Moreover, intranasal administration of human apoA-I to house dust mite-challenged mice reduced airway inflammation, with decreases in BAL fluid eosinophils, neutrophils, lymphocytes, and macrophages, as well as airway hyperreactivity and lung levels of cytokines such as IL-33, and increased airway epithelial cell tight junction proteins, as well as levels of lipoxin A4 [95]. Here, APOA1 is linked to inflammation.