Effect of Tritrichomonas foetus, Tf-31 (a cattle isolate) and Tff6 (a feline isolate) on TLR signaling pathway in cervical epithelial cells.

Abstract

Abstract Bovine trichomonosis is caused by Tritrichomonas foetus, which is widely prevalent in 33 US states, and is a reportable disease due to potential huge economic losses to cattle industry. T. foetus also causes chronic large-bowel diarrhoea in cats, complicated not only by its chronicity but for its difficulty to treat, with few registered or effective products available. T. foetus persistently colonize the lower genital tract of bulls but usually do not cause either major clinical signs or inflammation while vaginal inflammation is a common disease of the dairy cows’ reproductive tract. Mechanisms of immune response to this pathogen are poorly studied. This study for the first time, reports the effect of T. foetus; Tf-31-cattle isolate and Tff6-cat isolate, on activation of toll-like receptors (TLRs) and inflammatory response in vaginal epithelial cells. The expression levels of serial effectors related to the TLRs-MyD88/NF-κB signaling pathway (TLR2, TLR4, MyD88, NF-κB, IL-1β, IL-6, TNF-α, and IL-10) were measured with real-time polymerase chain reaction (RT-PCR), ELISA, and Western blot analyses. Of the 6 cell-membrane TLRs tested, TLR2 and TLR4 were activated by cells, as noted by increased mRNA expression levels of TLR2 and TLR4 in both Tf31 and Tff6 treated cervical epithelial cells relative to control cells. ELISA assays showed up-regulation on IL-10, both in Tf-31 and Tff6 treated epithelial cells. Treatment with inhibitors of MyD88 signaling pathway abolished the upregulation of downstream cytokines. These data indicate that T. foetus isolates activate TLR-MyD88 signaling pathway to induce innate immune response. However, further detailed in vitro and in vivo studies are required to confirm these findings. Supported by Biology department