期刊
JOURNAL OF MEDICAL VIROLOGY
卷 86, 期 1, 页码 58-63出版社
WILEY-BLACKWELL
DOI: 10.1002/jmv.23776
关键词
heterosexual infection; HIV entry; CCL20; IL-1 beta, female genital mucosa
类别
资金
- CAPES (the Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior), Brazil [BEX: 4083/09-1]
- University Jean Monnet of Saint-Etienne
Saliva can be considered as an important actor during sexual intercourse. However, there is no data concerning its influence on HIV sexual transmission. The aim of this study was to evaluate the role of whole saliva on the in vitro secretion of CCL20 by monolayered HEC-1A endocervical epithelium cells. HEC-1A cells were cultivated in 96-well microplates and incubated with specimens of whole saliva collected from 57 subjects tested seropositive (n = 34) or seronegative (n = 23) for HIV and presenting different oral conditions (healthy periodontally, n = 22, and gingivitis/periodontitis, n = 35). The production of CCL20 in the supernatants of HEC-1A cells after overnight incubation at 37 degrees C was quantified using ELISA. The salivary concentration of lactoferrin (Lf) and IL-1 beta was tested by ELISA. Saliva samples were found able to stimulate dramatically the production of CCL20 by epithelial cells, increasing this synthesis by a mean factor of 38.1 with reference to untreated cells. This stimulation was equivalent to that observed with IL-1 beta used as positive control. Although no difference was observed according to oral condition, HIV status or salivary concentration of Lf and IL-1 beta, the high salivary concentration of the latter protein could acknowledge in large part for the overproduction of CCL20 by HEC-1A cells when stimulated by saliva. Saliva was shown to significantly increase CCL20 secretion and may be responsible for an enhanced recruitment of dendritic/Langerhans cells at the genital level. These results suggest that saliva could facilitate HIV entry and possibly other pathogens through the genital mucosa during heterosexual intercourse. J. Med. Virol. 86:58-63, 2014. (c) 2013 Wiley Periodicals, Inc.
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