Abstract
Streptococcus uberis infection can cause serious inflammation and damage to mammary epithelial cells and tissues that can be significantly alleviated by taurine. Autophagy plays an important role in regulating immunity and clearing invasive pathogens and may be regulated by taurine. However, the relationships between taurine, autophagy, and S. uberis infection remain unclear. Herein, we demonstrate that taurine augments PTEN activity and inhibits Akt/mTOR signaling, which decreases phosphorylation of ULK1 and ATG13 by mTOR and activates autophagy. Activating autophagy accelerates the degradation of intracellular S. uberis, reduces intracellular bacterial load, inhibits over-activation of the NF-κB pathway, and alleviates the inflammation and damage caused by S. uberis infection. This study increases our understanding of the mechanism through which taurine regulates autophagy and is the first to demonstrate the role of autophagy in S. uberis infected MAC-T cells. Our study also provides a theoretical basis for employing nutritional elements (taurine) to regulate innate immunity and control S. uberis infection. It also provides theoretical support for the development of prophylactic strategies for this important pathogen.
Highlights
More than 150 different pathogens can cause mammary gland infection
These results suggest that taurine does not inhibit autophagosome degradation, but instead induces autophagic flux since additional increases of LC3B-II result from treatment with lysosome inhibitor reflecting the amount of newly produced autophagosomes
The results demonstrate that taurine activates the classic autophagic response characterized by the accumulation of LC3BII
Summary
More than 150 different pathogens can cause mammary gland infection. Bacteria are the most common cause of mastitis [1]. Antibiotics and vaccination are the primary therapeutic and prevention strategies for bovine mastitis; both can partially reduce the incidence of mammary infection and improve milk production and quality. The development of a variety of drug resistance bacterial mechanisms along with the plasticity of pathogens can produce drug-resistant strains and diversified antigens enabling pathogens to resist drugs and camouflage them from the immune system [2,3,4,5]. These mechanisms are especially common for intracellular pathogens. Developing effective methods to prevent and treat bovine mastitis is an urgent need
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