Mold-Specific Differences in Inflammatory Responses in the Lungs

R.A. Mintz-Cole AFFILIATIONS Cincinnati Children's Hospital Medical Center, Cincinnati, OH , A.M. Gibson, T. Reponen, G.K. Hershey

Author address: 

Cincinnati Children’s Hospital Medical Center, Cincinnati, OH, University of Cincinnati College of Medicine, Cincinnati, OH

Abstract: 

RATIONALE: Mold exposure is significantly associated with the development of allergy and asthma in children. Two species endemic to the Ohio River Valley are Aspergillus versicolor and Cladosporium cladosporioides. However, the mechanisms by which these molds contribute to the asthma phenotype is unknown. METHODS: We exposed 7-8 week old wild-type BALB/c mice to 104-106 A. versicolor or C. cladosporioides spores 9 times by intratracheal (IT) administration every other day (total of 17 days). One day after the last mold exposure (day 18) airway hyperresponsiveness (AHR) was assessed. Alveolar lavage fluid was collected to assess total cell counts, differential cell counts, and cytokine levels. Additionally, lung sections were evaluated by histology. RESULTS: Exposure to C. cladosporioides induces AHR, airway inflammation, and goblet cell hyperplasia even at a dose of 104 spores. In contrast, A. versicolor only induced AHR, airway inflammation, and goblet cell hyperplasia at the higher dose. A. versicolor induced a predominately neutrophilic response while C. cladosporioides induced a mixed eosinophilic and neutrophilic response. CONCLUSIONS: There are distinct immunologic responses that develop following exposure to A. versicolor or C. cladosporioides in a mouse exposure model. Exposure to C. cladosporioides induces more eosinophilia and AHR than exposure to A. versicolor. These data suggest that different mold exposures can contribute to the asthma phenotype via distinct mechanisms.
2010

abstract No: 

AB46

Full conference title: 

American Academy of Allergy Asthma & Immunology
    • AAAAI 2010 (66th)