肠道菌群在神经病理性疼痛中作用的研究进展

doi:10.16352/j.issn.1001-6325.2023.01.0188

基础医学与临床 ›› 2023, Vol. 43 ›› Issue (1): 188-191.doi: 10.16352/j.issn.1001-6325.2023.01.0188

肠道菌群在神经病理性疼痛中作用的研究进展

吕彦函, 余卓颖^*, 李民^*

北京大学第三医院麻醉科,北京 100191

收稿日期:2021-11-08 修回日期:2022-05-07 发布日期:2022-12-27
通讯作者: ^*liminanesth@bjmu.edu.cn; zhuoyingyu@bjmu.edu.cn
基金资助:
国家自然科学基金(82071411); 国家自然科学基金青年科学基金(82001329)

Research progress of gut microbiota in neuropathic pain

LYU Yanhan, YU Zhuoying^*, LI Min^*

Department of Anesthesiology, Peking University Third Hospital, Beijing 100191,China

Received:2021-11-08 Revised:2022-05-07 Published:2022-12-27
Contact: ^*liminanesth@bjmu.edu.cn; zhuoyingyu@bjmu.edu.cn

摘要/Abstract

摘要： 导致神经病理性疼痛(NP)的作用机制极其复杂。肠道菌群在诱发NP方面起着重要作用。肠道菌群及其代谢产物的改变可通过Toll 样受体(TLRs)促进免疫细胞和神经胶质细胞释放促炎因子,活化免疫系统及炎性反应,这可能是未来治疗NP的潜在靶点。

关键词: 肠道菌群, 神经病理性疼痛, Toll样受体

Abstract: The mechanism of neuropathic pain (NP) is extremely complicated, and current pharmacological treatments for NP are still unsatisfactory. The gut microbiota plays important roles in inducing NP. The changes of gut microbiota and gut microbiota-dependent metabolite could promote the immune cells and glial cells releasing pro-inflammatory cytokines, initiating the innate immune response and inflammation by activating Toll-like receptors (TLRs), which is believed to be a potential candidate to alleviate NP.

Key words: gut microbiota, neuropathic pain, Toll-like receptors

中图分类号:

R363

吕彦函, 余卓颖, 李民. 肠道菌群在神经病理性疼痛中作用的研究进展[J]. 基础医学与临床, 2023, 43(1): 188-191.

LYU Yanhan, YU Zhuoying, LI Min. Research progress of gut microbiota in neuropathic pain[J]. Basic & Clinical Medicine, 2023, 43(1): 188-191.

参考文献

[1] van Hecke O,Austin SK,Khan RA,et al. Neuropathic pain in the general population: A systematic review of epidemiological studies[J]. Pain,2014,155:654-662.
[2] Lin B,Wang Y,Zhang P,et al. Gut microbiota regulates neuropathic pain: potential mechanisms and therapeutic strategy[J]. J Headache Pain,2020,21:103.doi: 10.1186/s10194-020-01170-x.
[3] Defaye M,Gervason S,Altier C,et al. Microbiota: a novel regulator of pain[J]. J Neural Transm (Vienna),2020,127:445-465.
[4] Guo R,Chen LH,Xing C,et al. Pain regulation by gut microbiota: molecular mechanisms and therapeutic potential[J]. Br J Anaesth,2019,123:637-654.
[5] Ciesielska A,Matyjek M,Kwiatkowska K. Tlr4 and cd14 trafficking and its influence on LPS-induced pro-inflammatory signaling[J]. Cell Mol Life Sci,2021,78:1233-1261.
[6] Ji RR,Chamessian A,Zhang YQ. Pain regulation by non-neuronal cells and inflammation[J]. Science,2016,354:572-577.
[7] Yang C,Fang X,Zhan G,et al. Key role of gut microbiota in anhedonia-like phenotype in rodents with neuropathic pain[J]. Transl Psychiatry,2019,9:57.doi: 10.1038/s41398-019-0379-8.
[8] Zhou F,Wang X,Han B,et al. Short-chain fatty acids contribute to neuropathic pain via regulating microglia activation and polarization[J]. Mol Pain,2021,17:1744806921996520.doi: 10.1177/1744806921996520.
[9] Ding W,You Z,Chen Q,et al. Gut microbiota influences neuropathic pain through modulating proinflammatory and anti-inflammatory t cells[J]. Anesth Analg,2021,132:1146-1155.
[10] Zhong S,Zhou Z,Liang Y,et al. Targeting strategies for chemotherapy-induced peripheral neuropathy: Does gut microbiota play a role?[J]. Crit Rev Microbiol,2019,45:369-393.
[11] Shen S,Lim G,You Z,et al. Gut microbiota is critical for the induction of chemotherapy-induced pain[J]. Nat Neurosci,2017,20:1213-1216.
[12] Castelli V,Palumbo P,d'Angelo M,et al. Probiotic dsf counteracts chemotherapy induced neuropathic pain[J]. Oncotarget,2018,9:27998-28008.
[13] Cuozzo M,Castelli V,Avagliano C,et al. Effects of chronic oral probiotic treatment in paclitaxel-induced neuropathic pain[J]. Biomedicines,2021,9. doi: 10.3390/biomedicines9040346.
[14] Jamshidi P,Hasanzadeh S,Tahvildari A,et al. Is there any association between gut microbiota and type 1 diabetes? a systematic review[J]. Gut Pathog,2019,11:49.doi: 10.1080/19490976.2020.1870402.
[15] Adeshirlarijaney A,Gewirtz AT. Considering gut micro-biota in treatment of type 2 diabetes mellitus[J]. Gut Microbes,2020,11:253-264.
[16] Cai TT,Ye XL,Yong HJ,et al. Fecal microbiota transplantation relieve painful diabetic neuropathy: a case report[J]. Medicine (Baltimore),2018,97:e13543.doi: 10.1097/MD.0000000000013543.
[17] Bonomo RR,Cook TM,Gavini CK,et al. Fecal transplantation and butyrate improve neuropathic pain, modify immune cell profile, and gene expression in the pns of obese mice[J]. Proc Natl Acad Sci U S A,2020,117:26482-26493.
[18] Li L,Acioglu C,Heary RF,et al. Role of astroglial Toll-like receptors (TLRs) in central nervous system infec-tions, injury and neurodegenerative diseases[J]. Brain Behav Immun,2021,91:740-755.
[19] Zheng D,Liwinski T,Elinav E. Interaction between microbiota and immunity in health and disease[J]. Cell Res,2020,30:492-506.
[20] Meseguer V,Alpizar YA,Luis E,et al. Trpa1 channels mediate acute neurogenic inflammation and pain produced by bacterial endotoxins[J]. Nat Commun,2014,5:3125.doi: 10.1038/ncomms4125.
[21] Sorge RE,LaCroix-Fralish ML,Tuttle AH,et al. Spinal cord Toll-like receptor 4 mediates inflammatory and neuropathic hypersensitivity in male but not female mice[J]. J Neurosci,2011,31:15450-15454.
[22] Wardill HR,Gibson RJ,Van Sebille YZ,et al. Irinotecan-induced gastrointestinal dysfunction and pain are mediated by common TLR4-dependent mechanisms[J]. Mol Cancer Ther,2016,15:1376-1386.
[23] Lee JY,Sohn KH,Rhee SH,et al. Saturated fatty acids, but not unsaturated fatty acids, induce the expression of cyclooxygenase-2 mediated through Toll-like receptor 4[J]. J Biol Chem,2001,276:16683-16689.
[24] Yang H,Tian W,Wang S,et al. Tsg-6 secreted by bone marrow mesenchymal stem cells attenuates intervertebral disc degeneration by inhibiting the TLR2/NF-κB signaling pathway[J]. Lab Invest,2018,98:755-772.
[25] Yang H,Wu L,Deng H,et al. Anti-inflammatory protein tsg-6 secreted by bone marrow mesenchymal stem cells attenu-ates neuropathic pain by inhibiting the TLR2/Myd8/NF-κB signaling pathway in spinal microglia[J]. J Neuroinflammation,2020,17:154.doi: 10.1186/s12974-020-1731-x.
[26] Kim D,Kim MA,Cho IH,et al. A critical role of Toll-like receptor 2 in nerve injury-induced spinal cord glial cell activation and pain hypersensitivity[J]. J Biol Chem,2007,282:14975-14983.
[27] Xu ZZ,Kim YH,Bang S,et al. Inhibition of mechanical allodynia in neuropathic pain by TLR5-mediated a-fiber blockade[J]. Nat Med,2015,21:1326-1331.
[28] Das N,Dewan V,Grace PM,et al. Hmgb1 activates proinflammatory signaling via TLR5 leading to allodynia[J]. Cell Rep,2016,17:1128-1140.

肠道菌群在神经病理性疼痛中作用的研究进展

Research progress of gut microbiota in neuropathic pain

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