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DOI | 10.1038/s41467-019-12753-x |
Staphylococcus aureus produces pain through pore-forming toxins and neuronal TRPV1 that is silenced by QX-314 | |
Blake, Kimbria J.1; Baral, Pankaj1; Voisin, Tiphaine1; Lubkin, Ashira2; Pinho-Ribeiro, Felipe Almeida1; Adams, Kelsey L.1; Roberson, David P.3,4; Ma, Yuxin C.1; Otto, Michael5; Woolf, Clifford J.3,4; Torres, Victor J.2; Chiu, Isaac M.1 | |
2019-10-25 | |
发表期刊 | NATURE COMMUNICATIONS |
ISSN | 2041-1723 |
出版年 | 2018 |
卷号 | 9 |
文章类型 | Article |
语种 | 英语 |
国家 | USA |
英文摘要 | The hallmark of many bacterial infections is pain. The underlying mechanisms of pain during live pathogen invasion are not well understood. Here, we elucidate key molecular mechanisms of pain produced during live methicillin-resistant Staphylococcus aureus (MRSA) infection. We show that spontaneous pain is dependent on the virulence determinant agr and bacterial pore-forming toxins (PFTs). The cation channel, TRPV1, mediated heat hyperalgesia as a distinct pain modality. Three classes of PFTs-alpha-hemolysin (Hla), phenol-soluble modulins (PSMs), and the leukocidin HlgAB-directly induced neuronal firing and produced spontaneous pain. From these mechanisms, we hypothesized that pores formed in neurons would allow entry of the membrane-impermeable sodium channel blocker QX-314 into nociceptors to silence pain during infection. QX-314 induced immediate and long-lasting blockade of pain caused by MRSA infection, significantly more than lidocaine or ibuprofen, two widely used clinical analgesic treatments. |
领域 | 资源环境 |
收录类别 | SCI-E |
WOS记录号 | WOS:000419306000028 |
WOS关键词 | PHENOL-SOLUBLE MODULINS ; NONSTEROIDAL ANTIINFLAMMATORY DRUGS ; ALPHA-TOXIN ; INTRAOSSEOUS INJECTION ; VIRULENCE DETERMINANTS ; ANESTHETIC EFFICACY ; CHEMOKINE RECEPTORS ; IONIC CHANNELS ; INFECTION ; INFLAMMATION |
WOS类目 | Multidisciplinary Sciences |
WOS研究方向 | Science & Technology - Other Topics |
URL | 查看原文 |
引用统计 | |
文献类型 | 期刊论文 |
条目标识符 | http://119.78.100.173/C666/handle/2XK7JSWQ/204619 |
专题 | 资源环境科学 |
作者单位 | 1.Harvard Med Sch, Div Immunol, Dept Microbiol & Immunobiol, Boston, MA 02115 USA; 2.NYU, Sch Med, Dept Microbiol, New York, NY 10016 USA; 3.Harvard Med Sch, Dept Neurobiol, Boston, MA 02115 USA; 4.Boston Childrens Hosp, FM Kirby Neurobiol Ctr, Boston, MA 02155 USA; 5.NIAID, Pathogen Mol Genet Sect, Lab Bacteriol, NIH, Bethesda, MD 20814 USA |
推荐引用方式 GB/T 7714 | Blake, Kimbria J.,Baral, Pankaj,Voisin, Tiphaine,et al. Staphylococcus aureus produces pain through pore-forming toxins and neuronal TRPV1 that is silenced by QX-314[J]. NATURE COMMUNICATIONS,2019,9. |
APA | Blake, Kimbria J..,Baral, Pankaj.,Voisin, Tiphaine.,Lubkin, Ashira.,Pinho-Ribeiro, Felipe Almeida.,...&Chiu, Isaac M..(2019).Staphylococcus aureus produces pain through pore-forming toxins and neuronal TRPV1 that is silenced by QX-314.NATURE COMMUNICATIONS,9. |
MLA | Blake, Kimbria J.,et al."Staphylococcus aureus produces pain through pore-forming toxins and neuronal TRPV1 that is silenced by QX-314".NATURE COMMUNICATIONS 9(2019). |
条目包含的文件 | 条目无相关文件。 |
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