Dose-dependent allergic responses to an extract of Penicillium chrysogenum in BALB/c mice

Yong Joo Chung1, Najwa Haykal Coates, Michael E Viana

  • 1Department of Environmental Sciences and Engineering, School of Public Health, University of North Carolina, Chapel Hill, NC 27599, USA. chung.yongjoo@epa.gov

Toxicology
|February 24, 2005
PubMed

Insights

Indoor mold exposure, specifically Penicillium chrysogenum extract (PCE), can trigger allergic asthma responses in mice. Repeated PCE inhalation led to dose-dependent increases in allergic markers and airway hyperresponsiveness.

Area of Science:

  • Immunology
  • Environmental Health
  • Pulmonology

Background:

  • Indoor mold exposure is linked to allergic asthma development.
  • Penicillium chrysogenum is a common indoor mold with known allergens.
  • Previous studies show P. chrysogenum can induce allergic responses in a mouse model.

Purpose of the Study:

  • To investigate if soluble components of P. chrysogenum (PCE) can dose-dependently induce allergic asthma-like responses in BALB/c mice.
  • To evaluate the effects of repeated pulmonary exposure to PCE.

Main Methods:

  • Mice were exposed to varying doses of PCE (10-70 microg) via aspiration, four times over 4 weeks.
  • Serum and bronchoalveolar lavage fluid (BALF) were analyzed for immune markers and cell counts.
  • Airway hyperresponsiveness was assessed using barometric whole-body plethysmography.

Main Results:

  • PCE exposure caused dose-dependent increases in BALF total cells (including eosinophils), serum and BALF IgE, and BALF IL-5.
  • Histopathological lesions in the lungs increased with PCE dose.
  • Repeated high-dose PCE exposure led to immediate respiratory responses and non-specific airway hyperresponsiveness.

Conclusions:

  • Repeated pulmonary challenge with P. chrysogenum extract induces dose-dependent allergic asthma-like responses in mice.
  • PCE is a potent inducer of allergic airway inflammation and hyperresponsiveness.
  • These findings highlight the role of indoor mold components in asthma pathogenesis.

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