Innate Immunity Induced by the Major Allergen Alt a 1 From the Fungus Alternaria Is Dependent Upon Toll-Like Receptors 2/4 in Human Lung Epithelial Cells

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dc.contributor.authorHayes, Tristanen
dc.contributor.authorRumore, Amandaen
dc.contributor.authorHoward, Braden
dc.contributor.authorHe, Xinen
dc.contributor.authorLuo, Mengyaoen
dc.contributor.authorWuenschmann, Sabinaen
dc.contributor.authorChapman, Martin C.en
dc.contributor.authorKale, Shiv D.en
dc.contributor.authorLi, Liwuen
dc.contributor.authorKita, Hirohitoen
dc.contributor.authorLawrence, Christopher B.en
dc.contributor.departmentBiological Sciencesen
dc.contributor.departmentFralin Life Sciences Instituteen
dc.date.accessioned2019-08-28T14:20:18Zen
dc.date.available2019-08-28T14:20:18Zen
dc.date.issued2018-07-30en
dc.description.abstractAllergens are molecules that elicit a hypersensitive inflammatory response in sensitized individuals and are derived from a variety of sources. Alt a 1 is the most clinically important secreted allergen of the ubiquitous fungus, Alternaria. It has been shown to be a major allergen causing IgE-mediated allergic response in the vast majority of Alternaria-sensitized individuals. However, no studies have been conducted in regards to the innate immune eliciting activities of this clinically relevant protein. In this study, recombinant Alt a 1 was produced, purified, labeled, and incubated with BEAS-2B, NHBE, and DHBE human lung epithelial cells. Alt a 1 elicited strong induction of IL-8, MCP-1, and Groa/b/g. Using gene-specific siRNAs, blocking antibodies, and chemical inhibitors such as LPS-RS, it was determined that Alt a 1-induced immune responses were dependent upon toll-like receptors (TLRs) 2 and 4, and the adaptor proteins MYD88 and TIRAP. Studies utilizing human embryonic kidney cells engineered to express single receptors on the cell surface such as TLRs, further confirmed that Alt a 1-induced innate immunity is dependent upon TLR4 and to a lesser extent TLR2.en
dc.description.notesAwards from the National Institute of Allergy and Infectious Diseases 5R01AI071106 to HK and CL, 5R21AI115986 to CL, and 1R21AI094071 to CL supported this research.en
dc.description.sponsorshipNational Institute of Allergy and Infectious Diseases [5R01AI071106, 5R21AI115986, 1R21AI094071]en
dc.format.mimetypeapplication/pdfen
dc.identifier.doihttps://doi.org/10.3389/fimmu.2018.01507en
dc.identifier.issn1664-3224en
dc.identifier.other1507en
dc.identifier.pmid30100902en
dc.identifier.urihttp://hdl.handle.net/10919/93278en
dc.identifier.volume9en
dc.language.isoenen
dc.rightsCreative Commons Attribution 4.0 Internationalen
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/en
dc.subjectAlternariaen
dc.subjectallergenen
dc.subjectinnate immunityen
dc.subjecttoll-like receptorsen
dc.subjectmolden
dc.subjectfungus-host interactionen
dc.titleInnate Immunity Induced by the Major Allergen Alt a 1 From the Fungus Alternaria Is Dependent Upon Toll-Like Receptors 2/4 in Human Lung Epithelial Cellsen
dc.title.serialFrontiers in Immunologyen
dc.typeArticle - Refereeden
dc.type.dcmitypeTexten
dc.type.dcmitypeStillImageen

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