专题 脊髓损伤原因及机制

脊髓损伤患者肠道菌群属水平的特征及意义

  • 汪俊宇 ,
  • 庞日朝 ,
  • 王文春 ,
  • 王美玉 ,
  • 向武 ,
  • 赵小华 ,
  • 张安仁
展开
  • 1.中国人民解放军西部战区总医院康复医学科,四川成都市 610083
    2.四川大学生物治疗国家重点实验室,四川成都市 610041
    3.西南财经大学天府学院,四川成都市 610052
汪俊宇(1993-),男,汉族,重庆市人,硕士研究生,主要研究方向:脊髓损伤康复的临床及基础研究。

收稿日期: 2019-03-28

  修回日期: 2019-08-21

  网络出版日期: 2020-04-27

基金资助

1.国家自然科学基金面上项目(81674044);1.国家自然科学基金面上项目(81973927);2.四川省卫计委普及应用项目(18PJ509);3.四川省医学会青年创新科研课题(Q17007)

Characteristics of Genus-level Gut Microbiome in Patients with Spinal Cord Injury

  • Jun-yu WANG ,
  • Ri-zhao PANG ,
  • Wen-chun WANG ,
  • Mei-yu WANG ,
  • Wu XIANG ,
  • Xiao-hua ZHAO ,
  • An-ren ZHANG
Expand
  • 1. Department of Rehabilitation Medicine, the General Hospital of Western Theater Command, Chengdu, Sichuan 610083, China
    2. State Key Laboratory of Biotherapy of Sichuan University, Chengdu, Sichuan 610041, China
    3. Tianfu College, Southwestern University of Finance and Economics, Chengdu, Sichuan 610052, China

Received date: 2019-03-28

  Revised date: 2019-08-21

  Online published: 2020-04-27

Supported by

National Natural Science Foundation of China(81674044);National Natural Science Foundation of China(81973927);Popularization and Application Project of Sichuan Health Planning Commission(18PJ509);Youth Innovation Research Project of Sichuan Medical Association(Q17007)

摘要

目的 探讨脊髓损伤患者肠道菌群属水平变化特征及其在临床康复中的意义。方法 2018年1月至12月,纳入脊髓损伤患者23例(患者组)和健康受试者21例(对照组),采集粪便样本,应用16S rDNA高通量测序检测肠道菌群,并采用物种组成分析及随机森林机器学习等生物信息学方法分析两组间属水平的菌群分布及差异。结果 患者组丰度升高的重要标志性菌属分别是:瘤胃菌科的UBA1819、Ruminiclostridium 9、Ruminococcaceae NK4A214 group、Ruminococcus 2、Ruminococcaceae UCG-005、Ruminiclostridium 5、Flavonifractor;理研菌科的Alistipes、dgA-11 gut group、Rikenellaceae RC9 gut group;毛螺菌科的[Eubacterium] oxidoreducens group;消化链球菌科的Intestinibacter;肠杆菌科的Escherichia-Shigella (志贺菌属);以及Tannerellaceae的Parabacteroides (|U| > 1.962, P< 0.05)。患者组丰度降低的是梭杆菌科Fusobacterium菌属(|U| = -2.284, P< 0.05)。结论 脊髓损伤患者肠道菌群与健康对照组存在差异。脊髓损伤患者与抑郁相关的瘤胃菌科、与中枢神经系统疾病关系密切的瘤胃球菌,以及肠道内致病菌消化链球菌属、志贺菌属等的相对丰度增加;对肠道有益的产丁酸盐菌和抗炎性菌属的相对丰度降低。这些菌群变化可能有一定的临床意义。

本文引用格式

汪俊宇 , 庞日朝 , 王文春 , 王美玉 , 向武 , 赵小华 , 张安仁 . 脊髓损伤患者肠道菌群属水平的特征及意义[J]. 中国康复理论与实践, 2020 , 26(4) : 393 -399 . DOI: 10.3969/j.issn.1006-9771.2020.00.003

Abstract

Objective To investigate the changes of genus-level gut microbiome in patients with spinal cord injury and its significance in clinical rehabilitation.Methods Fecal samples were collected from 23 patients with spinal cord injury (patients group) and 21 healthy volunteers (control group). Gut microbiome was detected by 16S rDNA high-throughput sequencing. Bioinformatics methods such as species composition analysis and Random Forest were used to analyze the distribution and difference of genus-level gut microbiome between two groups. Results Compared with the control group, the increased important marker genera in the patients group were as follows: UBA1819, Ruminiclostridium 9, Ruminococcaceae NK4A214 group, Ruminococcus 2, Ruminococceae UCG-005, Ruminiclostridium 5, Flavonifractor belonging to Ruminococceae; Aglistes, dgA-11 gut group, Rikenaceae RC9 gut group belonging to Rikenellaceae; [Eubacterium] oxidoreducens group belonging to Lachnospiraceae; Intestinibacter belonging to Peptostreptococcaceae; Escherichia-Shigella belonging to Enterobacteriaceae; Tannerellaceae belonging to Parabacteroides (|U| > 1.962, P< 0.05). The decreased marker genera in the patients group was Fusobacterium of Fusobacteriaceae (|U| = -2.284, P< 0.05).Conclusion There are significant differences of gut microbiome in spinal cord injury patients. The relative abundance of Ruminococcaceae relating to depression, Ruminococcus relating to central nervous system diseases, and enteropathogenic bacteria such as Escherichia-Shigella and Erysipelothrix increase; and the relative abundance of butyrate-producing bacteria and anti-inflammatory bacteria benefitting to the intestine decrease; which may play a role in clinic.

参考文献

[1] Savage D C. Microbial ecology of the gastrointestinal tract[J]. Annu Rev Microbiol, 1977, 31:107-133.
[2] Backhed F, Ley R E, Sonnenburg J L, et al. Host-bacterial mutualism in the human intestine[J]. Science, 2005, 307:1915-1920.
[3] Belkaid Y, Naik S. Compartmentalized and systemic control of tissue immunity by commensals[J]. Nat Immunol, 2013, 14(7):646-653.
[4] Round J L. The gut microbiota shapes intestinal immune responses during health and disease[J]. Nat Rev Immunol, 2009, 9(8):600.
[5] Hooper L V, Littman D R, Macpherson A J, et al. Interactions between the microbiota and the immune system[J]. Science, 2012, 336(6086):1268-1273.
[6] Nicholson J K, Holmes E, Kinross J, et al. Host-gut microbiota metabolic interactions[J]. Science, 2012, 336(6086):1262-1267.
[7] Scheperjans F, Aho V, Pereira P A, et al. Gut microbiota are related to Parkinson's disease and clinical phenotype[J]. Mov Disord, 2015, 30(3):350-358.
[8] Mielcarz D W, Kasper L H. The gut microbiome in multiple sclerosis[J]. Curr Treat Options Neurol, 2015, 17(4):344.
[9] Vogt N M, Kerby R L, Dill-Mcfarland K A, et al. Gut microbiome alterations in Alzheimer’s disease[J]. Sci Rep, 2017, 7(1):13537.
[10] Wang L, Conlon M A, Christophersen C T, et al. Gastrointesti- nal microbiota and metabolite biomarkers in children with autism spectrum disorders[J]. Biomark Med, 2014, 8(3):331-344.
[11] Mazzini L, Mogna L, De Marchi F, et al. Potential role of gut microbiota in ALS pathogenesis and possible novel therapeutic strategies[J]. J Clin Gastroenterol, 2018, 52 (Suppl 1). Proceedings from the 9th Probiotics, Prebiotics and New Foods, Nutraceuticals and Botanicals for Nutrition & Human and Microbiota Health Meeting, held in Rome, Italy from September 10 to 12, 2017:S68-S70. doi: 10.1097/MCG.0000000000001042.
[12] Kigerl K A, Hall J C E, Wang L, et al. Gut dysbiosis impairs recovery after spinal cord injury[J]. J Exp Med, 2016, 213(12):2603-2620.
[13] Gungor B, Adiguzel E, Gursel I, et al. Intestinal microbiota in patients with spinal cord injury[J]. PLoS One, 2016, 11(1):e0145878.
[14] 张洁, 李建军, 张超, 等. 急性创伤性完全性脊髓损伤患者肠道菌群多样性研究[J]. 中国康复理论与实践, 2019, 25(12):1450-1457.
[15] 美国脊髓损伤协会, 国际脊髓损伤学会. 脊髓损伤神经学分类国际标准(2011年修订)[J]. 李建军,王方永,译. 中国康复理论与实践, 2011, 17(10):963-972.
[16] 王一吉, 周红俊, 李建军, 等. 脊髓损伤神经学分类国际标准检查表最新修订及解读[J]. 中国康复理论与实践, 2015, 21(8):879-882.
[17] Caporaso J G, Lauber C L, Walters W A, et al. Global patterns of 16S rRNA diversity at a depth of millions of sequences per sample[J]. Proc Natl Acad Sci USA, 2011, 108(Suppl 1):4516-4522.
[18] Liu C, Yao M J, Stegen J C, et al. Long-term nitrogen addition affects the phylogenetic turnover of soil microbial community responding to moisture pulse[J]. Sci Rep, 2017, 7:17492.
[19] 李欣, 刘冯铂, 杜若飞, 等. 残疾人领悟社会支持对其社交回避及苦恼的影响:自尊的调节作用[J]. 心理技术与应用, 2016, 4(11):648-655.
[20] 荣晗, 徐丹, 刘铁榜, 等. 抑郁症患者肠道菌群丰度和种类及基因功能通路的病例对照研究[J]. 中华精神科杂志, 2017, 50(3):208-213.
[21] Mar G, Sevasti G, Santos P G, et al. Microbiota-driven transcriptional changes in prefrontal cortex override genetic differences in social behavior[J]. eLife, 2016, 5:e13442.
[22] Mudd A T, Berding K, Wang M, et al. Serum cortisol mediates the relationship between fecal Rumi- nococcus & brain N-acetylaspartate in the young pig[J]. Gut Microbes, 2017, 8(6):589-600.
[23] Zhao L, Huang Y, Lu L, et al. Saturated long-chain fatty acid-producing bacteria contribute to enhanced colonic motility in rats[J]. Microbiome, 2018, 6(1):107.
[24] 彭俊平, 杨剑, 金奇, 等. 志贺菌研究进展[J]. 中国科学:生命科学, 2010(1):14-22.
[25] Meijer K, de Vos P, Priebe M G. Butyrate and other short-chain fatty acids as modulators of immunity: what relevance for health?[J]. Curr Opin Clin Nutr Metab Care, 2010, 13(6):715-721.
[26] Fung K Y, Cosgrove L, Lockett T, et al. A review of the potential mechanisms for the lowering of colorectal oncogenesis by butyrate[J]. Br J Nutr, 2012, 108(5):820-831.
[27] Vinolo M A, Rodrigues H G, Hatanaka E, et al. Suppressive effect of short-chain fatty acids on production of proinflammatory mediators by neutrophils[J]. J Nutr Biochem, 2011, 22(9):849-855.
[28] Park J S, Woo M S, Kim S Y, et al. Repression of interferon-gamma-induced inducible nitric oxide synthase (iNOS) gene expression in microglia by sodium butyrate is mediated through specific inhibition of ERK signaling pathways[J]. J Neuroimmunol, 2005, 168(1-2):56-64.
[29] Chen P S, Wang C C, Bortner C D, et al. Valproic acid and other histone deace- tylase inhibitors induce microglial apoptosis and attenuate lipopolysacchar- ide-induced dopaminergic neurotoxicity[J]. Neuroscience, 2007, 149(1):203-212.
文章导航

/

〈 〉