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Immune Phenotype and IL-6 Deficiency Modulate the Inflammatory Response in a Mouse Model of Irritant Contact Dermatitis



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  • Personal Author:
  • 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]
  • Subjects:
  • Keywords:
  • ISSN:
    0022-1767
  • Document Type:
  • Funding:
  • Genre:
  • Place as Subject:
  • CIO:
  • Topic:
  • Location:
  • Volume:
    196
  • Issue:
    1
  • NIOSHTIC Number:
    nn:20057004
  • Citation:
    J Immunol 2016 May; 196(1)(Suppl):126.34
  • Federal Fiscal Year:
    2016
  • NORA Priority Area:
  • Performing Organization:
    University of Oklahoma Health Sciences Center, Oklahoma City
  • Peer Reviewed:
    False
  • Start Date:
    20130901
  • Source Full Name:
    The Journal of Immunology
  • Supplement:
    Supplement
  • End Date:
    20180831
  • Collection(s):
  • Main Document Checksum:
    urn:sha-512:2e067a56233c2c603d474207334a3130e5e3ceed6e5b0c3ec30d85d48c0a28ed296650ea4794c6d795d3950a9eacbda82467c172919384c7e1c7be0563767a24
  • Download URL:
  • File Type:
    Filetype[PDF - 84.33 KB ]
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