title: Dectin-1 and IL-17A suppress murine asthma induced by Aspergillus versicolor but not Cladosporium cladosporioides due to differences in β-glucan surface exposure.
abstract: There is considerable evidence supporting a role for mold exposure in the pathogenesis and expression of childhood asthma. Aspergillus versicolor and Cladosporium cladosporioides are common molds that have been implicated in asthma. In a model of mold-induced asthma, mice were repeatedly exposed to either A. versicolor or C. cladosporioides spores. The two molds induced distinct phenotypes, and this effect was observed in both BALB/c and C57BL/6 strains. C. cladosporioides induced robust airway hyperresponsiveness (AHR), eosinophilia, and a predominately Th2 response, whereas A. versicolor induced a strong Th17 response and neutrophilic inflammation, but very mild AHR. Neutralization of IL-17A resulted in strong AHR and eosinophilic inflammation following A. versicolor exposure. In Dectin-1-deficient mice, A. versicolor exposure resulted in markedly attenuated IL-17A and robust AHR compared with wild-type mice. In contrast, C. cladosporioides induced AHR and eosinophilic inflammation independent of IL-17A and Dectin-1. A. versicolor, but not C. cladosporioides, spores had increased exposure of β-glucans on their surface and were able to bind Dectin-1. Thus, the host response to C. cladosporioides was IL-17A- and Dectin-1-independent, whereas Dectin-1- and IL-17A-dependent pathways were protective against the development of asthma after exposure to A. versicolor.
authors.affiliation: Division of Asthma Research, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.
authors.forename: Rachael A
authors.initials: RA
authors.lastname: Mintz-Cole
authors.forename: Aaron M
authors.initials: AM
authors.lastname: Gibson
authors.forename: Stacey A
authors.initials: SA
authors.lastname: Bass
authors.forename: Alison L
authors.initials: AL
authors.lastname: Budelsky
authors.forename: Tiina
authors.initials: T
authors.lastname: Reponen
authors.forename: Gurjit K Khurana
authors.initials: GK
authors.lastname: Hershey
mesh_terms: D000818:Animals; D018927:Anti-Asthmatic Agents / Q000008:administration & dosage* / Q000378:metabolism; D001230:Aspergillus / Q000276:immunology* / Q000378:metabolism; D001249:Asthma / Q000276:immunology* / Q000473:pathology* / Q000517:prevention & control; D016535:Bronchial Hyperreactivity / Q000276:immunology / Q000473:pathology / Q000517:prevention & control; D002963:Cladosporium / Q000276:immunology* / Q000378:metabolism; D004804:Eosinophils / Q000276:immunology / Q000473:pathology; D016130:Immunophenotyping; D018836:Inflammation Mediators / Q000008:administration & dosage; D020381:Interleukin-17 / Q000008:administration & dosage*; D037181:Lectins, C-Type / Q000008:administration & dosage* / Q000172:deficiency / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009504:Neutrophils / Q000276:immunology / Q000473:pathology; D013172:Spores, Fungal / Q000276:immunology / Q000378:metabolism; D013499:Surface Properties; D047071:beta-Glucans / Q000008:administration & dosage* / Q000378:metabolism; D000099181:Dectin-1
chemical_list: D018927:Anti-Asthmatic Agents; D018836:Inflammation Mediators; D020381:Interleukin-17; D037181:Lectins, C-Type; D047071:beta-Glucans; D000099181:Dectin-1