EXPRESSION OF BETA-DEFENSINS IN RESPONSE TO HIV-1 IN AN ORAL TISSUE MODEL VS MONOLAYER CULTURES.

This study by researchers at the University of Washington and the Fred Hutchinson Cancer Research Center demonstrated that MatTek’s EpiOral in vitro human buccal (inner cheek) tissue equivalent can be used to investigate the expression of human beta-defensins (hBD) in response to exposure to HIV-1 virus. HIV transmission through the oral route is inefficient. Epithelial structure and antimicrobial peptides including human beta-defensins (hBD), produced by the epithelium, may contribute to the relative lack of viral infection through the oral cavity. The objective of this study was to determine the expression of hBD in response to HIV-1. Researchers at the University of Washington and the Fred Hutchinson Cancer Research Center (USA) used EpiOral, a multilayered, organotypic tissue model of the human buccal epithelium (MatTek Corp., Ashland, MA), and monolayer cultures of primary gingival epithelial cells, under different conditions: unstimulated, in the presence of cell-free vs. cell-associated X4-tropic or R5-tropic HIV-1, applied to either the top or the bottom of the tissues, and in the presence of the pro-inflammatory cytokines IL-1á or TNF-á. Expression of hBD2 mRNA was determined by reverse transcriptase polymerase chain reaction and quantitative real-time PCR. In the EpiOral tissue model and in the monolayer cell cultures, hBD2 mRNA expression was not significantly higher after HIV-1 challenge than in unstimulated media controls. Expression of hBD2 mRNA was strongly up-regulated in response to TNF-á and weakly to IL-1á. Researchers concluded that hBD2 expression was induced by some components in the media, for example proteins derived from the fetal bovine serum, rather than by the virus itself.

EpiOral , HIV-1, Human beta-defensins (hBD), Human buccal epithelium, IL-1a, Messenger RNA (mRNA), Monolayer cultures, Oral tissue model, Primary gingival epithelial cells , R5-trophic, TNF-a, X4-trophic

IL-1a, TNF-a