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Murine Model of Allergen Induced Asthma
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Published on: May 14, 2012

Gene-environment interactions influence airways function in laboratory animal workers.

Karin A Pacheco1, Cecile S Rose, Lori J Silveira

  • 1Department of Medicine, Division of Environmental and Occupational Health Sciences, National Jewish Health, Denver, CO 80206, USA. pachecok@njhealth.org

The Journal of Allergy and Clinical Immunology
|June 29, 2010
PubMed
Summary

Environmental endotoxin exposure and CD14 gene variants significantly impact lung function in laboratory animal workers. Specific CD14 alleles combined with high endotoxin levels worsen airways function, especially in atopic individuals.

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Area of Science:

  • Environmental health
  • Genetics
  • Occupational medicine

Background:

  • Gene-environment interactions are crucial in diseases like asthma.
  • CD14 gene variants negatively influence lung function in individuals exposed to environmental allergens and endotoxin.

Purpose of the Study:

  • To investigate the hypothesis that CD14 gene polymorphisms interact with inhaled endotoxin and/or mouse allergen exposure to reduce airways function in laboratory animal workers.

Main Methods:

  • 369 Caucasian laboratory animal workers underwent questionnaires, skin prick testing, and spirometry.
  • Exposure estimates for endotoxin and murine allergen were calculated.
  • Real-time PCR assessed CD14 gene variants (-1619, -550, -159).
  • Multiple linear regression analyzed gene-environment interactions affecting lung function.

Main Results:

  • Workers with the endotoxin-responsive CD14/-1619 G allele and high endotoxin exposure showed significantly reduced FEV1 and FEF25-75.
  • This gene-environment effect was more pronounced in atopic workers.
  • No significant impact on lung function was observed for CD14/-159 or -550 variants, or for murine allergen exposure.

Conclusions:

  • A significant gene-environment interaction between CD14/-1619 genotype and endotoxin exposure impacts airways function in laboratory animal workers.
  • High endotoxin exposure combined with the CD14/-1619G allele leads to decreased lung function (FEV1, FEF25-75).
  • Atopic status exacerbates the negative effects of cumulative endotoxin exposure on lung function.