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House dust and storage mite extracts influence skin keratinocyte and fibroblast function
Larry G Arlian1, Marjorie S Morgan, Kevin T Peterson
1Department of Biological Sciences, Wright State University, Dayton, Ohio 45435, USA. larry.arlian@wright.edu
Background:
The bodies of allergy-causing dust and storage mites likely contain many bioreactive molecules, including some that are allergenic. These molecules may penetrate the epidermis and dermis of the skin. However, little is known about the effects that most of the molecules from mites have on the function of cells in the skin, the overall inflammatory and immune reactions and the manifestation of allergic disease. The purpose of this research was to determine the response of cultured skin cells (keratinocytes and fibroblasts) to extracts of house dust and storage mites.
Methods:
Normal human epidermal keratinocytes and dermal fibroblasts were cultured with varying doses of extracts of the storage mites Acarus siro, Chortoglyphus arcuatus or Lepidoglyphus destructor or of the house dust mites Dermatophagoides farinae, D. pteronyssinus or Euroglyphus maynei in the absence or presence of lipopolysaccharide. Culture supernatants were collected 24 h later and assayed for the presence of various chemokines and cytokines.
Results:
Keratinocytes constitutively secreted interleukin (IL)-1 receptor antagonist/IL-1F3, growth-related oncogene alpha and transforming growth factor alpha, and these secretions were modulated by extracts of 1 or more of the mites tested. Mite extracts also modulated the production of IL-6, IL-8, monocyte chemoattractant protein 1, macrophage colony-stimulating factor and vascular endothelial growth factor from fibroblasts.
Conclusions:
The effects that mite extracts exerted on both keratinocytes and fibroblasts varied among the house dust mite species, among the storage mite species and between the house dust and storage mites. This study showed that extracts of mites contain substances that modulate the production of proinflammatory cytokines and chemokines secreted by normal human epidermal keratinocytes and dermal fibroblasts, and therefore may influence the course of pathophysiology in the skin in atopic dermatitis.
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