Immune Phenotype and IL-6 Deficiency Modulate the Inflammatory Response in a Mouse Model of Irritant Contact Dermatitis
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2016/05/01
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Description:Skin diseases are the second most common occupational illness with associated per annum costs exceeding $1 billion. Irritant contact dermatitis (ICD), the most common occupational skin disease, is characterized as an acute inflammatory response that manifests as a result of topical irritant exposure. Immune phenotype, such as Th1- and Th2- dominance, is postulated to contribute to the variability seen between patients. In addition, interleukin 6, which is known to have variably both Th1 and Th2 properties, has been shown to play a key role in ICD. C57BL/6J ("Th1 dominant"), Balb/c ("Th2 dominant"), and IL-6KO mice were utilized to investigate ICD induced by exposure to the occupational irritants, benzoalkonium chloride (BKC) and JP-8 jet fuel. Histopathology revealed epidermal thickening and dermal cellular infiltration in dermatitis lesions, with IL-6KO skin exhibiting the most severe damage. Analysis of skin cytokine and chemokine protein expression showed that IL-1β, TNF-a, TGF-β, CCL2, CCL3 and CXCL1, were elevated in mice exposed to BKC regardless of immune phenotype. In contrast, IL-1β, TNF-a, TGF-β, and CXCL1 varied between mouse strains when JP-8 was compared to control exposure. Flow cytometric analysis and immunohistochemistry indicated neutrophil and monocyte presence within dermatitis lesions; however, IL-6KO showed a greater amount of neutrophils following BKC exposure and decreased neutrophil presence after JP-8 exposure when compared to C57 mice. Overall, it appears that immune phenotype and IL-6 deficiency alters the skin inflammatory response in ICD via differential cytokine and chemokine expression that influence the type of inflammatory cells that infiltrate into the skin. [Description provided by NIOSH]
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ISSN:0022-1767
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Volume:196
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Issue:1
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NIOSHTIC Number:nn:20057004
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Citation:J Immunol 2016 May; 196(1)(Suppl):126.34
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Federal Fiscal Year:2016
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Performing Organization:University of Oklahoma Health Sciences Center, Oklahoma City
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Peer Reviewed:False
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Start Date:20130901
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Source Full Name:The Journal of Immunology
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Supplement:Supplement
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End Date:20180831
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Main Document Checksum:urn:sha-512:2e067a56233c2c603d474207334a3130e5e3ceed6e5b0c3ec30d85d48c0a28ed296650ea4794c6d795d3950a9eacbda82467c172919384c7e1c7be0563767a24
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