High level expression of human epithelial β-defensins hBD-1, 2 and 3 in papillomavirus induced lesionsReportar como inadecuado

High level expression of human epithelial β-defensins hBD-1, 2 and 3 in papillomavirus induced lesions - Descarga este documento en PDF. Documentación en PDF para descargar gratis. Disponible también para leer online.

Virology Journal

, 3:75

First Online: 08 September 2006Received: 08 July 2006Accepted: 08 September 2006


BackgroundEpithelial defensins including human β-defensins hBDs and α-defensins HDs are antimicrobial peptides that play important roles in the mucosal defense system. However, the role of defensins in papillomavirus induced epithelial lesions is unknown.

ResultsPapilloma tissues were prospectively collected from 15 patients with recurrent respiratory papillomatosis RRP and analyzed for defensins and chemokine IL-8 expression by quantitative, reverse-transcriptase polymerase chain reaction RT-PCR assays. HBD-1 -2 and -3 mRNAs were detectable in papilloma samples from all RRP patients and the levels were higher than in normal oral mucosal tissues from healthy individuals. Immunohistochemical analysis showed that both hBD-1 and 2 were localized in the upper epithelial layers of papilloma tissues. Expression of hBD-2 and hBD-3 appeared to be correlated as indicated by scatter plot analysis r = 0.837, p < 0.01 suggesting that they were co-inducible in papillomavirus induced lesions. Unlike hBDs, only low levels of HD5 and HD6 were detectable in papillomas and in oral mucosa.

ConclusionHuman β-defensins are upregulated in respiratory papillomas. This novel finding suggests that hBDs might contribute to innate and adaptive immune responses targeted against papillomavirus-induced epithelial lesions.

Electronic supplementary materialThe online version of this article doi:10.1186-1743-422X-3-75 contains supplementary material, which is available to authorized users.

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Autor: Kong T Chong - Liangbin Xiang - Xiaohong Wang - Eunjoo L Jun - Long-fu Xi - John M Schweinfurth

Fuente: https://link.springer.com/

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