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The genomic mechanisms that underlie pulmonary immune responses to fungal bioaerosols have remained unclear.<\/jats:p><\/jats:sec><jats:sec><jats:title>Objective<\/jats:title><jats:p>The impact of fungal viability on the pulmonary micro<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> and messenger <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> profiles that regulate murine immune responses was evaluated following subchronic inhalation exposure to <jats:italic>Aspergillus fumigatus<\/jats:italic> conidia.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Three groups of na\u00efve B6C3F1\/N mice were exposed via nose\u2010only inhalation to <jats:italic>A. fumigatus<\/jats:italic> viable conidia, heat\u2010inactivated conidia (HIC), or <jats:styled-content style=\"fixed-case\">HEPA<\/jats:styled-content>\u2010filtered air twice a week for 13 weeks. Total <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> was isolated from whole lung 24 and 48 h postfinal exposure and was further processed for gene expression and micro<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> array analysis. The molecular network pathways between viable and HIC groups were evaluated.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Comparison of data sets revealed increased <jats:italic>Il4<\/jats:italic>,<jats:italic> Il13<\/jats:italic> and <jats:italic>Il33<\/jats:italic> expression in mice exposed to viable vs. HIC. Of 415 micro<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>s detected, approximately 50% were altered in mice exposed to viable vs. HIC 48 h postexposure. Significantly down\u2010regulated (<jats:italic>P<\/jats:italic> \u2264 0.05) miR\u201029a\u20103p was predicted to regulate <jats:italic><jats:styled-content style=\"fixed-case\">TGF<\/jats:styled-content>\u2010<\/jats:italic>\u03b2<jats:italic>3<\/jats:italic> and <jats:italic>Clec7a<\/jats:italic>, genes involved in innate responses to viable <jats:italic>A. fumigatus<\/jats:italic>. Also significantly down\u2010regulated (<jats:italic>P<\/jats:italic> \u2264 0.05), miR\u201023b\u20103p regulates genes involved in pulmonary <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201013 and <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201033 responses and <jats:italic><jats:styled-content style=\"fixed-case\">SMAD<\/jats:styled-content>2<\/jats:italic>, downstream of <jats:styled-content style=\"fixed-case\">TGF<\/jats:styled-content>\u2010\u03b2 signalling. Using Ingenuity Pathway Analysis, a novel interaction was identified between viable conidia and <jats:italic><jats:styled-content style=\"fixed-case\">SMAD<\/jats:styled-content>2\/3<\/jats:italic>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions and Clinical Relevance<\/jats:title><jats:p>Examination of the pulmonary genetic profiles revealed differentially expressed genes and micro<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>s following subchronic inhalation exposure to <jats:italic>A. fumigatus<\/jats:italic>. Micro<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>s regulating genes involved in the pulmonary immune responses were those with the greatest fold change. Specifically, germinating <jats:italic>A. fumigatus<\/jats:italic> conidia were associated with <jats:italic>Clec7a<\/jats:italic> and were predicted to interact with <jats:italic>Il13<\/jats:italic> and <jats:italic>Il33<\/jats:italic>. Furthermore, altered micro<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>s may serve as potential biomarkers to evaluate fungal exposure.<\/jats:p><\/jats:sec>","DOI":"10.1111\/cea.12783","type":"journal-article","created":{"date-parts":[[2016,9,16]],"date-time":"2016-09-16T09:33:49Z","timestamp":1474018429000},"page":"1315-1327","source":"Crossref","is-referenced-by-count":46,"title":["Influence of <i>Aspergillus fumigatus<\/i> conidia viability on murine pulmonary micro<scp>RNA<\/scp> and m<scp>RNA<\/scp> expression following subchronic inhalation exposure"],"prefix":"10.1111","volume":"46","author":[{"given":"T. L.","family":"Croston","sequence":"first","affiliation":[{"name":"Allergy and Clinical Immunology Branch Health Effects Laboratory Division Centers for Disease Control and Prevention National Institute for Occupational Safety and Health Morgantown WV USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A. P.","family":"Nayak","sequence":"additional","affiliation":[{"name":"Allergy and Clinical Immunology Branch Health Effects Laboratory Division Centers for Disease Control and Prevention National Institute for Occupational Safety and Health Morgantown WV USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A. R.","family":"Lemons","sequence":"additional","affiliation":[{"name":"Allergy and Clinical Immunology Branch Health Effects Laboratory Division Centers for Disease Control and Prevention National Institute for Occupational Safety and Health Morgantown WV USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"W. T.","family":"Goldsmith","sequence":"additional","affiliation":[{"name":"Engineering and Control Technology Branch Health Effects Laboratory Division Centers for Disease Control and Prevention National Institute for Occupational Safety and Health Morgantown WV USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J. 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