelling, scratching behavior, inflammatory cell infiltration, dermal edema, and cutaneous expression of Il4, Il13, and Il33. DON also increased dendritic, activated CD4+ T, and IgE+ B cell populations; type 2 cytokine production; and serum IgE levels. Oral CS administration attenuated local and systemic allergic responses. Contrastingly, CS exerted limited effects on allergic inflammation in mice not exposed to DON, indicating that its protective activity was primarily associated with the mitigation of DON toxicity rather than with nonspecific immunosuppression. Both conventional and pulverized CS reduced several DON-associated inflammatory responses. An in vitro binding assay confirmed that CS decreased residual DON concentrations. These findings demonstrate that CS reduces the bioavailability and immunotoxic effects of DON and may represent a functional dietary strategy for preventing the mycotoxin-associated exacerbation of allergic inflammation.