Accumulation of C-reactive protein in basal keratinocytes of normal skins. Issue 1 (July 2016)

• Record Type: Journal Article
• Authors: Ono, Koji; Fujimoto, Norihiro; Akiyama, Minoru; Satoh, Takahiro; Tajima, Shingo
• Is Part Of: Journal of dermatological science. Volume 83:Issue 1(2016:Jul.)
• Page Start: 26
• Page End: 33
• Publication Date: 2016-07
• Subjects: C-reactive protein -- Keratinocyte -- IL-1β -- IL-8 -- Endothelial cell; Dermatology -- Periodicals; Skin Diseases -- Periodicals; Dermatologie -- Périodiques; 616.5005
• DOI: 10.1016/j.jdermsci.2016.04.002
• Languages: English
• ISSNs: 0923-1811

Abstract

Highlights: CRP deposition was found on the basal keratinocyte membrane in normal human skins. CRP in the basal keratinocytes can be derived from local dermal microvasculatures. Treatment of cultured keratinocytes with heat-denatured CRP induced IL-8 expression. CRP inhibited the adhesion of keratinocytes in culture. Skin inflammation may be regulated by CRP modulation of keratinocytes. Abstract: Background: C-reactive protein (CRP) is a prototypic acute phase protein which increases dramatically in the blood during the first 48 h of tissue inflammation and has been recognized as a risk factor for atherosclerosis. CRP interacts with a variety of proteins. Objective: To know the role of accumulated CRP in the skin. Methods: Interaction of CRP with basal keratinocytes was studied using immunohistochemical method and keratinocyte culture system. Results: We found an immunohistochemical deposition of CRP on the basal keratinocyte membrane in some normal human skins (23 out of 46 skins). When added to cultured keratinocytes, heat-denatured but not native CRP was found to adhere to keratinocyte cell membrane after 1 h, then internalized into cytoplasm after 24 h. The heat-denatured CRP recognized at least four keratinocyte polypeptides with the molecular weights of 56, 42, 32 and 24 kDa. Ligand binding assays suggested that multiple populations of receptor-ligand interactions were involved in the binding between CRP and keratinocyte. Cultured dermal microvascular endothelial cells were found to express CRP of which expression was greatly induced by interleukin-1β (IL-1β) treatment, suggesting that the deposited CRP in the basal keratinocytes can be derived from local dermal microvasculatures as well as from systemic circulation (serum). Treatment of cultured keratinocytes with heat-denatured CRP induced interleukin-8 (IL-8) expression, a potent leukocyte chemotactic cytokine. CRP in the medium (liquid phase) and CRP-coated dishes (solid phase) both inhibited the adhesion of keratinocytes in culture. Conclusion: Accumulation of CRP may regulate the skin inflammation and keratinocyte proliferation by modulating keratinocyte cytokine expression and adhesion to substrate.