Staphylococcus aureus increases Prostaglandin E2 secretion in cow neutrophils by activating TLR2, TLR4, and NLRP3 inflammasome signaling pathways

Frontiers in Microbiology

Microbiology

Jinshan Cao¹  Xueying Jiang¹  Shuangyi Zhang¹  Wei Mao¹  Yan Jia¹  Kai Zhang¹  Bo Liu¹  Yinghong Qian²  Yongli Song³ 

[1] College of Veterinary Medicine, Inner Mongolia Agricultural University, Huhhot, China;Key Laboratory of Animal Clinical Treatment Technology, Ministry of Agriculture, Huhhot, China;Inner Mongolia Academy of Agricultural and Animal Husbandry Sciences, Huhhot, China;Stem Cell and Microbiology, Inner Mongolia University, Huhhot, China;

关键词: Staphylococcus aureus;    Prostaglandin E;    neutrophils;    toll-like receptor 2;    toll-like receptor 4;    NLR pyrin domain-containing 3;   

DOI  :  10.3389/fmicb.2023.1163261

 received in 2023-02-27, accepted in 2023-03-24,  发布年份 2023

来源: Frontiers

【 摘 要 】

IntroductionIn clinical settings, dairy cows are often attacked by pathogenic bacteria after delivery, especially Staphylococcus aureus (S. aureus). Neutrophils have long been regarded as essential for host defense against S. aureus. Prostaglandin E2 (PGE2) can additionally be used as an inflammatory mediator in pathological conditions to promote the repair of inflammatory injuries. However, whether S. aureus can promote the accumulation of PGE2 after the infection of neutrophils in cows and its mechanism remain unclear. Lipoprotein is an important immune bioactive ingredient of S. aureus.MethodsIn this study, the changes in neutrophils were monitored in dairy cows infected with wild-type S. aureus (SA113) and an S. aureus lipoprotein-deficient strain (Δlgt); meanwhile, we established whether pattern recognition receptors mediate this process and whether S. aureus lipoproteins are necessary for causing the release of PGE2 from cow neutrophils.ResultsThe results showed that Δlgt was less effective than SA113 in inducing the production of IL-1β, IL-6, IL-8, IL-10, and PGE2 within neutrophils; furthermore, TLR2, TLR4, and NLRP3 receptors were found to mediate the inducible effect of lipoprotein on the above inflammation mediators and cytokines, which depended on MAPK and Caspase-1 signaling pathways. In addition, TLR2, TLR4, and NLRP3 inhibitors significantly inhibited PGE2 and cytokine secretion, and PGE2 was involved in the interaction of S. aureus and neutrophils in dairy cows, which could be regulated by TLR2, TLR4, and NLRP3 receptors. We also found that S. aureus was more likely to be killed by neutrophils when it lacked lipoprotein and TLR2, TLR4, and NLRP3 were involved, but PGE2 seemed to have no effect.DiscussionTaken together, these results suggest that lipoprotein is a crucial component of S. aureus in inducing cytokine secretion by neutrophils as well as killing within neutrophils, which could be accomplished by the accumulation of PGE2 by activating MAPK and the Caspase-1 signaling pathways through TLR2, TLR4, and NLRP3 receptors. These results will contribute to a better understanding of the interaction between S. aureus and host immune cells in dairy cows.

【 授权许可】

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Copyright © 2023 Zhang, Jia, Qian, Jiang, Zhang, Liu, Cao, Song and Mao.