Abstract Asthma impacts over 24 million people and costs about $56 billion annually in the United States. Airway neutrophil accumulation and high levels of IL-17 are characteristic of severe asthma. However, mechanisms underlying IL-17/neutrophilic inflammation in severe asthma remain poorly defined. Scavenger receptor class B type I (SR-BI) is a multi-recognition receptor that regulates cholesterol trafficking. We previously reported SR-BI dampens pulmonary innate immune responses during bacterial pneumonia, but the role of SR-BI in asthma is unknown. We hypothesize pulmonary SR-BI expression is protective against house dust mite (HDM)-induced IL-17-dependent neutrophilic asthma. SR-BI+/+ and SR-BI−/− mice were sensitized with 10 μg HDM by oropharyngeal aspiration on day 0 and 7, and challenged with 2 μg HDM on day 14, 15, 16. Airway inflammation and cytokine production were quantified on day 17. SR-BI−/− mice had increased neutrophils but decreased eosinophils in bronchoalveolar lavage (BAL) after HDM challenge compared to SR-BI+/+ mice. BAL levels of neutrophil chemoattractants CXCL1, CXCL2 and CXCL5 were not significantly different between SR-BI+/+ and SR-BI−/− mice. SR-BI−/− mice had increased pulmonary IL-17A and GM-CSF production and decreased IL-5 production. To identify cellular sources of airspace IL-17, single cells isolated from lung were labeled with antibodies for flow cytometry. IL-17A increased in neutrophils (CD45+Ly6G+) and macrophages (CD45+CD64+CD11b−CD11c+) but not T cells (CD45+CD4+) of asthmatic SR-BI−/− mice suggesting myeloid cells rather than Th17 cells as sources of IL-17. Overall, SR-BI expression in the lung suppresses neutrophilic inflammation and IL-17 production in HDM-induced asthma model.