肠道菌群及其代谢产物在重症急性胰腺炎相关急性呼吸窘迫综合征中的作用

熊洋洋; 吴东; 钱家鸣

doi:10.3969/j.issn.1001-5256.2021.01.052

肠道菌群及其代谢产物在重症急性胰腺炎相关急性呼吸窘迫综合征中的作用

DOI: 10.3969/j.issn.1001-5256.2021.01.052

中国医学科学院，北京协和医学院，北京协和医院消化内科，北京 100730

基金项目:

北京市自然科学基金面上项目 (7192162);

中国医学科学院临床与转化医学研究项目 (2019XK320036)

作者贡献声明：熊洋洋负责检索文献，资料分析，撰写论文；吴东和钱家鸣负责拟定写作思路，修改论文，指导撰写文章并最后定稿。

详细信息

作者简介:
熊洋洋(1989—)，男，主要从事急性胰腺炎、炎症性肠病方面的研究

通信作者:
吴东，wudong@pumch.cn

中图分类号: R576
计量
- 文章访问数: 618
- HTML全文浏览量: 194
- PDF下载量: 53
- 被引次数: 0
出版历程
- 收稿日期: 2020-06-03
- 录用日期: 2020-06-28
- 出版日期: 2021-01-20

Role of gut microbiota and its metabolites in severe acute pancreatitis-related acute respiratory distress syndrome

Chinese Academy of Medical Sciences; Peking Union Medical College; Department of Gastroenterology, Peking Union Medical College Hospital, Beijing 100730, China

摘要

摘要: 急性呼吸窘迫综合征(ARDS)是重症急性胰腺炎(SAP)常见的并发症，也是导致SAP患者早期死亡的首要原因，目前发病机制尚不清楚。近年来肠道菌群及其代谢产物参与调控SAP相关ARDS日益受到关注，深入探究“肠-肺轴”的发病机制有助于为SAP-ARDS的药物研发提供新的思路。总结了近年来肠道菌群及其代谢产物在SAP-ARDS领域的研究进展。
- 胰腺炎 /
- 胃肠道微生物组 /
- 呼吸窘迫综合征，成人
Abstract: Acute respiratory distress syndrome (ARDS) is a common complication of severe acute pancreatitis (SAP) and a leading cause of early death in SAP patients, but its pathogenesis is still unclear. In recent years, the role of gut microbiota and its metabolites in regulating SAP-related ARDS has attracted more and more attention, and in-depth studies on the pathogenesis of "intestine-lung axis" may provide new ideas for the research and development of drugs for SAP-related ARDS. This article summarizes the recent research advances in gut microbiota and its metabolites in SAP-related ARDS.
- Pancreatitis /
- Gastrointestinal Microbiome /
- Respiratory Distress Syndrome, Adult

HTML全文

参考文献(49)

[1]	Pancreas Study Group, Chinese Society of Gastroenterology, Chinese Medical Association; Editorial Board of Chinese Journal of Pancreatology; Editorial Board of Chinese Journal of Digestion. Chinese guidelines for the management of acute pancreatitis (Shenyang, 2019)[J]. J Clin Hepatol, 2019, 35(12): 2706-2711. (in Chinese) 中华医学会消化病学分会胰腺疾病学组, 《中华胰腺病杂志》编辑委员会, 《中华消化杂志》编辑委员会. 中国急性胰腺炎诊治指南(2019, 沈阳)[J]. 临床肝胆病杂志, 2019, 35(12): 2706-2711.
[2]	LANKISCH PG, APTE M, BANKS PA. Acute pancreatitis[J]. Lancet, 2015, 386(9988): 85-96. DOI: 10.1016/S0140-6736(14)60649-8
[3]	GBD 2017 Disease and Injury Incidence and Prevalence Collaborators. Global, regional, and national incidence, prevalence, and years lived with disability for 354 diseases and injuries for 195 countries and territories, 1990-2017: A systematic analysis for the Global Burden of Disease Study 2017[J]. Lancet, 2018, 392(10159): 1789-1858. DOI: 10.1016/S0140-6736(18)32279-7
[4]	van DIJK SM, HALLENSLEBEN N, van SANTVOORT HC, et al. Acute pancreatitis: Recent advances through randomised trials[J]. Gut, 2017, 66(11): 2024-2032. DOI: 10.1136/gutjnl-2016-313595
[5]	WU D, QIAN JM. Fluid therapy for acute pancreatitis: Timing of resuscitation, type of fluid, and monitoring methods[J]. J Clin Hepatol, 2017, 33(1): 12-16. (in Chinese) DOI: 10.3969/j.issn.1001-5256.2017.01.001 吴东, 钱家鸣. 急性胰腺炎的液体治疗: 复苏时机、液体种类及监测方法[J]. 临床肝胆病杂志, 2017, 33(1): 12-16. DOI: 10.3969/j.issn.1001-5256.2017.01.001
[6]	JACOBS ML, DAGGETT WM, CIVETTE JM, et al. Acute pancreatitis: Analysis of factors influencing survival[J]. Ann Surg, 1977, 185(1): 43-51. DOI: 10.1097/00000658-197701000-00007
[7]	WU D, LU B, XUE HD, et al. Validation of Modified Determinant-Based Classification of severity for acute pancreatitis in a tertiary teaching hospital[J]. Pancreatology, 2019, 19(2): 217-223. DOI: 10.1016/j.pan.2019.01.003
[8]	GRIFFITHS M, MCAULEY DF, PERKINS GD, et al. Guidelines on the management of acute respiratory distress syndrome[J]. BMJ Open Respir Res, 2019, 6(1): e000420. DOI: 10.1136/bmjresp-2019-000420
[9]	KIM JH, HONG SK, KIM KC, et al. Influence of full-time intensivist and the nurse-to-patient ratio on the implementation of severe sepsis bundles in Korean intensive care units[J]. J Crit Care, 2012, 27(4): 414.e11-21. DOI: 10.1016/j.jcrc.2012.03.010
[10]	RUBENFELD GD, CALDWELL E, PEABODY E, et al. Incidence and outcomes of acute lung injury[J]. N Engl J Med, 2005, 353(16): 1685-1693. DOI: 10.1056/NEJMoa050333
[11]	ZHOU MT, CHEN CS, CHEN BC, et al. Acute lung injury and ARDS in acute pancreatitis: Mechanisms and potential intervention[J]. World J Gastroenterol, 2010, 16(17): 2094-2099. DOI: 10.3748/wjg.v16.i17.2094
[12]	WU D, TANG M, ZHAO Y, et al. Impact of seasons and festivals on the onset of acute pancreatitis in Shanghai, China[J]. Pancreas, 2017, 46(4): 496-503. DOI: 10.1097/MPA.0000000000000795
[13]	MOGGIA E, KOTI R, BELGAUMKAR AP, et al. Pharmacological interventions for acute pancreatitis[J]. Cochrane Database Syst Rev, 2017, 4: CD011384.
[14]	van MINNEN LP, BLOM M, TIMMERMAN HM, et al. The use of animal models to study bacterial translocation during acute pancreatitis[J]. J Gastrointest Surg, 2007, 11(5): 682-689.
[15]	ZHU Y, HE C, LI X, et al. Gut microbiota dysbiosis worsens the severity of acute pancreatitis in patients and mice[J]. J Gastroenterol, 2019, 54(4): 347-358. DOI: 10.1007/s00535-018-1529-0
[16]	JIN M. IL-22 Protective effect and mechanism of IL-22 on acute pancreatitis and intestinal barrier function[D]. Beijing: Chinese Academy of Medical Sciences & Peking Union Medical College, 2019. (in Chinese) 金梦. IL-22对急性胰腺炎及其肠道屏障功能的保护作用及机制探究[D]. 北京: 中国医学科学院北京协和医学院, 2019.
[17]	YU S, XIONG Y, XU J, et al. Identification of dysfunctional gut microbiota through rectal swab in patients with different severity of acute pancreatitis[J]. Dig Dis Sci, 2020.[Online ahead of print]
[18]	GIANOTTI L, MUNDA R, ALEXANDER JW, et al. Bacterial translocation: A potential source for infection in acute pancreatitis[J]. Pancreas, 1993, 8(5): 551-558. DOI: 10.1097/00006676-199309000-00004
[19]	WANG H, LI C, JIANG Y, et al. Effects of bacterial translocation and autophagy on acute lung injury induced by severe acute pancreatitis[J]. Gastroenterol Res Pract, 2020, 2020: 8953453.
[20]	DICKSON RP, SCHULTZ MJ, van der POLL T, et al. Lung microbiota predict clinical outcomes in critically ill patients[J]. Am J Respir Crit Care Med, 2020, 201(5): 555-563. DOI: 10.1164/rccm.201907-1487OC
[21]	ALDRIDGE AJ. Role of the neutrophil in septic shock and the adult respiratory distress syndrome[J]. Eur J Surg, 2002, 168(4): 204-214. DOI: 10.1080/11024150260102807
[22]	WELTY-WOLF KE, CARRAWAY MS, ORTEL TL, et al. Coagulation and inflammation in acute lung injury[J]. Thromb Haemost, 2002, 88(1): 17-25.
[23]	DOERSCHUG KC, POWERS LS, MONICK MM, et al. Antibiotics delay but do not prevent bacteremia and lung injury in murine sepsis[J]. Crit Care Med, 2004, 32(2): 489-494. DOI: 10.1097/01.CCM.0000109450.66450.23
[24]	YAN X, LU QG, ZENG L, et al. Synergistic protection of astragalus polysaccharides and matrine against ulcerative colitis and associated lung injury in rats[J]. World J Gastroenterol, 2020, 26(1): 55-69. DOI: 10.3748/wjg.v26.i1.55
[25]	PENG H, ZHI-FEN W, SU-MEI J, et al. Blocking abdominal lymphatic flow attenuates acute hemorrhagic necrotizing pancreatitis -associated lung injury in rats[J]. J Inflamm (Lond), 2013, 10(1): 9. DOI: 10.1186/1476-9255-10-9
[26]	ZHANG D, TSUI N, LI Y, et al. Thoracic duct ligation in the rat attenuates lung injuries in acute pancreatitis[J]. Lymphology, 2013, 46(3): 144-149.
[27]	LANDAHL P, ANSARI D, ANDERSSON R. Severe acute pancreatitis: Gut barrier failure, systemic inflammatory response, acute lung injury, and the role of the mesenteric lymph[J]. Surg Infect (Larchmt), 2015, 16(6): 651-656. DOI: 10.1089/sur.2015.034
[28]	KOH A, de VADDER F, KOVATCHEVA-DATCHARY P, et al. From dietary fiber to host physiology: Short-chain fatty acids as key bacterial metabolites[J]. Cell, 2016, 165(6): 1332-1345. DOI: 10.1016/j.cell.2016.05.041
[29]	MAKKI K, DEEHAN EC, WALTER J, et al. The impact of dietary fiber on gut microbiota in host health and disease[J]. Cell Host Microbe, 2018, 23(6): 705-715. DOI: 10.1016/j.chom.2018.05.012
[30]	BOETS E, GOMAND SV, DEROOVER L, et al. Systemic availability and metabolism of colonic-derived short-chain fatty acids in healthy subjects: A stable isotope study[J]. J Physiol, 2017, 595(2): 541-555. DOI: 10.1113/JP272613
[31]	CANANI RB, COSTANZO MD, LEONE L, et al. Potential beneficial effects of butyrate in intestinal and extraintestinal diseases[J]. World J Gastroenterol, 2011, 17(12): 1519-1528. DOI: 10.3748/wjg.v17.i12.1519
[32]	PAN X, FANG X, WANG F, et al. Butyrate ameliorates caerulein-induced acute pancreatitis and associated intestinal injury by tissue-specific mechanisms[J]. Br J Pharmacol, 2019, 176(23): 4446-4461. DOI: 10.1111/bph.14806
[33]	ZHANG T, XIA M, ZHAN Q, et al. Sodium butyrate reduces organ injuries in mice with severe acute pancreatitis through inhibiting HMGB1 expression[J]. Dig Dis Sci, 2015, 60(7): 1991-1999. DOI: 10.1007/s10620-015-3586-z
[34]	LI N, LIU XX, HONG M, et al. Sodium butyrate alleviates LPS-induced acute lung injury in mice via inhibiting HMGB1 release[J]. Int Immunopharmacol, 2018, 56: 242-248. DOI: 10.1016/j.intimp.2018.01.017
[35]	LIU J, CHANG G, HUANG J, et al. Sodium butyrate inhibits the inflammation of lipopolysaccharide-induced acute lung injury in mice by regulating the toll-like receptor 4/nuclear factor κB signaling pathway[J]. J Agric Food Chem, 2019, 67(6): 1674-1682. DOI: 10.1021/acs.jafc.8b06359
[36]	NI YF, WANG J, YAN XL, et al. Histone deacetylase inhibitor, butyrate, attenuates lipopolysaccharide-induced acute lung injury in mice[J]. Respir Res, 2010, 11: 33. DOI: 10.1186/1465-9921-11-33
[37]	TONG LC, WANG Y, WANG ZB, et al. Propionate ameliorates dextran sodium sulfate-induced colitis by improving intestinal barrier function and reducing inflammation and oxidative stress[J]. Front Pharmacol, 2016, 7: 253.
[38]	JIMINEZ JA, UWIERA TC, ABBOTT DW, et al. Butyrate supplementation at high concentrations alters enteric bacterial communities and reduces intestinal inflammation in mice infected with citrobacter rodentium[J]. mSphere, 2017, 2(4): e00243-17.
[39]	KOTUNIA A, WOLIN'SKI J, LAUBITZ D, et al. Effect of sodium butyrate on the small intestine development in neonatal piglets fed[correction of feed] by artificial sow[J]. J Physiol Pharmacol, 2004, 55(Suppl 2): 59-68.
[40]	MASLOWSKI KM, VIEIRA AT, NG A, et al. Regulation of inflammatory responses by gut microbiota and chemoattractant receptor GPR43[J]. Nature, 2009, 461(7268): 1282-1286. DOI: 10.1038/nature08530
[41]	XU M, WANG C, LI N, et al. Intraperitoneal injection of acetate protects mice against lipopolysaccharide (LPS)-Induced acute lung injury through its anti-inflammatory and anti-oxidative ability[J]. Med Sci Monit, 2019, 25: 2278-2288. DOI: 10.12659/MSM.911444
[42]	TROMPETTE A, GOLLWITZER ES, YADAVA K, et al. Gut microbiota metabolism of dietary fiber influences allergic airway disease and hematopoiesis[J]. Nat Med, 2014, 20(2): 159-166. DOI: 10.1038/nm.3444
[43]	TIAN X, HELLMAN J, HORSWILL AR, et al. Corrigendum: Elevated gut microbiome-derived propionate levels are associated with reduced sterile lung inflammation and bacterial immunity in mice[J]. Front Microbiol, 2019, 10: 518. DOI: 10.3389/fmicb.2019.00518
[44]	LI J, ZHAO XL, LIU YX, et al. 1HNMR-based metabolomic profile of rats with experimental acute pancreatitis[J]. BMC Gastroenterol, 2014, 14: 115. DOI: 10.1186/1471-230X-14-115
[45]	ALDHAHRANI A, VERDON B, WARD C, et al. Effects of bile acids on human airway epithelial cells: Implications for aerodigestive diseases[J]. ERJ Open Res, 2017, 3(1): 00107-2016.
[46]	BRONOWICKA-ADAMSKA P, HUTSCH T, GAWRYS'-KO- PCZYN'SKA M, et al. Hydrogen sulfide formation in experimental model of acute pancreatitis[J]. Acta Biochim Pol, 2019, 66(4): 611-618.
[47]	RAGY MM, ALI FF, TONI N. Comparing the preventive effect of sodium hydrosulfide, leptin, and curcumin against Larginine induced acute pancreatitis in rats: Role of corticosterone and inducible nitric oxide synthase[J]. Endocr Regul, 2019, 53(4): 221-230. DOI: 10.2478/enr-2019-0022
[48]	FALLER S, HAUSLER F, GOEFT A, et al. Hydrogen sulfide limits neutrophil transmigration, inflammation, and oxidative burst in lipopolysaccharide-induced acute lung injury[J]. Sci Rep, 2018, 8(1): 14676. DOI: 10.1038/s41598-018-33101-x
[49]	XU X, LI H, GONG Y, et al. Hydrogen sulfide ameliorated lipopolysaccharide-induced acute lung injury by inhibiting autophagy through PI3K/Akt/mTOR pathway in mice[J]. Biochem Biophys Res Commun, 2018, 507(1-4): 514-518. DOI: 10.1016/j.bbrc.2018.11.081