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Schizophyllum commune  is a ubiquitous basidiomycetous fungus typically found across the world, which has been detected in indoor and outdoor air. Some studies indicated that sensitization to  S. commune  is correlated with asthma severity in patients. Patients with chronic severe or acute fatal asthma have neutrophil-dominant airway inflammation. We hypothesized that  S. commune  can exacerbate asthma. To test this hypothesis, we evaluated the direct immunomodulatory activities of  S. commune  in allergic airway inflammation induced by non-fungal sensitization. Ovalbumin (OVA)-induced asthma model mice were generated using wild-type (WT) and  Il-17a  −/−  Il-17f  −/−  mice that were intratracheally exposed to  S. commune , then immune responses in the lungs were assessed after 24 h. Intratracheal administration of  S. commune  in OVA-induced asthma model mice enhanced neutrophilic airway inflammation, increased the mRNA expression of  CXCL1  and  CXCL2  in the lungs, and provoked IL-17A, and IL-17F production in BAL fluid. In addition, neutrophilic airway inflammation was significantly inhibited in  Il-17a  −/−  Il-17f  −/−  mice compared with those found in WT mice. We demonstrated that  S. commune  induces neutrophilic airway inflammation in OVA-induced asthma model mice, and IL-17A and IL-17F had central roles in this activity. As  S. commune  inhabits the general environment, including indoor and outdoor air, our results suggested that  S. commune  is a causative agent of asthma exacerbation. This study has provided clues regarding the mechanisms behind fungi and asthma exacerbation.

Schizophyllum commune induces IL-17-mediated neutrophilic airway inflammation in OVA-induced asthma model mice