Influence of Chlamydia trachomatis infection on the barrier function of porcine oviduct epithelial cells

Chlamydia trachomatis (Ct) infections cause the most prevalent bacterial sexually transmitted disease worldwide causing infertility and ectopic pregnancies. An additional detrimental side effect of Ct infections is that patients are at higher risk of experiencing co-infections with sexually transmitted viruses such as human immunodeficiency virus (HIV). It has been previously demonstrated that Ct infection of porcine oviduct epithelial cells (pOECs) redirects claudin-4, a tight-junction protein, from the cell surface to the intracellular Ct inclusions. This redirection of claudin-4 indicates that Ct-infected cells have a lower tight-junction barrier function. Thus, this study aims to show the effect of Ct infection on pOECs regarding their barrier integrity. pOECs were isolated and infected with Ct to measure the trans-epithelial electrical resistance (TEER). By comparing the TEER between Ct-infected and non-infected pOECs, we could demonstrate that Ct infection leads to a significant decrease in the TEER of pOECs as early as eight hours post-infection (hpi) with Ct titers ranging from 1:8 through 1:128,000. This effect was dose-dependent. The reproductive cycle of Ctin pOEC takes ~48 hours before Ct are released via cell lysis. Since Ct inhibits host cell apoptosis and a drop in TEER was observed as early as 8hpi, it is unlikely that this effect is caused by Ct-induced cell death. Taken together this data suggests a Ct-induced disruption of the epithelial barrier integrity which could explain the higher risk of Ct patients for co-infections with HIV. Thereby, this project justifies further investigation into how Ct infection might affect the permeability of pOECs barriers for viruses like HIV.