肠道微生态与血流动力学

潘晓俊; 陈德昌

doi:10.12290/xhyxzz.2022-0468

肠道微生态与血流动力学

doi: 10.12290/xhyxzz.2022-0468

潘晓俊,
陈德昌^,

上海交通大学医学院附属瑞金医院重症医学科，上海 200025

基金项目:

国家自然科学基金 81873944

国家自然科学基金 82172152

上海市科学技术委员会 20DZ2200500

详细信息

通讯作者:
陈德昌, E-mail: cdc12064@rjh.com.cn

中图分类号: R441.9;R-1
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- 文章访问数: 2448
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- PDF下载量: 90
- 被引次数: 0
出版历程
- 收稿日期: 2022-08-24
- 录用日期: 2022-10-20
- 网络出版日期: 2022-10-27
- 刊出日期: 2022-11-30

Gut Microbiota in Hemodynamics

PAN Xiaojun,
CHEN Dechang^,

Department of Critical Care Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China

Funds:

National Natural Science Foundation of China 81873944

National Natural Science Foundation of China 82172152

Shanghai Science and Technology Commission 20DZ2200500

More Information

Corresponding author: CHEN Dechang, E-mail: cdc12064@rjh.com.cn

摘要

摘要: 肠道微生态是由原核微生物(细菌)、真核微生物(包括真菌以及原生动物)和病毒构成的强大“器官”，在机体营养代谢、维持肠道黏膜上皮屏障的完整性、免疫调节中发挥至关重要的作用。已有研究表明，肠道微生态与多种疾病的发病机制相关，如神经精神性疾病、自身免疫性疾病、癌症以及慢性代谢性疾病等。近年来的研究发现，肠道微生态能够通过氧化三甲胺和短链脂肪酸及其受体途径对血流动力学发挥调控作用; 同时，肠道微生态失调、易位激活机体炎症反应可影响机体血流动力学的稳定。本文梳理二者之间的关系，以期为进一步开展相关研究提供借鉴。
- 肠道微生态 /
- 血流动力学 /
- 重症
Abstract: The gut microbiota is a powerful "organ" composed of prokaryotic organisms (bacteria), eukaryotic microorganisms (including fungi and protozoa) and viruses, which plays a crucial role in the nutrition metabolism, maintenance of the integrity of intestinal mucosal barrier, and immune regulation of the body. Researches have shown that intestinal microecology is related to the pathogenesis of many diseases, such as neuropsychiatric diseases, autoimmune diseases, cancer and chronic metabolic diseases. Recent studies have found that gut microbiota can regulate hemodynamics through the oxidation of trimethylamine and short chain fatty acids. At the same time, gut microbiota disorder and translocation can activate the body's inflammatory response, affecting the stability of the body's hemodynamics.In this article, we summarize the relationship between gut microbiota and hemodymamics, in order to provide reference for further research.
- gut microbiota /
- hemodynamics /
- critical care
注释:

作者贡献：潘晓俊负责文献查阅及论文撰写; 陈德昌负责选题设计、审核及修订。

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参考文献(59)

[1]	Socała K, Doboszewska U, Szopa A, et al. The role of microbiota-gut-brain axis in neuropsychiatric and neurological disorders[J]. Pharmacol Res, 2021, 172: 105840. doi: 10.1016/j.phrs.2021.105840
[2]	Xiao L, Liu Q, Luo M, et al. Gut Microbiota-Derived Metabolites in Irritable Bowel Syndrome[J]. Front Cell Infect Microbiol, 2021, 11: 729346. doi: 10.3389/fcimb.2021.729346
[3]	Doroszkiewicz J, Groblewska M, Mroczko B. The Role of Gut Microbiota and Gut-Brain Interplay in Selected Diseases of the Central Nervous System[J]. Int J Mol Sci, 2021, 22: 10028. doi: 10.3390/ijms221810028
[4]	Hou H, Chen D, Zhang K, et al. Gut microbiota-derived short-chain fatty acids and colorectal cancer: Ready for clinical translation?[J]. Cancer Lett, 2022, 526: 225-235. doi: 10.1016/j.canlet.2021.11.027
[5]	Zaky A, Glastras SJ, Wong MYW, et al. The Role of the Gut Microbiome in Diabetes and Obesity-Related Kidney Disease[J]. Int J Mol Sci, 2021, 22: 9641. doi: 10.3390/ijms22179641
[6]	Cai J, Sun L, Gonzalez FJ. Gut microbiota-derived bile acids in intestinal immunity, inflammation, and tumori-genesis[J]. Cell Host Microbe, 2022, 30: 289-300. doi: 10.1016/j.chom.2022.02.004
[7]	Adhikari AA, Ramachandran D, Chaudhari SN, et al. A Gut-Restricted Lithocholic Acid Analog as an Inhibitor of Gut Bacterial Bile Salt Hydrolases[J]. ACS Chem Biol, 2021, 16: 1401-1412. doi: 10.1021/acschembio.1c00192
[8]	Campbell C, McKenney PT, Konstantinovsky D, et al. Bacterial metabolism of bile acids promotes generation of peripheral regulatory T cells[J]. Nature, 2020, 581: 475-479. doi: 10.1038/s41586-020-2193-0
[9]	Jin WB, Li TT, Huo D, et al. Genetic manipulation of gut microbes enables single-gene interrogation in a complex microbiome[J]. Cell, 2022, 185: 547-562. e522. doi: 10.1016/j.cell.2021.12.035
[10]	Franzosa EA, Sirota-Madi A, Avila-Pacheco J, et al. Gut microbiome structure and metabolic activity in inflammatory bowel disease[J]. Nat Microbiol, 2019, 4: 293-305. doi: 10.1038/s41564-018-0306-4
[11]	Gadaleta RM, Garcia-Irigoyen O, Cariello M, et al. Fibroblast Growth Factor 19 modulates intestinal microbiota and inflammation in presence of Farnesoid X Receptor[J]. EBioMedicine, 2020, 54: 102719. doi: 10.1016/j.ebiom.2020.102719
[12]	Doden HL, Wolf PG, Gaskins HR, et al. Completion of the gut microbial epi-bile acid pathway[J]. Gut Microbes, 2021, 13: 1-20.
[13]	Turner JR. Intestinal mucosal barrier function in health and disease[J]. Nat Rev Immunol, 2009, 9: 799-809. doi: 10.1038/nri2653
[14]	Tang WHW, Li DY, Hazen SL. Dietary metabolism, the gut microbiome, and heart failure[J]. Nat Rev Cardiol, 2019, 16: 137-154. doi: 10.1038/s41569-018-0108-7
[15]	Rajilić-Stojanović M, de Vos WM. The first 1000 cultured species of the human gastrointestinal microbiota[J]. FEMS Microbiol Rev, 2014, 38: 996-1047. doi: 10.1111/1574-6976.12075
[16]	Kamada N, Seo SU, Chen GY, et al. Role of the gut microbiota in immunity and inflammatory disease[J]. Nat Rev Immunol, 2013, 13: 321-335. doi: 10.1038/nri3430
[17]	Stanley EG, Bailey NJ, Bollard ME, et al. Sexual dimorphism in urinary metabolite profiles of Han Wistar rats revealed by nuclear-magnetic-resonance-based metabonomics[J]. Anal Biochem, 2005, 343: 195-202. doi: 10.1016/j.ab.2005.01.024
[18]	Tang WHW, Bäckhed F, Landmesser U, et al. Intestinal Microbiota in Cardiovascular Health and Disease: JACC State-of-the-Art Review[J]. J Am Coll Cardiol, 2019, 73: 2089-2105.
[19]	Wang Z, Klipfell E, Bennett BJ, et al. Gut flora metabolism of phosphatidylcholine promotes cardiovascular disease[J]. Nature, 2011, 472: 57-63. doi: 10.1038/nature09922
[20]	Zhu W, Buffa JA, Wang Z, et al. Flavin monooxygenase 3, the host hepatic enzyme in the metaorganismal trimethyla-mine N-oxide-generating pathway, modulates platelet responsiveness and thrombosis risk[J]. J Thromb Haemost, 2018, 16: 1857-1872. doi: 10.1111/jth.14234
[21]	Bergeron N, Williams PT, Lamendella R, et al. Diets high in resistant starch increase plasma levels of trimethylamine-N-oxide, a gut microbiome metabolite associated with CVD risk[J]. Br J Nutr, 2016, 116: 2020-2029. doi: 10.1017/S0007114516004165
[22]	Hauet T, Baumert H, Gibelin H, et al. Noninvasive monitoring of citrate, acetate, lactate, and renal medullary osmolyte excretion in urine as biomarkers of exposure to ischemic reperfusion injury[J]. Cryobiology, 2000, 41: 280-291. doi: 10.1006/cryo.2000.2291
[23]	Griffin JL, Wang X, Stanley E. Does our gut microbiome predict cardiovascular risk? A review of the evidence from metabolomics[J]. Circ Cardiovasc Genet, 2015, 8: 187-191. doi: 10.1161/CIRCGENETICS.114.000219
[24]	Seldin MM, Meng Y, Qi H, et al. Trimethylamine N-Oxide Promotes Vascular Inflammation Through Signaling of Mitogen-Activated Protein Kinase and Nuclear Factor-κB[J]. J Am Heart Assoc, 2016, 5.
[25]	Makrecka-Kuka M, Volska K, Antone U, et al. Trimethylamine N-oxide impairs pyruvate and fatty acid oxidation in cardiac mitochondria[J]. Toxicol Lett, 2017, 267: 32-38. doi: 10.1016/j.toxlet.2016.12.017
[26]	Savi M, Bocchi L, Bresciani L, et al. Trimethylamine-N-Oxide (TMAO)-Induced Impairment of Cardiomyocyte Function and the Protective Role of Urolithin B-Glucuronide[J]. Molecules, 2018, 23.
[27]	Jacobs J, Braun J. Host genes and their effect on the intestinal microbiome garden[J]. Genome Med, 2014, 6: 119. doi: 10.1186/s13073-014-0119-x
[28]	Moron R, Galvez J, Colmenero M, et al. The Importance of the Microbiome in Critically Ⅲ Patients: Role of Nutrition[J]. Nutrients, 2019, 11.
[29]	Valdés-Duque BE, Giraldo-Giraldo NA, Jaillier-Ramírez AM, et al. Stool Short-Chain Fatty Acids in Critically Ⅲ Patients with Sepsis[J]. J Am Coll Nutr, 2020, 39: 706-712. doi: 10.1080/07315724.2020.1727379
[30]	Arpaia N, Campbell C, Fan X, et al. Metabolites produced by commensal bacteria promote peripheral regulatory T-cell generation[J]. Nature, 2013, 504: 451-455. doi: 10.1038/nature12726
[31]	Pluznick J. A novel SCFA receptor, the microbiota, and blood pressure regulation[J]. Gut Microbes, 2014, 5: 202-207. doi: 10.4161/gmic.27492
[32]	Pluznick JL, Protzko RJ, Gevorgyan H, et al. Olfactory receptor responding to gut microbiota-derived signals plays a role in renin secretion and blood pressure regulation[J]. Proc Natl Acad Sci U S A, 2013, 110: 4410-4415. doi: 10.1073/pnas.1215927110
[33]	Samuel BS, Shaito A, Motoike T, et al. Effects of the gut microbiota on host adiposity are modulated by the short-chain fatty-acid binding G protein-coupled receptor, Gpr41[J]. Proc Natl Acad Sci U S A, 2008, 105: 16767-16772. doi: 10.1073/pnas.0808567105
[34]	Maslowski KM, Vieira AT, Ng A, et al. Regulation of inflammatory responses by gut microbiota and chemoattractant receptor GPR43[J]. Nature, 2009, 461: 1282-1286. doi: 10.1038/nature08530
[35]	Le Poul E, Loison C, Struyf S, et al. Functional characterization of human receptors for short chain fatty acids and their role in polymorphonuclear cell activation[J]. J Biol Chem, 2003, 278: 25481-25489. doi: 10.1074/jbc.M301403200
[36]	Tazoe H, Otomo Y, Karaki S, et al. Expression of short-chain fatty acid receptor GPR41 in the human colon[J]. Biomed Res, 2009, 30: 149-156. doi: 10.2220/biomedres.30.149
[37]	Samuel BS, Gordon JI. A humanized gnotobiotic mouse model of host-archaeal-bacterial mutualism[J]. Proc Natl Acad Sci U S A, 2006, 103: 10011-10016. doi: 10.1073/pnas.0602187103
[38]	Durazzi F, Sala C, Castellani G, et al. Comparison between 16S rRNA and shotgun sequencing data for the taxonomic characterization of the gut microbiota[J]. Sci Rep, 2021, 11: 3030. doi: 10.1038/s41598-021-82726-y
[39]	Osuka A, Shimizu K, Ogura H, et al. Prognostic impact of fecal pH in critically ill patients[J]. Crit Care, 2012, 16: R119. doi: 10.1186/cc11413
[40]	Yamada T, Shimizu K, Ogura H, et al. Rapid and Sustained Long-Term Decrease of Fecal Short-Chain Fatty Acids in Critically Ill Patients With Systemic Inflammatory Response Syndrome[J]. JPEN J Parenter Enteral Nutr, 2015, 39: 569-577. doi: 10.1177/0148607114529596
[41]	Ladopoulos T, Giannaki M, Alexopoulou C, et al. Gastrointestinal dysmotility in critically ill patients[J]. Ann Gastroenterol, 2018, 31: 273-281.
[42]	Imhann F, Bonder MJ, Vich Vila A, et al. Proton pump inhibitors affect the gut microbiome[J]. Gut, 2016, 65: 740-748. doi: 10.1136/gutjnl-2015-310376
[43]	Rogers MAM, Aronoff DM. The influence of non-steroidal anti-inflammatory drugs on the gut microbiome[J]. Clin Microbiol Infect, 2016, 22: 178. e171-e178. e179.
[44]	Habes QLM, van Ede L, Gerretsen J, et al. Norepinephrine Contributes to Enterocyte Damage in Septic Shock Patients: A Prospective Cohort Study[J]. Shock, 2018, 49: 137-143. doi: 10.1097/SHK.0000000000000955
[45]	Fink MP. Intestinal epithelial hyperpermeability: update on the pathogenesis of gut mucosal barrier dysfunction in critical illness[J]. Curr Opin Crit Care, 2003, 9: 143-151. doi: 10.1097/00075198-200304000-00011
[46]	De-Souza DA, Greene LJ. Intestinal permeability and systemic infections in critically ill patients: effect of gluta-mine[J]. Crit Care Med, 2005, 33: 1125-1135. doi: 10.1097/01.CCM.0000162680.52397.97
[47]	Wang C, Li Q, Ren J. Microbiota-Immune Interaction in the Pathogenesis of Gut-Derived Infection[J]. Front Immunol, 2019, 10: 1873. doi: 10.3389/fimmu.2019.01873
[48]	Andriamihaja M, Lan A, Beaumont M, et al. The deleteri-ous metabolic and genotoxic effects of the bacterial metabolite p-cresol on colonic epithelial cells[J]. Free Radic Biol Med, 2015, 85: 219-227. doi: 10.1016/j.freeradbiomed.2015.04.004
[49]	Simonen M, Dali-Youcef N, Kaminska D, et al. Conjugated bile acids associate with altered rates of glucose and lipid oxidation after Roux-en-Y gastric bypass[J]. Obes Surg, 2012, 22: 1473-1480. doi: 10.1007/s11695-012-0673-5
[50]	le Roux CW, Bloom SR. Why do patients lose weight after Roux-en-Y gastric bypass?[J]. J Clin Endocrinol Metab, 2005, 90: 591-592. doi: 10.1210/jc.2004-2211
[51]	Ince C, Mayeux PR, Nguyen T, et al. The Endothelium in Sepsis[J]. Shock, 2016, 45: 259-270. doi: 10.1097/SHK.0000000000000473
[52]	Kakihana Y, Ito T, Nakahara M, et al. Sepsis-induced myocardial dysfunction: pathophysiology and management[J]. J Intensive Care, 2016, 4: 22. doi: 10.1186/s40560-016-0148-1
[53]	Hollenberg SM. Understanding stress cardiomyopathy[J]. Intensive Care Med, 2016, 42: 432-435. doi: 10.1007/s00134-015-4018-4
[54]	Stanzani G, Duchen MR, Singer M. The role of mitochondria in sepsis-induced cardiomyopathy[J]. Biochim Biophys Acta Mol Basis Dis, 2019, 1865: 759-773. doi: 10.1016/j.bbadis.2018.10.011
[55]	Yin J, Liao SX, He Y, et al. Dysbiosis of Gut Microbiota With Reduced Trimethylamine-N-Oxide Level in Patients With Large-Artery Atherosclerotic Stroke or Transient Ischemic Attack[J]. J Am Heart Assoc, 2015, 4: e002699. doi: 10.1161/JAHA.115.002699
[56]	Wang F, Li Q, Wang C, et al. Dynamic alteration of the colonic microbiota in intestinal ischemia-reperfusion injury[J]. PLoS One, 2012, 7: e42027. doi: 10.1371/journal.pone.0042027
[57]	Nagatomo Y, Tang WH. Intersections Between Microbiome and Heart Failure: Revisiting the Gut Hypothesis[J]. J Card Fail, 2015, 21: 973-980. doi: 10.1016/j.cardfail.2015.09.017
[58]	Harikrishnan S. Diet, the Gut Microbiome and Heart Failure[J]. Card Fail Rev, 2019, 5: 119-122. doi: 10.15420/cfr.2018.39.2
[59]	Wozniak H, Beckmann TS, Fröhlich L, et al. The central and biodynamic role of gut microbiota in critically ill patients[J]. Crit Care, 2022, 26: 250. doi: 10.1186/s13054-022-04127-5

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肠道微生态与血流动力学

doi: 10.12290/xhyxzz.2022-0468

通讯作者:
陈德昌, E-mail: cdc12064@rjh.com.cn

计量

Gut Microbiota in Hemodynamics

Corresponding author: CHEN Dechang, E-mail: cdc12064@rjh.com.cn

计量

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留言板

肠道微生态与血流动力学

doi: 10.12290/xhyxzz.2022-0468

通讯作者: 陈德昌, E-mail: cdc12064@rjh.com.cn

计量

出版历程

Gut Microbiota in Hemodynamics

Corresponding author: CHEN Dechang, E-mail: cdc12064@rjh.com.cn

计量

出版历程

目录

通讯作者:
陈德昌, E-mail: cdc12064@rjh.com.cn