The role of Ca 2+ mediated signaling pathways on the effect of taurine against Streptococcus uberis infection

Dai, Bin; Zhang, Jinqiu; Liu, Ming; Lu, Jia; Zhang, Yuanshu; Xu, Yuanyuan; Miao, Jinfeng; Yin, Yulong

doi:10.1016/j.vetmic.2016.06.008

Cited by 23 publications

(19 citation statements)

References 34 publications

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“…Numerous studies have established that oxidative phosphorylation in mitochondria is the main pathway for mROS production and the main source of ROS [43]. Expressing catalase in mitochondria could effectively reduce the production of mROS, thereby reducing the killing effect of macrophages on pathogens, indicating that mROS is a key driver in the process of antibacterial activity [10]. Our previous study shows that TLR2 regulates the generation of ROS including mROS during S. uberis infection both in vivo and in vitro [4].…”

Section: Discussionmentioning

confidence: 98%

“…These studies indicate that MECs could have a pivotal role in host defense with TLRs as their huge number in the mammary gland. Our laboratory has done a lot of research on the function of TLRs and MECs against S. uberis infection in vivo and in vitro models [4,[10][11][12]. We find that TLRs, mainly TLR2 but not excluding TLR4, initiates a complex signaling network characterized by NF-κB and nuclear factor in activated T cells.…”

Section: Introductionmentioning

confidence: 95%

“…PCR was carried out as previously described [10]. Total RNA was extracted by TRIzol reagent (TaKaRa, Dalian, China).…”

Section: Rna Extraction and Quantitative Real-time Polymerase Chain Rmentioning

confidence: 99%

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TLR2 Signaling Pathway Combats Streptococcus uberis Infection by Inducing Mitochondrial Reactive Oxygen Species Production

Wan

Wang

et al. 2020

Cells

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Mastitis caused by Streptococcus uberis (S. uberis) is a common and difficult-to-cure clinical disease in dairy cows. In this study, the role of Toll-like receptors (TLRs) and TLR-mediated signaling pathways in mastitis caused by S. uberis was investigated using mouse models and mammary epithelial cells (MECs). We used S. uberis to infect mammary glands of wild type, TLR2−/− and TLR4−/− mice and quantified the adaptor molecules in TLR signaling pathways, proinflammatory cytokines, tissue damage, and bacterial count. When compared with TLR4 deficiency, TLR2 deficiency induced more severe pathological changes through myeloid differentiation primary response 88 (MyD88)-mediated signaling pathways during S. uberis infection. In MECs, TLR2 detected S. uberis infection and induced mitochondrial reactive oxygen species (mROS) to assist host in controlling the secretion of inflammatory factors and the elimination of intracellular S. uberis. Our results demonstrated that TLR2-mediated mROS has a significant effect on S. uberis-induced host defense responses in mammary glands as well as in MECs.

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Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 95%

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TLR2 Signaling Pathway Combats Streptococcus uberis Infection by Inducing Mitochondrial Reactive Oxygen Species Production

Wan

Wang

et al. 2020

Cells

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“…PCR was carried out as previously described [41]. Total RNA was extracted by TRIzol reagent (TaKaRa, Dalian, China).…”

Section: Methodsmentioning

confidence: 99%

TLR2 signaling pathway combats Streptococcus uberis infection by inducing production of mitochondrial reactive oxygen species

Wan

Wang

et al. 2019

Preprint

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14Mastitis caused by Streptococcus uberis is a hazardous clinical disease in dairy 15 animals. In this study, the role of Toll-like receptors (TLRs) and TLR-mediated 16 signaling pathways in mastitis caused by S. uberis was investigated using mouse 17 models and mammary epithelial cells (MECs). We used S. uberis to infect mammary 18 glands of wild type, TLR2 / and TLR4 / mice and quantified the adaptor molecules in 19 TLR signaling pathways, proinflammatory cytokines, tissue damage and bacterial 20 count in mammary glands. When compared with TLR4 deficiency, TLR2 deficiency 21 induced more severe pathological changes through myeloid differentiation primary 22 response 88 (MyD88)-mediated signaling pathways during S. uberis infection. In 23 MECs, TLR2 detected S. uberis infection and induced mitochondrial reactive oxygen 24 species (mROS) to assist host control of secretion of inflammatory factors and 25 elimination of intracellular S. uberis. Our results demonstrate that TLR2-mediated 26 mROS have a significant effect on S. uberis-induced host defense responses in 27 mammary glands as well as MECs.28 29 Author summary 30 S. uberis contributes significantly to global mastitis and remains a major obstacle for 31inflammation elimination due to its ability to form persistent infection in mammary 32 tissue. The Toll-like receptor (TLR) family plays a significant role in identifying 33 infections of intracellular bacteria and further triggering inflammatory reactions in 34 immune cells. However, the detailed molecular mechanism by which TLR is regulated, 35 and whether MECs, as the main cells in mammary gland, are tightly involved in these 36 processes is poorly understood. Here, we used S. uberis to infect mammary glands of 37 wild type, TLR2 / , TLR4 / mice and MECs to assess pathogenesis, proinflammatory 38 cytokines, ROS as well as mROS levels during infection. We found that during S.uberis 39 infection, it is TLR2 deficiency that induced more severe pathological changes 40 through MyD88-mediated signaling pathways. In addition, our work demonstrates 41 that mROS mediated by TLR2 has an important role in host defense response to 42 combat S. uberis infection in mammary glands as well as MECs. 43 44 45 Mastitis is a type of inflammation mainly caused by intramammary infection and 46 causes great harm to the dairy industry [1]. Streptococcus uberis is an environmental 47 pathogen that is emerging as the most important mastitis-causing agent in some 48 regions [2]. Previous studies in our laboratory have demonstrated that persistent 49 inflammation including swelling, secretory epithelial cell degeneration, and 50 polymorphonuclear neutrophilic leukocyte (PMN) infiltration occurs in mammary 51 tissue following injection with S. uberis [3]. The inflammatory responce caused by 52 S. uberis is lighter than that caused by E. coli [3].These pathological response 53 connected with intracellular infection of S. uberis as it escaped the elimination of 54 immune cells and formed persistent infection. 55 Activation o...

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“…Taurine-conjugated bile acids are identified as inhibitors of biofilm formation against both Vibrio cholerae and Pseudomonas aeruginosa [47]. Taurine complementation attenuates pro-inflammatory response in mammary epithelial cells after Streptococcus uberis challenge [48] and in a bovine mammary epithelial cell (MEC) line (MAC-T) or a mouse mammary epithelial cell line (EpH4-Ev) infected with Escherichia coli and Staphylococcus aureus [30]. In addition, exogenous taurine also promotes the anti-infective ability against viruses and fungi [49,50].…”

Section: Discussionmentioning

confidence: 99%

Malate enhances survival of zebrafish against Vibrio alginolyticus infection in the same manner as taurine

Yang

et al. 2020

Virulence

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Development of low-cost and eco-friendly approaches to fight bacterial pathogens is especially needed in aquaculture. We previously showed that exogenous malate reprograms zebrafish's metabolome to potentiate zebrafish survival against Vibrio alginolyticus infection. However, the underlying mechanism is unknown. Here, we use GC-MS based metabolomics to identify the malate-triggered metabolic shift. An activated TCA cycle and elevated taurine are identified as the key metabolic pathways and the most crucial biomarker of the reprogrammed metabolome, respectively. Taurine elevation is attributed to the activated TCA cycle, which is further supported by the increased expression of genes in the metabolic pathway of taurine biosynthesis from the isocitrate of the TCA cycle to taurine. Exogenous taurine increases the survival of zebrafish against V. alginolyticus infection as malate did. Moreover, exogenous taurine and malate regulate the expression of innate immunity genes and promote the generation of reactive oxygen species and nitrogen oxide in a similar way. The two metabolites can alleviate the excessive immune response to bacterial challenge, which protects fish from bacterial infection. These results indicate that malate enhances the survival of zebrafish to V. alginolyticus infection via taurine. Thus, our study highlights a metabolic approach to enhance a host's ability to fight bacterial infection.

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The role of Ca 2+ mediated signaling pathways on the effect of taurine against Streptococcus uberis infection

Cited by 23 publications

References 34 publications

TLR2 Signaling Pathway Combats Streptococcus uberis Infection by Inducing Mitochondrial Reactive Oxygen Species Production

TLR2 Signaling Pathway Combats Streptococcus uberis Infection by Inducing Mitochondrial Reactive Oxygen Species Production

TLR2 signaling pathway combats Streptococcus uberis infection by inducing production of mitochondrial reactive oxygen species

Malate enhances survival of zebrafish against Vibrio alginolyticus infection in the same manner as taurine

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