4.6 Article

Fungal Chitin from Asthma-Associated Home Environments Induces Eosinophilic Lung Infiltration

Journal

JOURNAL OF IMMUNOLOGY
Volume 187, Issue 5, Pages 2261-2267

Publisher

AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1100972

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Funding

  1. National Institutes of Health [AI030663, AI077439, R01 ES10906]
  2. Howard Hughes Medical Institute
  3. Sandler Asthma Basic Research Center at the University of California

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Development of asthma and allergic inflammation involves innate immunity, but the environmental contributions remain incompletely defined. Analysis of dust collected from the homes of asthmatic individuals revealed that the polysaccharide chitin is environmentally widespread and associated with beta-glucans, possibly from ubiquitous fungi. Cell wall preparations of Aspergillus isolated from house dust induced robust recruitment of eosinophils into mouse lung, an effect that was attenuated by enzymatic degradation of cell wall chitin and beta-glucans. Mice expressing constitutively active acidic mammalian chitinase in the lungs demonstrated a significant reduction in eosinophil infiltration after fungal challenge. Conversely, chitinase inhibition prolonged the duration of tissue eosinophilia. Thus, fungal chitin derived from home environments associated with asthma induces eosinophilic allergic inflammation in the lung, and mammalian chitinases, including acidic mammalian chitinase, limit this process. The Journal of Immunology, 2011, 187: 2261-2267.

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