The role of Ca2+ mediated signaling pathways on the effect of taurine against Streptococcus uberis infection

- MECs were with S. uberis and TLR-2/Ca2+ mediated signaling pathways were quantified.
- S. uberis increases the expression of the TLR-2/Ca2+ mediated signaling pathways.
- Taurine administration downregulated all these indices.

To provide insight into the mechanisms of taurine attenuation of pro-inflammatory response in mouse mammary epithelial cell line (EpH4-Ev, purchased by ATCC, USA) after Streptococcus uberis (S. uberis, 0140J) challenge, we infected MECs with S. uberis (2.5 × 107 cfu mL−1, MOI = 10) for 3 h and quantified changes in TLR-2 and calcium (Ca2+) mediated signaling pathways. The results indicate that S. uberis infection significantly increases the expression of TLR-2, intracellular Ca2+ levels, PLC-γ1 and PKC-α, the activities of transcription factors NF-κB and NFAT, and related cytokines (TNF-α, IL-1β, IL-6, G-CSF, IL-2, KC, IL-15, FasL, MCP-1, and LIX) in culture supernatants. Taurine administration downregulated all these indices, the activities of NF-κB and NFAT. Cytokine secretions were similar using special PKC inhibitor Go 6983 and NFAT inhibitor VIVIT. Our data indicate that S. uberis infection induces pro-inflammatory response of MECs through a TLR-2 mediated signaling pathway. In addition, taurine can prevent MEC damage by affecting both PLC-γ1-Ca2+-PKC-α-NF-κB and PLC-γ1-Ca2+-NFATs signaling pathways. This is the first report to demonstrate the mechanisms of taurine attenuated pro-inflammatory response in MECs after S. uberis challenge.