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


Akgül, B; Bostanci, N; Westphal, K; Nindl, I; Navsaria, H; Storey, A; Pfister, H (2010). Human papillomavirus 5 and 8 E6 downregulate interleukin-8 secretion in primary human keratinocytes. Journal of General Virology, 91(4):888-892.

Abstract

Human papillomaviruses (HPVs) of genus beta appear to be involved in the early stages of skin cancer development because both the prevalence and viral load are higher in precancerous actinic keratoses than in skin cancers. IL-8 is an inflammatory cytokine, which 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.

Abstract

Human papillomaviruses (HPVs) of genus beta appear to be involved in the early stages of skin cancer development because both the prevalence and viral load are higher in precancerous actinic keratoses than in skin cancers. IL-8 is an inflammatory cytokine, which 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.

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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Center for Dental Medicine > Institute of Oral Biology
Dewey Decimal Classification:610 Medicine & health
Language:English
Date:2010
Deposited On:27 Feb 2010 08:06
Last Modified:05 Apr 2016 14:02
Publisher:Society for General Microbiology
ISSN:0022-1317
Additional Information:This is an author manuscript that has been accepted for publication in Journal of General Virology, copyright Society for General Microbiology, but has not been copy-edited, formatted or proofed. Cite this article as appearing in Journal of General Virology. This version of the manuscript may not be duplicated or reproduced, other than for personal use or within the rule of ‘Fair Use of Copyrighted Materials’ (section 17, Title 17, US Code), without permission from the copyright owner, Society for General Microbiology. The Society for General Microbiology disclaims any responsibility or liability for errors or omissions in this version of the manuscript or in any version derived from it by any other parties. The final copy-edited, published article, which is the version of record, can be found at http://vir.sgmjournals.org, and is freely available without a subscription.
Publisher DOI:https://doi.org/10.1099/vir.0.016527-0
PubMed ID:20007354

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