Chlamydial infection may impact epithelial cell health directly by downregulating adherens junction molecule nectin-1 [37], disrupting epithelial tissue homeostasis [38] and inducing epithelialmesenchyme transition [39] and we observed that these pathways, as well as pathways promoting chlamydial entry into cells [18] and subsequent growth [19, 20] were over-represented amongst the most dynamic human transcripts in our small sample population. This evidence concerns the gene NECTIN1 and chlamydia trachomatis infectious disease.