House dust mite allergen exerts no direct proinflammatory effects on human keratinocytes

Francesca Mascia, Valentina Mariani, Alberto Giannetti, Giampiero Girolomoni, Saveria Pastore

Research output: Contribution to journalArticle

Abstract

Background: Dermatophagoides pteronyssinus is a trigger of atopic dermatitis. Many D pteronyssinus allergens are proteases that can elicit airway inflammation by stimulating the release of cytokines and chemokines by bronchial epithelial cells. Objective: We sought to investigate whether D pteronyssinus allergens can exert a similar activity on skin keratinocytes. Methods: Primary cultures of keratinocytes from healthy subjects or patients with atopic dermatitis and normal human bronchial epithelial cells were compared for cytokine production in response to D pteronyssinus extract. Results: Keratinocytes, but not bronchial epithelial cells, displayed a modest dose-dependent release of IL-1α and IL-1 receptor antagonist but no induction of their mRNA after exposure to D pteronyssinus. However, D pteronyssinus also degraded these cytokines. On the other hand, D pteronyssinus extract induced bronchial epithelial cells, but not keratinocytes, to increased expression of IL-8/CXCL8 and GM-CSF mRNA and protein. These effects were efficiently abrogated by a mixture of cysteine and serine protease inhibitors. Both IL-8 and GM-CSF were fully resistant to D pteronyssinus proteolytic attack. No induction of monocyte chemoattractant protein 1/CCL2, RANTES/CCL5, or IFN-γ-induced protein of 10 kd/CXCL10 was detected in either cell type. Only bronchial epithelial cells expressed protease-activated receptor (PAR) 4 mRNA, whereas PAR-1, PAR-2, and PAR-3 mRNA was found in both cell types. D pteronyssinus did not affect PAR mRNA signals. Conclusions: Although D pteronyssinus can cause proteolysis-dependent release of cytokines from keratinocytes, it appears incapable of activating de novo expression of cytokines and chemokines, arguing against a direct proinflammatory activity of house dust mite on the skin.

Original languageEnglish
Pages (from-to)532-538
Number of pages7
JournalJournal of Allergy and Clinical Immunology
Volume109
Issue number3
DOIs
Publication statusPublished - 2002

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Dermatophagoides Antigens
Keratinocytes
Epithelial Cells
Cytokines
Messenger RNA
Atopic Dermatitis
Granulocyte-Macrophage Colony-Stimulating Factor
Interleukin-8
Chemokines
Allergens
Proteinase-Activated Receptors
PAR-2 Receptor
PAR-1 Receptor
Dermatophagoides pteronyssinus
Cysteine Proteinase Inhibitors
Chemokine CCL5
Pyroglyphidae
Skin
Serine Proteinase Inhibitors
Interleukin-1 Receptors

Keywords

  • Atopic dermatitis
  • Chemokines
  • Cytokines
  • Dermatophagoides pteronyssinus
  • Epithelial cells

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this

House dust mite allergen exerts no direct proinflammatory effects on human keratinocytes. / Mascia, Francesca; Mariani, Valentina; Giannetti, Alberto; Girolomoni, Giampiero; Pastore, Saveria.

In: Journal of Allergy and Clinical Immunology, Vol. 109, No. 3, 2002, p. 532-538.

Research output: Contribution to journalArticle

Mascia, Francesca ; Mariani, Valentina ; Giannetti, Alberto ; Girolomoni, Giampiero ; Pastore, Saveria. / House dust mite allergen exerts no direct proinflammatory effects on human keratinocytes. In: Journal of Allergy and Clinical Immunology. 2002 ; Vol. 109, No. 3. pp. 532-538.
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abstract = "Background: Dermatophagoides pteronyssinus is a trigger of atopic dermatitis. Many D pteronyssinus allergens are proteases that can elicit airway inflammation by stimulating the release of cytokines and chemokines by bronchial epithelial cells. Objective: We sought to investigate whether D pteronyssinus allergens can exert a similar activity on skin keratinocytes. Methods: Primary cultures of keratinocytes from healthy subjects or patients with atopic dermatitis and normal human bronchial epithelial cells were compared for cytokine production in response to D pteronyssinus extract. Results: Keratinocytes, but not bronchial epithelial cells, displayed a modest dose-dependent release of IL-1α and IL-1 receptor antagonist but no induction of their mRNA after exposure to D pteronyssinus. However, D pteronyssinus also degraded these cytokines. On the other hand, D pteronyssinus extract induced bronchial epithelial cells, but not keratinocytes, to increased expression of IL-8/CXCL8 and GM-CSF mRNA and protein. These effects were efficiently abrogated by a mixture of cysteine and serine protease inhibitors. Both IL-8 and GM-CSF were fully resistant to D pteronyssinus proteolytic attack. No induction of monocyte chemoattractant protein 1/CCL2, RANTES/CCL5, or IFN-γ-induced protein of 10 kd/CXCL10 was detected in either cell type. Only bronchial epithelial cells expressed protease-activated receptor (PAR) 4 mRNA, whereas PAR-1, PAR-2, and PAR-3 mRNA was found in both cell types. D pteronyssinus did not affect PAR mRNA signals. Conclusions: Although D pteronyssinus can cause proteolysis-dependent release of cytokines from keratinocytes, it appears incapable of activating de novo expression of cytokines and chemokines, arguing against a direct proinflammatory activity of house dust mite on the skin.",
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AU - Mascia, Francesca

AU - Mariani, Valentina

AU - Giannetti, Alberto

AU - Girolomoni, Giampiero

AU - Pastore, Saveria

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N2 - Background: Dermatophagoides pteronyssinus is a trigger of atopic dermatitis. Many D pteronyssinus allergens are proteases that can elicit airway inflammation by stimulating the release of cytokines and chemokines by bronchial epithelial cells. Objective: We sought to investigate whether D pteronyssinus allergens can exert a similar activity on skin keratinocytes. Methods: Primary cultures of keratinocytes from healthy subjects or patients with atopic dermatitis and normal human bronchial epithelial cells were compared for cytokine production in response to D pteronyssinus extract. Results: Keratinocytes, but not bronchial epithelial cells, displayed a modest dose-dependent release of IL-1α and IL-1 receptor antagonist but no induction of their mRNA after exposure to D pteronyssinus. However, D pteronyssinus also degraded these cytokines. On the other hand, D pteronyssinus extract induced bronchial epithelial cells, but not keratinocytes, to increased expression of IL-8/CXCL8 and GM-CSF mRNA and protein. These effects were efficiently abrogated by a mixture of cysteine and serine protease inhibitors. Both IL-8 and GM-CSF were fully resistant to D pteronyssinus proteolytic attack. No induction of monocyte chemoattractant protein 1/CCL2, RANTES/CCL5, or IFN-γ-induced protein of 10 kd/CXCL10 was detected in either cell type. Only bronchial epithelial cells expressed protease-activated receptor (PAR) 4 mRNA, whereas PAR-1, PAR-2, and PAR-3 mRNA was found in both cell types. D pteronyssinus did not affect PAR mRNA signals. Conclusions: Although D pteronyssinus can cause proteolysis-dependent release of cytokines from keratinocytes, it appears incapable of activating de novo expression of cytokines and chemokines, arguing against a direct proinflammatory activity of house dust mite on the skin.

AB - Background: Dermatophagoides pteronyssinus is a trigger of atopic dermatitis. Many D pteronyssinus allergens are proteases that can elicit airway inflammation by stimulating the release of cytokines and chemokines by bronchial epithelial cells. Objective: We sought to investigate whether D pteronyssinus allergens can exert a similar activity on skin keratinocytes. Methods: Primary cultures of keratinocytes from healthy subjects or patients with atopic dermatitis and normal human bronchial epithelial cells were compared for cytokine production in response to D pteronyssinus extract. Results: Keratinocytes, but not bronchial epithelial cells, displayed a modest dose-dependent release of IL-1α and IL-1 receptor antagonist but no induction of their mRNA after exposure to D pteronyssinus. However, D pteronyssinus also degraded these cytokines. On the other hand, D pteronyssinus extract induced bronchial epithelial cells, but not keratinocytes, to increased expression of IL-8/CXCL8 and GM-CSF mRNA and protein. These effects were efficiently abrogated by a mixture of cysteine and serine protease inhibitors. Both IL-8 and GM-CSF were fully resistant to D pteronyssinus proteolytic attack. No induction of monocyte chemoattractant protein 1/CCL2, RANTES/CCL5, or IFN-γ-induced protein of 10 kd/CXCL10 was detected in either cell type. Only bronchial epithelial cells expressed protease-activated receptor (PAR) 4 mRNA, whereas PAR-1, PAR-2, and PAR-3 mRNA was found in both cell types. D pteronyssinus did not affect PAR mRNA signals. Conclusions: Although D pteronyssinus can cause proteolysis-dependent release of cytokines from keratinocytes, it appears incapable of activating de novo expression of cytokines and chemokines, arguing against a direct proinflammatory activity of house dust mite on the skin.

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KW - Epithelial cells

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