%0 Journal Article %A Sun, Jingru %A Kintner, Jennifer %A Schoborg, Robert V. %T The host adherens junction molecule nectin-1 is downregulated in Chlamydia trachomatis-infected genital epithelial cells %D 2008 %J Microbiology, %V 154 %N 5 %P 1290-1299 %@ 1465-2080 %R https://doi.org/10.1099/mic.0.2007/015164-0 %K TJ, tight junction %K CPAF, chlamydial protease/proteasome-like activity factor %K FAK, focal adhesion kinase %K h.p.i., hours post-infection %K EB, elementary body %K RB, reticulate body %K MOMP, major outer-membrane protein %K DS, desmosome %K GAPDH, glyceraldehyde-3-phosphate dehydrogenase %K AJ, adherens junction %I Microbiology Society, %X Nectin-1, a member of the immunoglobulin superfamily, is a Ca2+-independent cell adhesion protein implicated in the organization of E-cadherin-based adherens junctions (AJs) and claudin-based tight junctions (TJs) in epithelial cells. Nectin-1 also regulates cell–cell adhesion and cell polarization in a Cdc42- and Rac-dependent manner. Western blot analyses demonstrated that accumulation of host nectin-1 is decreased by 85 % at 48 hours post-infection (h.p.i.) in Chlamydia trachomatis serovar E-infected HeLa cells. Time-course experiments demonstrated that this decrease was sustained to 60 h.p.i. Nectin-1 downregulation in C. trachomatis-infected cells was prevented by both chloramphenicol exposure and prior inactivation of the chlamydiae with UV light, demonstrating that active C. trachomatis replication was required. Penicillin G-exposure studies demonstrated that nectin-1 accumulation was also altered during persistent infection. Finally, RT-PCR analyses indicated that chlamydial infection did not alter accumulation of any nectin-1 transcripts, demonstrating that nectin-1 accumulation is reduced at a post-transcriptional level. Intesrestingly, N-cadherin-dependent cell–cell junctions can be disrupted by C. trachomatis infection, as reported by Prozialeck et al. (2002) . Because interaction of nectin molecules on adjacent cells is essential for AJ formation, these data suggest that C. trachomatis may disrupt AJs, at least in part, by diminishing nectin-1 accumulation. Notably, release of chlamydiae-infected epithelial cells has been observed both in vitro from polarized monolayers and in vivo from tissues, suggesting that chlamydia-modulated downregulation of adhesion molecules and the subsequent disruption of host cell adherence may be involved in chlamydial dissemination or pathogenesis. %U https://www.microbiologyresearch.org/content/journal/micro/10.1099/mic.0.2007/015164-0