Epidermal Hyperplasia and Elevated HB-EGF are More Prominent in Retinoid Dermatitis Compared with Irritant Contact Dermatitis Induced by Benzalkonium Chloride

Abstract

Background: 'Retinoid dermatitis' is a retinoid-induced irritant contact dermatitis (ICD). The mechanism of retinoid dermatitis may be different from that of other ICDs. However, it remains uncertain how topical retinoid induce ICD. Objective: We compared several aspects of contact dermatitis induced by topical retinol and benzalkonium chloride (BKC) on hairless mice skin. Methods: 2% retinol or 2.5% BKC was applied to hairless mice and transepidermal water loss (TEWL), ear thickness, histologic and immunohistochemical findings were compared. We also compared mRNA expression of inflammatory cytokines, epidermal differential markers, cyclooxygenases (COXs) and heparin binding epidermal growth factor like growth factor (HB-EGF). Results: Topical application of 2% retinol and 2.5% BKC increased TEWL and ear thickness in similar intensity. Epidermal hyperplasia was more prominent in retinol treated skin. Proliferating cell nuclear antigen, involucrin and loricrin expression were higher in retinol-treated skin than in BKC-treated skin. Filaggrin, however, was more expressed in BKC-treated skin. The mRNA expression of IL-8, TNF-α, COX-2, involucrin, loricrin and filaggrin were increased in both retinol-and BKC-treated skin in similar intensity. HB-EGF was more significantly increased in retinol-treated skin. Conclusion: Elevated HB-EGF and epidermal hyperplasia are more prominent features of retinoid dermatitis than in BKC-induced ICD. (Ann Dermatol 22(3) 290∼299,

Inhibition of benzalkonium chloride-induced skin inflammation in mice by an indol-1-ylpropan-2-one inhibitor of cytosolic phospholipase A2α

“…Therefore, we cultivated primary murine keratinocytes from the ears of BALB/c mice and stimulated them with BAC (8 μmol L −1 ) for 24 h. At this concentration, cells were still viable, but the irritant led to the expression or upregulation of TNF‐α, S100A8, S100A9, IL‐1α, IL‐1β, IL‐6, MIP‐1α and MIP‐1β as well as COX2 (Fig. 8), as previously described 36–38,44 . Thus, BAC directly induces expression of proinflammatory mediators by cultured keratinocytes.…”

“…In order to investigate the effect of compound 1 on the expression of mediators or signals induced by BAC in vivo , we carried out real‐time PCR to analyse tissue‐derived gene expression. As previously described for ICD with BAC, the application of BAC induced an upregulation of many cytokines with a known function in inflammatory response, such as interleukin (IL)‐1α, IL‐1β and especially TNF‐α 37–41 …”

“…As previously described for ICD with BAC, the application of BAC induced an upregulation of many cytokines with a known function in inflammatory response, such as interleukin (IL)-1a, IL-1b and especially TNF-a. [37][38][39][40][41] After treatment with compound 1 the induction of mRNA of IL-1a, IL-1b and TNF-a was downregulated as was the induction of mRNA for proinflammatory cytokines such as IL-6, macrophage inflammatory protein (MIP)-1a and MIP-1b ( Fig. 7).…”

“…8), as previously described. [36][37][38]44 Thus, BAC directly induces expression of proinflammatory mediators by cultured keratinocytes. The same mediators are also expressed by keratinocytes in vivo and are known to be the major inducers for the ensuing inflammatory infiltrate.…”

Effects of Egg Shell Membrane Hydrolysates on UVB-radiation-induced Wrinkle Formation in SKH-1 Hairless Mice

“…Keratin is very resistant to physical, chemical, and biological reactions ( Kim et al ., 2009 ). ESM has been suggested for use in formulations for moisturizers, wound recovery, skin growth, anti-wrinkle agents, whitening, and anti-microbial activity ( Cong et al ., 2008 ; Kim, 2009 ; Lee, 2010 ).…”