Human papillomavirus 5 and 8 E6 downregulate interleukin-8 secretion in primary human keratinocytes

被引:21
作者
Akguel, Baki [1 ]
Bostanci, Nagihan [2 ]
Westphal, Kathi [3 ]
Nindl, Ingo [3 ]
Navsaria, Harshad [4 ]
Storey, Alan [5 ]
Pfister, Herbert [1 ]
机构
[1] Univ Cologne, Inst Virol, D-5000 Cologne 41, Germany
[2] Univ Zurich, Inst Oral Biol, ZZMK, Fac Med, CH-8032 Zurich, Switzerland
[3] Skin Canc Ctr Charite, Charite, Dept Dermatol, Berlin, Germany
[4] Univ London, Ctr Cutaneous Res, Queen Marys Sch Med & Dent, London, England
[5] Univ Oxford, John Radcliffe Hosp, Dept Mol Oncol, Oxford OX3 9DU, England
关键词
EPIDERMODYSPLASIA-VERRUCIFORMIS; EPIDERMAL-KERATINOCYTES; ACTINIC KERATOSES; DNA LOADS; HIGH-RISK; SKIN; PROTEINS; DIFFERENTIATION; PREVALENCE; EXPRESSION;
D O I
10.1099/vir.0.016527-0
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Human papillomaviruses (HPVs) of the genus Betapapilloma virus appear to be involved in the early stages of skin cancer development, since both the prevalence and viral load are higher in precancerous actinic keratoses than in skin cancers. Interleukin-8 (IL-8) is an inflammatory cytokine that serves to alert the surrounding tissue after UV-induced damage. We examined the effects of the E2, E6 and E7 proteins of HPV8 and the E6 proteins of various HPV genotypes on IL-8 secretion from primary keratinocytes. HPV5 and HPV8 E6 showed the highest downregulation of basal IL-8 secretion. HPV8 E6 also negatively modulated IL-8 mRNA expression and protein secretion upon UVB irradiation. The downregulation of IL-8 in actinic keratoses may weaken the response to UV-induced damage and thus favour the accumulation of UVB-induced mutations.
引用
收藏
页码:888 / 892
页数:5
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