The chemokine receptor CCR3 participates in tissue remodeling during atopic skin inflammation

Krisztian Gaspar, Gabriela Kukova, Erich Bunemann, Bettina Alexandra Buhren, Eniko Sonkoly, Attila Gabor Szollosi, Anja Muller, Terhi Savinko, Antti I. Lauerma, Harri Alenius, L. Kemény, Marie Caroline Dieu-Nosjean, Sonja Stander, Jens W. Fischer, Thomas Ruzicka, Albert Zlotnik, A. Szegedi, Bernhard Homey

Research output: Article

17 Citations (Scopus)

Abstract

Background: Recent studies provided insights into the recruitment and activation pathways of leukocytes in atopic dermatitis, however, the underlying mechanisms of tissue remodeling in atopic skin inflammation remain elusive. Objective: To identify chemokine-mediated communication pathways regulating tissue remodeling during atopic skin inflammation. Methods: Analysis of the chemokine receptor repertoire of human dermal fibroblasts using flow cytometry and immunofluorescence. Quantitative real-time polymerase chain reaction and immunohistochemical analyses of chemokine expression in atopic vs. non-atopic skin inflammation. Investigation of the function of chemokine receptor CCR3 on human dermal fibroblasts through determining intracellular Ca2+ mobilization, cell proliferation, migration, and repair capacity. Results: Analyses on human dermal fibroblasts showed abundant expression of the chemokine receptor CCR3 in vitro and in vivo. Among its corresponding ligands (CCL5, CCL8, CCL11, CCL24 and CCL26) CCL26 demonstrated a significant and specific up-regulation in atopic when compared to psoriatic skin inflammation. In vivo, epidermal keratinocytes showed most abundant CCL26 protein expression in lesional atopic skin. In structural cells of the skin, TH2-cytokines such as IL-4 and IL-13 were dominant inducers of CCL26 expression. In dermal fibroblasts, CCL26 induced CCR3 signaling resulting in intracellular Ca2+ mobilization, as well as enhanced fibroblast migration and repair capacity, but no proliferation. Conclusion: Taken together, findings of the present study suggest that chemokine-driven communication pathways from the epidermis to the dermis may modulate tissue remodeling in atopic skin inflammation.

Original languageEnglish
Pages (from-to)12-21
Number of pages10
JournalJournal of Dermatological Science
Volume71
Issue number1
DOIs
Publication statusPublished - júl. 2013

Fingerprint

Chemokine Receptors
Skin
Fibroblasts
Tissue
Inflammation
Chemokines
Repair
Interleukin-13
Flow cytometry
Polymerase chain reaction
Communication
Cell proliferation
Interleukin-4
Chemical activation
Cytokines
Ligands
Atopic Dermatitis
Dermis
Keratinocytes
Epidermis

ASJC Scopus subject areas

  • Dermatology
  • Biochemistry
  • Molecular Biology

Cite this

Gaspar, K., Kukova, G., Bunemann, E., Buhren, B. A., Sonkoly, E., Szollosi, A. G., ... Homey, B. (2013). The chemokine receptor CCR3 participates in tissue remodeling during atopic skin inflammation. Journal of Dermatological Science, 71(1), 12-21. https://doi.org/10.1016/j.jdermsci.2013.04.011

The chemokine receptor CCR3 participates in tissue remodeling during atopic skin inflammation. / Gaspar, Krisztian; Kukova, Gabriela; Bunemann, Erich; Buhren, Bettina Alexandra; Sonkoly, Eniko; Szollosi, Attila Gabor; Muller, Anja; Savinko, Terhi; Lauerma, Antti I.; Alenius, Harri; Kemény, L.; Dieu-Nosjean, Marie Caroline; Stander, Sonja; Fischer, Jens W.; Ruzicka, Thomas; Zlotnik, Albert; Szegedi, A.; Homey, Bernhard.

In: Journal of Dermatological Science, Vol. 71, No. 1, 07.2013, p. 12-21.

Research output: Article

Gaspar, K, Kukova, G, Bunemann, E, Buhren, BA, Sonkoly, E, Szollosi, AG, Muller, A, Savinko, T, Lauerma, AI, Alenius, H, Kemény, L, Dieu-Nosjean, MC, Stander, S, Fischer, JW, Ruzicka, T, Zlotnik, A, Szegedi, A & Homey, B 2013, 'The chemokine receptor CCR3 participates in tissue remodeling during atopic skin inflammation', Journal of Dermatological Science, vol. 71, no. 1, pp. 12-21. https://doi.org/10.1016/j.jdermsci.2013.04.011
Gaspar, Krisztian ; Kukova, Gabriela ; Bunemann, Erich ; Buhren, Bettina Alexandra ; Sonkoly, Eniko ; Szollosi, Attila Gabor ; Muller, Anja ; Savinko, Terhi ; Lauerma, Antti I. ; Alenius, Harri ; Kemény, L. ; Dieu-Nosjean, Marie Caroline ; Stander, Sonja ; Fischer, Jens W. ; Ruzicka, Thomas ; Zlotnik, Albert ; Szegedi, A. ; Homey, Bernhard. / The chemokine receptor CCR3 participates in tissue remodeling during atopic skin inflammation. In: Journal of Dermatological Science. 2013 ; Vol. 71, No. 1. pp. 12-21.
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abstract = "Background: Recent studies provided insights into the recruitment and activation pathways of leukocytes in atopic dermatitis, however, the underlying mechanisms of tissue remodeling in atopic skin inflammation remain elusive. Objective: To identify chemokine-mediated communication pathways regulating tissue remodeling during atopic skin inflammation. Methods: Analysis of the chemokine receptor repertoire of human dermal fibroblasts using flow cytometry and immunofluorescence. Quantitative real-time polymerase chain reaction and immunohistochemical analyses of chemokine expression in atopic vs. non-atopic skin inflammation. Investigation of the function of chemokine receptor CCR3 on human dermal fibroblasts through determining intracellular Ca2+ mobilization, cell proliferation, migration, and repair capacity. Results: Analyses on human dermal fibroblasts showed abundant expression of the chemokine receptor CCR3 in vitro and in vivo. Among its corresponding ligands (CCL5, CCL8, CCL11, CCL24 and CCL26) CCL26 demonstrated a significant and specific up-regulation in atopic when compared to psoriatic skin inflammation. In vivo, epidermal keratinocytes showed most abundant CCL26 protein expression in lesional atopic skin. In structural cells of the skin, TH2-cytokines such as IL-4 and IL-13 were dominant inducers of CCL26 expression. In dermal fibroblasts, CCL26 induced CCR3 signaling resulting in intracellular Ca2+ mobilization, as well as enhanced fibroblast migration and repair capacity, but no proliferation. Conclusion: Taken together, findings of the present study suggest that chemokine-driven communication pathways from the epidermis to the dermis may modulate tissue remodeling in atopic skin inflammation.",
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AU - Gaspar, Krisztian

AU - Kukova, Gabriela

AU - Bunemann, Erich

AU - Buhren, Bettina Alexandra

AU - Sonkoly, Eniko

AU - Szollosi, Attila Gabor

AU - Muller, Anja

AU - Savinko, Terhi

AU - Lauerma, Antti I.

AU - Alenius, Harri

AU - Kemény, L.

AU - Dieu-Nosjean, Marie Caroline

AU - Stander, Sonja

AU - Fischer, Jens W.

AU - Ruzicka, Thomas

AU - Zlotnik, Albert

AU - Szegedi, A.

AU - Homey, Bernhard

PY - 2013/7

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N2 - Background: Recent studies provided insights into the recruitment and activation pathways of leukocytes in atopic dermatitis, however, the underlying mechanisms of tissue remodeling in atopic skin inflammation remain elusive. Objective: To identify chemokine-mediated communication pathways regulating tissue remodeling during atopic skin inflammation. Methods: Analysis of the chemokine receptor repertoire of human dermal fibroblasts using flow cytometry and immunofluorescence. Quantitative real-time polymerase chain reaction and immunohistochemical analyses of chemokine expression in atopic vs. non-atopic skin inflammation. Investigation of the function of chemokine receptor CCR3 on human dermal fibroblasts through determining intracellular Ca2+ mobilization, cell proliferation, migration, and repair capacity. Results: Analyses on human dermal fibroblasts showed abundant expression of the chemokine receptor CCR3 in vitro and in vivo. Among its corresponding ligands (CCL5, CCL8, CCL11, CCL24 and CCL26) CCL26 demonstrated a significant and specific up-regulation in atopic when compared to psoriatic skin inflammation. In vivo, epidermal keratinocytes showed most abundant CCL26 protein expression in lesional atopic skin. In structural cells of the skin, TH2-cytokines such as IL-4 and IL-13 were dominant inducers of CCL26 expression. In dermal fibroblasts, CCL26 induced CCR3 signaling resulting in intracellular Ca2+ mobilization, as well as enhanced fibroblast migration and repair capacity, but no proliferation. Conclusion: Taken together, findings of the present study suggest that chemokine-driven communication pathways from the epidermis to the dermis may modulate tissue remodeling in atopic skin inflammation.

AB - Background: Recent studies provided insights into the recruitment and activation pathways of leukocytes in atopic dermatitis, however, the underlying mechanisms of tissue remodeling in atopic skin inflammation remain elusive. Objective: To identify chemokine-mediated communication pathways regulating tissue remodeling during atopic skin inflammation. Methods: Analysis of the chemokine receptor repertoire of human dermal fibroblasts using flow cytometry and immunofluorescence. Quantitative real-time polymerase chain reaction and immunohistochemical analyses of chemokine expression in atopic vs. non-atopic skin inflammation. Investigation of the function of chemokine receptor CCR3 on human dermal fibroblasts through determining intracellular Ca2+ mobilization, cell proliferation, migration, and repair capacity. Results: Analyses on human dermal fibroblasts showed abundant expression of the chemokine receptor CCR3 in vitro and in vivo. Among its corresponding ligands (CCL5, CCL8, CCL11, CCL24 and CCL26) CCL26 demonstrated a significant and specific up-regulation in atopic when compared to psoriatic skin inflammation. In vivo, epidermal keratinocytes showed most abundant CCL26 protein expression in lesional atopic skin. In structural cells of the skin, TH2-cytokines such as IL-4 and IL-13 were dominant inducers of CCL26 expression. In dermal fibroblasts, CCL26 induced CCR3 signaling resulting in intracellular Ca2+ mobilization, as well as enhanced fibroblast migration and repair capacity, but no proliferation. Conclusion: Taken together, findings of the present study suggest that chemokine-driven communication pathways from the epidermis to the dermis may modulate tissue remodeling in atopic skin inflammation.

KW - Atopic dermatitis

KW - CCR3

KW - Chemokines

KW - Fibroblast

KW - Remodeling

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