title: Chronic intranasal administration of Aspergillus fumigatus spores leads to aggravation of airway inflammation and remodelling in asthmatic rats.
abstract: OBJECTIVE
  Epidemiological evidence indicates a close link between exposure to fungi and deterioration of asthma. However, the role of fungi as an exogenous precipitant for initiation and progression of asthma has been incompletely explored. In this study, the effects of Aspergillus fumigatus exposure on airway inflammation and remodelling in a rat model of chronic asthma were investigated.
  
  
  METHODS
  The rat model of chronic asthma was established by systemic sensitization and repeated challenge with ovalbumin (OVA). The asthmatic rats were exposed to chronic intranasal inhalation of A. fumigatus spores. Changes in airway inflammation, remodelling and BHR were measured after exposure to the fungus.
  
  
  RESULTS
  Chronic inhalation of A. fumigatus spores elevated the production of T helper 2 (Th2) cytokines, increased the concentration of total serum IgE, and resulted in the recruitment of eosinophils and lymphocyte infiltration into the airways of asthmatic rats. Goblet cell hyperplasia, mucus hyperproduction and subepithelial collagen deposition were also induced by inhalation of the fungus. The remodelling changes induced by inhalation of the fungus paralleled the changes in BHR in this rat model of asthma.
  
  
  CONCLUSIONS
  Chronic exposure to A. fumigatus aggravated Th2 airway inflammation, promoted airway remodelling and increased BHR in OVA-sensitized and -challenged rats.
authors.affiliation: Department of Respiratory Medicine, First People's Hospital Affiliated to Shanghai Jiao Tong University, Shanghai, China.
authors.forename: Fu-Sheng
authors.initials: FS
authors.lastname: Gao
authors.forename: Jian-Ou
authors.initials: JO
authors.lastname: Qiao
authors.forename: Yi
authors.initials: Y
authors.lastname: Zhang
authors.forename: Xian-Qiao
authors.initials: XQ
authors.lastname: Jin
mesh_terms: D000281:Administration, Intranasal; D000818:Animals; D001232:Aspergillus fumigatus / Q000472:pathogenicity; D001249:Asthma / Q000139:chemically induced / Q000382:microbiology* / Q000473:pathology*; D002465:Cell Movement; D002908:Chronic Disease; D003094:Collagen / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D004804:Eosinophils / Q000473:pathology; D007073:Immunoglobulin E / Q000097:blood; D008297:Male; D010047:Ovalbumin; D011014:Pneumonia / Q000378:metabolism / Q000382:microbiology* / Q000473:pathology*; D051381:Rats; D017208:Rats, Wistar; D012130:Respiratory Hypersensitivity / Q000378:metabolism / Q000382:microbiology / Q000473:pathology; D013172:Spores, Fungal; D018418:Th2 Cells / Q000378:metabolism / Q000473:pathology
chemical_list: D016207:Cytokines; D007073:Immunoglobulin E; D010047:Ovalbumin; D003094:Collagen