The severity of imiquimod-induced mouse skin inflammation is independent of endogenous IL-38 expression.

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  • Additional Information
    • Source:
      Publisher: Public Library of Science Country of Publication: United States NLM ID: 101285081 Publication Model: eCollection Cited Medium: Internet ISSN: 1932-6203 (Electronic) Linking ISSN: 19326203 NLM ISO Abbreviation: PLoS One Subsets: MEDLINE
    • Publication Information:
      Original Publication: San Francisco, CA : Public Library of Science
    • Subject Terms:
      Aminoquinolines*; Dermatitis/*genetics ; Drug Eruptions/*genetics ; Inflammation/*chemically induced ; Interleukin-1/*genetics ; Interleukins/*genetics ; Skin/*metabolism; Animals ; Cells, Cultured ; Dermatitis/metabolism ; Dermatitis/pathology ; Disease Models, Animal ; Drug Eruptions/metabolism ; Drug Eruptions/pathology ; Female ; Imiquimod ; Inflammation/genetics ; Inflammation/pathology ; Interleukin-1/metabolism ; Interleukins/metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Knockout ; Severity of Illness Index ; Skin/pathology
    • Abstract:
      The IL-1 cytokine family includes eleven members, among which Il-36α, β and γ, IL-36Ra and IL-38. The IL-36 cytokines are involved in the pathogenesis of psoriasis. IL-38 is also expressed in the skin and was previously proposed to act as an IL-36 antagonist. In this study, we thus examined expression and function of Il-38 in a mouse model of imiquimod (IMQ)-induced skin inflammation. Il-38 mRNA was detected in the epidermis and in primary mouse keratinocytes, but not in dermal fibroblasts. At the peak of IMQ-induced inflammation, skin Il-38 mRNA levels were reduced, whereas Il-36ra mRNA expression increased. The severity of IMQ-induced skin inflammation, as assessed by recording ear thickness and histological changes, was similar in Il-38 KO and WT littermate control mice, while, in contrast, Il-36ra-deficient mice displayed more severe skin pathology than their WT littermates. Il-38-deficiency had no impact on IMQ-induced expression of proinflammatory mediators in the skin in vivo, on the basal expression of various cytokines or chemokines by cultured primary keratinocytes and dermal fibroblasts in vitro, or on the response of these cells to Il-36β. Finally, after cessation of topical IMQ application, the resolution of skin inflammation was also not altered in Il-38 KO mice. In conclusion, Il-38-deficiency did not impact the development or resolution of IMQ-induced skin inflammation. Our observations further suggest that endogenous Il-38 does not exert Il-36 inhibitory activity in this model, or in cultured skin cells. A potential anti-inflammatory function of Il-38 in mouse skin thus still remains to be demonstrated.
    • References:
      PLoS One. 2011 Apr 04;6(4):e18266. (PMID: 21483750)
      Biochem Biophys Rep. 2015 Oct 31;4:386-391. (PMID: 29124228)
      Immunity. 2013 Dec 12;39(6):1003-18. (PMID: 24332029)
      Nat Rev Rheumatol. 2010 Apr;6(4):232-41. (PMID: 20177398)
      Ann Rheum Dis. 2012 Jun;71(6):885-90. (PMID: 22312160)
      J Clin Invest. 2012 Nov;122(11):3965-76. (PMID: 23064362)
      Clin Exp Immunol. 2016 May;184(2):159-73. (PMID: 26701127)
      J Mol Cell Biol. 2016 Feb 17;:null. (PMID: 26892022)
      Blood. 2012 Oct 25;120(17):3478-87. (PMID: 22968459)
      Australas J Dermatol. 2004 Feb;45(1):47-50. (PMID: 14961909)
      Scand J Rheumatol. 2010 May;39(3):190-6. (PMID: 20141484)
      J Leukoc Biol. 2015 Apr;97(4):645-52. (PMID: 25673295)
      Nature. 2007 Feb 22;445(7130):866-73. (PMID: 17314973)
      Eur J Immunol. 2013 Dec;43(12 ):3138-46. (PMID: 24254490)
      J Dermatol Sci. 2015 Nov;80(2):150-2. (PMID: 26319074)
      Arthritis Rheumatol. 2015 Dec;67(12):3219-25. (PMID: 26314375)
      Proc Natl Acad Sci U S A. 2012 Feb 21;109(8):3001-5. (PMID: 22315422)
      J Biol Chem. 2001 Jun 8;276(23):20597-602. (PMID: 11278614)
      J Immunol. 2014 Jul 15;193(2):921-30. (PMID: 24935927)
      Ann Rheum Dis. 2006 Aug;65(8):1106-9. (PMID: 16361275)
      Cell Mol Biol (Noisy-le-grand). 2016 Apr 30;62(4):31-4. (PMID: 27188731)
      Int Immunopharmacol. 2016 Nov;40:452-457. (PMID: 27723569)
      Immunobiology. 2017 Mar;222(3):483-493. (PMID: 27769564)
      Lancet. 2015 Sep 5;386(9997):983-94. (PMID: 26025581)
      J Immunol. 2009 May 1;182(9):5836-45. (PMID: 19380832)
      Ann Rheum Dis. 2017 Jul;76(7):1304-1312. (PMID: 28288964)
      N Engl J Med. 2009 Jul 30;361(5):496-509. (PMID: 19641206)
      Clin Exp Immunol. 2015 Aug;181(2):230-8. (PMID: 25902739)
      Clin Exp Dermatol. 2006 Jan;31(1):140-1. (PMID: 16309513)
      J Exp Med. 2007 Oct 29;204(11):2603-14. (PMID: 17908936)
      Hum Mutat. 2013 Jan;34(1):176-83. (PMID: 22903787)
      Nat Rev Immunol. 2014 May;14(5):289-301. (PMID: 24722477)
      J Dermatolog Treat. 2016;27(1):19-26. (PMID: 26138406)
      Arthritis Rheum. 2006 Jul;54(7):2321-5. (PMID: 16918024)
      Nat Commun. 2013;4:1560. (PMID: 23463003)
    • Accession Number:
      0 (Aminoquinolines)
      0 (Il1f10 protein, mouse)
      0 (Interleukin-1)
      0 (Interleukins)
      P1QW714R7M (Imiquimod)
    • Publication Date:
      Date Created: 20180320 Date Completed: 20180723 Latest Revision: 20181202
    • Publication Date:
      20231215
    • Accession Number:
      PMC5858842
    • Accession Number:
      10.1371/journal.pone.0194667
    • Accession Number:
      29554104