S. Aureus Lipoteichoic Acid Failed to Activate NLRP3, but Downregulated the Transduction of NLRP3/MAPK and NF-κB Signaling Pathway in Mouse Mastitis Induced by S. Aureus

Abstract

Background It was confirmed that S. aureus infection activated the expression of NLRP3. As a major component of S. aureus cell wall, what about LTA? Firstly, in this study a mouse model was built following LTA intramammary infection for 0, 12, 24, 48 and 72 h, the characterization of mammary inflammatory response induced by LTA was observed. Subsequently, mouse mammary preconditioned with LTA was modelling. The effect of LTA treatment on the activation of NLRP3/ MAPK and NF-κB signaling pathways induced by S. aureus were detected.Results Results shown that the LTA intramammary infection induce mild but rapid recovery inflammation in mammary gland whereas failed to stimulate NLRP3. LTA treatment protected mammary gland against S. aureus infection by suppressed the activation of NLRP3/ MAPK and NF-κB signaling pathways. Meanwhile it is noteworthy that the expression of NLRP3/MAPK JNK induced by S. aureus was not regulated by LTA treatment.Conclusions These results suggested LTA induced mammary gland inflammation was mild and self-limiting. LTA treatment revealed a good anti-inflammation effect through downregulating the transduction of NLRP3/MAPK and NF-κB signaling pathways in mouse mastitis induced by S. aureus. Our research highlights the importance of an LTA during the innate immune response of the mammary gland and offer novel insights for new approaches concerning effective immunomodulation against a local bacterial infection.