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Interferon-gamma promotes exaggerated cytokine production in keratinocytes cultured from patients with atopic dermatitis.
J Allergy Clin Immunol. 1998 Apr; 101(4 Pt 1):538-44.JA

Abstract

Recent studies suggest that skin keratinocytes from patients with atopic dermatitis (AD) and nonatopic subjects differ in their intrinsic ability to respond to proinflammatory stimuli. In this study keratinocyte cultures established from the normal-looking skin of six adult patients with AD and six healthy, nonatopic control subjects were compared in their response to interferon (IFN)-gamma, a potent proinflammatory lymphokine whose expression is increased in chronic AD lesions. Basal expression of IFN-gamma receptor as well as IFN-gamma-induced membrane expression of HLA-DR and intercellular adhesion molecule (ICAM)-1 were evaluated by flow cytometry. Keratinocyte release of IL-1alpha, IL-1 receptor antagonist (IL-1ra), granulocyte-macrophage colony stimulating factor (GM-CSF), and tumor necrosis factor (TNF)-alpha were measured by ELISA on culture supernatants after treatment with IFN-gamma or medium alone. Expression of membrane IFN-gamma receptor was similar in keratinocytes cultured from nonatopic subjects and subjects with AD. IFN-gamma (10 to 500 U/ml) induced comparable levels of membrane HLA-DR and ICAM-1 in both groups of keratinocytes. In contrast, spontaneous release of IL-1alpha, IL-1ra, GM-CSF, and TNF-alpha was increased in the supernatants of unstimulated keratinocytes from patients with AD compared with keratinocytes from control subjects, with IL-1ra and GM-CSF reaching statistically significant difference. Moreover, IFN-gamma-induced release of all the cytokines tested was much higher for keratinocytes from patients with AD, but the IL-1ra/IL-1alpha ratio for the two groups of keratinocytes was not substantially different, either basally or after IFN-gamma stimulation. The results indicate that keratinocytes from patients with AD are hyperresponsive to IFN-gamma in terms of cytokine release.

Authors+Show Affiliations

Laboratory of Immunology, Istituto Dermopatico dell'Immacolata, IRCCS, Rome, Italy.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

9564808

Citation

Pastore, S, et al. "Interferon-gamma Promotes Exaggerated Cytokine Production in Keratinocytes Cultured From Patients With Atopic Dermatitis." The Journal of Allergy and Clinical Immunology, vol. 101, no. 4 Pt 1, 1998, pp. 538-44.
Pastore S, Corinti S, La Placa M, et al. Interferon-gamma promotes exaggerated cytokine production in keratinocytes cultured from patients with atopic dermatitis. J Allergy Clin Immunol. 1998;101(4 Pt 1):538-44.
Pastore, S., Corinti, S., La Placa, M., Didona, B., & Girolomoni, G. (1998). Interferon-gamma promotes exaggerated cytokine production in keratinocytes cultured from patients with atopic dermatitis. The Journal of Allergy and Clinical Immunology, 101(4 Pt 1), 538-44.
Pastore S, et al. Interferon-gamma Promotes Exaggerated Cytokine Production in Keratinocytes Cultured From Patients With Atopic Dermatitis. J Allergy Clin Immunol. 1998;101(4 Pt 1):538-44. PubMed PMID: 9564808.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Interferon-gamma promotes exaggerated cytokine production in keratinocytes cultured from patients with atopic dermatitis. AU - Pastore,S, AU - Corinti,S, AU - La Placa,M, AU - Didona,B, AU - Girolomoni,G, PY - 1998/5/9/pubmed PY - 1998/5/9/medline PY - 1998/5/9/entrez SP - 538 EP - 44 JF - The Journal of allergy and clinical immunology JO - J Allergy Clin Immunol VL - 101 IS - 4 Pt 1 N2 - Recent studies suggest that skin keratinocytes from patients with atopic dermatitis (AD) and nonatopic subjects differ in their intrinsic ability to respond to proinflammatory stimuli. In this study keratinocyte cultures established from the normal-looking skin of six adult patients with AD and six healthy, nonatopic control subjects were compared in their response to interferon (IFN)-gamma, a potent proinflammatory lymphokine whose expression is increased in chronic AD lesions. Basal expression of IFN-gamma receptor as well as IFN-gamma-induced membrane expression of HLA-DR and intercellular adhesion molecule (ICAM)-1 were evaluated by flow cytometry. Keratinocyte release of IL-1alpha, IL-1 receptor antagonist (IL-1ra), granulocyte-macrophage colony stimulating factor (GM-CSF), and tumor necrosis factor (TNF)-alpha were measured by ELISA on culture supernatants after treatment with IFN-gamma or medium alone. Expression of membrane IFN-gamma receptor was similar in keratinocytes cultured from nonatopic subjects and subjects with AD. IFN-gamma (10 to 500 U/ml) induced comparable levels of membrane HLA-DR and ICAM-1 in both groups of keratinocytes. In contrast, spontaneous release of IL-1alpha, IL-1ra, GM-CSF, and TNF-alpha was increased in the supernatants of unstimulated keratinocytes from patients with AD compared with keratinocytes from control subjects, with IL-1ra and GM-CSF reaching statistically significant difference. Moreover, IFN-gamma-induced release of all the cytokines tested was much higher for keratinocytes from patients with AD, but the IL-1ra/IL-1alpha ratio for the two groups of keratinocytes was not substantially different, either basally or after IFN-gamma stimulation. The results indicate that keratinocytes from patients with AD are hyperresponsive to IFN-gamma in terms of cytokine release. SN - 0091-6749 UR - https://www.unboundmedicine.com/medline/citation/9564808/Interferon_gamma_promotes_exaggerated_cytokine_production_in_keratinocytes_cultured_from_patients_with_atopic_dermatitis_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0091-6749(98)70361-6 DB - PRIME DP - Unbound Medicine ER -