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A network-based analysis of the late-phase reaction of the skin
Department of Pediatrics, Queen Silvia Children's Hospital, Gothenburg, Sweden.
Department of Computer Science, University of Tennessee, Knoxville, USA.
Laboratory for Clinical and Experimental Allergy Research, Department of Oto-Rhino-Laryngology, Malmö University Hospital, Lund University, Malmö, Sweden.
Department of Clinical Immunology, Sahlgrenska Academy, Gothenburg, Sweden.
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2006 (Engelska)Ingår i: Journal of Allergy and Clinical Immunology, ISSN 0091-6749, E-ISSN 1097-6825, Vol. 118, nr 1, s. 220-225Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Background

The late-phase reaction (LPR) of the skin is an in vivo model of allergic inflammation.

Objective

We sought to identify disease-associated pathways in the LPR using a network-based analysis.

Methods

The LPR was examined by means of DNA microarray analysis of skin biopsy specimens from 10 patients with allergic rhinitis and 10 healthy control subjects. The results were further analyzed in 2 different materials consisting of nasal fluids and allergen-challenged CD4+ T cells from patients with allergic rhinitis.

Results

The DNA microarray analysis revealed several genes of known relevance to allergy. The eosinophil marker Charcot-Leyden crystal protein (CLC) that encodes Charcot-Leyden crystal protein differed most in expression. A network-based analysis showed upregulation of IL-4– and CCL4-dependent pathways and downregulation of a TGF-β–induced pathway. CCL4 is expressed by CD4+ T cells and chemotactic for eosinophils. We hypothesized that allergen induces release of CCL4 from TH2 cells and that this contributes to influx of eosinophils. Further analysis showed increase of CCL4 protein in nasal fluids from allergic patients during the season. Allergen challenge of PBMCs resulted in proliferation of TH2 cells and increased production of CCL4 in CD4+ T cells from allergic patients. An analysis of the DNA microarray data revealed a significant correlation between CCL4 and the eosinophil marker CLC.

Conclusion

A network-based analysis of the LPR showed increased activity of IL-4– and CCL4- dependent pathways and downregulation of the TGF-β–induced pathway. Allergen-induced release of CCL4 from TH2 cells might contribute to influx of eosinophils during the LPR.

Clinical implications

Involvement of multiple interacting pathways indicates that it might be difficult to identify one single mediator as a biomarker or drug target in allergic inflammation.

Ort, förlag, år, upplaga, sidor
Elsevier, 2006. Vol. 118, nr 1, s. 220-225
Nyckelord [en]
DNA microarrays; gene expression; late-phase reaction
Nationell ämneskategori
Medicin och hälsovetenskap
Identifikatorer
URN: urn:nbn:se:liu:diva-98562DOI: 10.1016/j.jaci.2006.03.006ISI: 000239184800027PubMedID: 16815159OAI: oai:DiVA.org:liu-98562DiVA, id: diva2:654963
Tillgänglig från: 2013-10-09 Skapad: 2013-10-09 Senast uppdaterad: 2017-12-06Bibliografiskt granskad

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