PI3K/Akt/mTOR signaling pathway participates in Streptococcus uberis-induced inflammation in mammary epithelial cells in concert with the classical TLRs/NF-κB pathway

Mammary epithelial cells (MECs) play an important role in debating Streptococcus uberis (S. uberis) infection. Toll like receptor (TLR) engagement leads to the recruitment of phosphatidylinositol 3 kinases (PI3K). In order to investigate the relationship of TLRs/NF-kappa B and PI3K/Akt/mTOR signaling pathways in S. uberis infection in MECs, we challenged MECs (EpH4-Ev) with S. uberis 0140 J and quantified the adaptor molecules in these two signaling pathways, as-well-as proinflammatory cytokines and cell damage. The results indicate that the host's responses to virulent S. uberis infection are complex. In MECs, both TLR2 and TLR4 are detecting S. uberis infection and TLR2 is the principal receptor. The role of the PI3K/Akt/mTOR pathway in inflammatory regulation is independent of the activation of TLRs/NF-kappa B. Cross-talk between PI3K/Akt/mTOR and TLRs/NF-kappa B signaling pathways promote inflammation. This study increases our understanding of the molecular defense mechanisms of MECs in S. uberis mastitis, and provides theoretical support for the prevention of this disease.