[1]李博昊,谈林华.创伤脓毒症的免疫和代谢改变[J].医学信息,2022,35(06):5-9.[doi:10.3969/j.issn.1006-1959.2022.06.002]
 LI Bo-hao,TAN Lin-hua.Immune and Metabolic Changes in Traumatic Sepsis[J].Medical Information,2022,35(06):5-9.[doi:10.3969/j.issn.1006-1959.2022.06.002]
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创伤脓毒症的免疫和代谢改变()
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医学信息[ISSN:1006-1959/CN:61-1278/R]

卷:
35卷
期数:
2022年06期
页码:
5-9
栏目:
出版日期:
2022-03-15

文章信息/Info

Title:
Immune and Metabolic Changes in Traumatic Sepsis
文章编号:
1006-1959(2022)06-0005-05
作者:
李博昊谈林华
(浙江大学医学院附属儿童医院外科重症监护室,浙江 杭州 310051)
Author(s):
LI Bo-haoTAN Lin-hua
(Department of Surgical Intensive Care Unit,Children’s Hospital Affiliated to Medical College of Zhejiang University,Hangzhou 310051,Zhejiang,China)
关键词:
创伤脓毒症免疫失调代谢紊乱
Keywords:
TraumasepsisImmunedisordersMetabolic disorder
分类号:
R631.01
DOI:
10.3969/j.issn.1006-1959.2022.06.002
文献标志码:
A
摘要:
脓毒症是创伤患者死亡的主要原因之一,且目前降低创伤脓毒症死亡率的治疗选择有限。研究认为,代谢途径的紊乱、宿主的缺氧反应以及免疫系统的过度驱动是创伤和脓毒症分子水平上的主要特征,且创伤和脓毒症中免疫失调与代谢过程的改变之间有很强的相互关系,这种免疫代谢紊乱会严重影响患者的预后。本文主要对创伤脓毒症的免疫代谢以及潜在的治疗措施进行综述,以帮助临床更好的认识创伤脓毒症。
Abstract:
Sepsis is one of the main causes of death in trauma patients, and the treatment options for reducing the mortality of trauma sepsis are limited. Studies have shown that metabolic disorders, the host’s hypoxic response and excessive drive of the immune system are the main characteristics of trauma and sepsis at the molecular level, and there is a strong correlation between immune disorders and metabolic processes in trauma and sepsis, which seriously affects the prognosis of patients. This article mainly reviews the immune metabolism and potential treatment measures of traumatic sepsis, in order to help clinical better understand traumatic sepsis.

参考文献/References:

[1]Singer M,Deutschman CS,Seymour CW,et al.The third international consensus definitions for sepsis and septic shock (sepsis-3)[J].JAMA,2016,315(8):801-810.[2]Seymour CW,Kennedy JN,Wang S,et al.Derivation, validation, and potential treatment implications of novel clinical phenotypes for sepsis[J].JAMA,2019,321(20):2003-2017.[3]Bhavani SV,Carey KA,Gilbert ER,et al.Identifying novel sepsis subphenotypesusing temperature trajectories[J].Am J Respir Crit Care Med,2019,200(3):327-335.[4]DiMaggio C,Ayoung-Chee P,Shinseki M,et al.Traumatic injury in the United States: in-patient epidemiology 2000-2011[J].Injury,2016,47(7):1393-1403.[5]Poulose N,Raju R.Aging and injury: alterations in cellular energetics and organ function[J].Aging Dis,2014,5(2):101-108.[6]Eguia E,Bunn C,Kulshrestha S,et al.Trends, cost, and mortality from sepsis after trauma in the United States: an evaluation of the national inpatient sample of hospitalizations, 2012-2016[J].Crit Care Med,2020,48(9):1296-1303.[7]Brealey D,Brand M,Hargreaves I,et al.Association between mitochondrial dysfunction and severity and outcome of septic shock[J].Lancet,2002,360(9328):219-223.[8]Matkovich SJ,Al Khiami B,Efimov IR,et al.Widespread down-regulation of cardiac mitochondrial and sarcomericgenes in patients with sepsis[J].Crit Care Med,2017,45(3):407-414.[9]Eyenga P,Roussel D,Morel J,et al.Time course of liver mitochondrial function and intrinsic changes in oxidative phosphorylation in a rat model of sepsis[J].Intensive Care Med Exp,2018,6(1):31.[10]Makrecka-Kuka M,Korzh S,Vilks K,et al.Mitochondrial function in the kidney and heart, but not the brain, is mainly altered in an experimental model of endotoxaemia[J].Shock Augusta Ga,2019,52(6):e153-e162.[11]Carchman EH,Whelan S,Loughran P,et al.Experimental sepsis-induced mitochondrial biogenesis is dependent on autophagy, TLR4, and TLR9 signaling in liver[J].FASEB J,2013,27(12):4703-4711.[12]Cuzzocrea S,Mazzon E,di Paola R,et al.A role for nitric oxide-mediated peroxynitrite formation in a model of endotoxin-induced shock[J].JPharmacol Exp Ther,2006,319(1):73-81.[13]Youle R J,van der Bliek AM.Mitochondrial fission,fusion,and stress[J].Science,2012,337(6098):1062-1065.[14]Carchman EH,Rao J,Loughran PA,et al.Heme oxygenase-1-mediated autophagy protects against hepatocyte cell death and hepatic injury from infection/sepsis in mice[J].Hepatology,2011,53(6):2053-2062.[15]B’Chir W,Maurin AC,Carraro V,et al.The eIF2α/ATF4 pathway is essential for stress-induced autophagy gene expression[J].Nucleic Acids Res,2013,41(16):7683-7699.[16]Hamasaki M,Furuta N,Matsuda A,et al.Autophagosomes form at ER-mitochondria contact sites[J].Nature,2013,495(7441):389-393.[17]Jian BX,Hsieh CH,Chen JG,et al.Activation of endoplasmic reticulum stress response following trauma-hemorrhage[J].Biochim Biophys Acta,2008,1782(11):621-626.[18]Jeschke MG,Finnerty CC,Herndon DN,et al.Severe injury is associated with insulin resistance, endoplasmic reticulum stress response, and unfolded protein response[J].Ann Surg,2012,255(2):370-378.[19]Kraft BD,Chen LY,Suliman HB,et al.Peripheral blood mononuclear cells demonstrate mitochondrial damage clearance during sepsis[J].Crit Care Med,2019,47(5):651-658.[20]Zhou B,Liu J,Zeng L,et al.Extracellular SQSTM1 mediates bacterial septic death in mice through insulin receptor signalling[J].Nat Microbiol,2020,5(12):1576-1587.[21]Yin X,Xin H,Mao S,et al.The role of autophagy in sepsis: protection and injury to organs[J].Front Physiol,2019(10):1071.[22]Heyland D,Muscedere J,Wischmeyer PE,et al.A randomized trial of glutamine and antioxidants in critically ill patients[J].N Engl J Med,2013,368(16):1489-1497.[23]van Zanten AR,Sztark F,Kaisers UX,et al.High-protein enteral nutrition enriched with immune-modulating nutrients vs standard high-protein enteral nutrition and nosocomial infections in the ICU: a randomized clinical trial[J].JAMA,2014,312(5):514-524.[24]Escobar DA,Botero-Quintero AM,Kautza BC,et al.Adenosine monophosphate-activated protein kinase activation protects against sepsis-induced organ injury and inflammation[J].J Surg Res,2015,194(1):262-272.[25]Inata Y,Piraino G,Hake PW,et al.Age-dependent cardiac function during experimental sepsis:effect of pharmacological activation of AMP-activated protein kinase by AICAR[J].Am J Physiol Heart Circ Physiol,2018,315(4):H826-H837.[26]Hall DT,Griss T,Ma JF,et al.The AMPK agonist 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR), but not metformin, prevents inflammation-associated cachectic muscle wasting[J].EMBO Mol Med,2018,10(7):e8307.[27]Ismail Hassan F,Didari T,Khan F,et al.A review on the protective effects of metformin in sepsis-induced organ failure[J].Cell J,2020,21(4):363-370.[28]McBride MA,Owen AM,Stothers CL,et al.The metabolic basis of immune dysfunction following sepsis and trauma[J].Front Immunol,2020(11):1043.[29]Liu LM,Wu HL,Zang JT,et al.4-phenylbutyric acid reveals good beneficial effects on vital organ function via anti-endoplasmic reticulum stress in septic rats[J].Crit Care Med,2016,44(8):e689-e701.[30]Assimakopoulos SF,Triantos C,Thomopoulos K,et al.Gut-origin sepsis in the critically ill patient: pathophysiology and treatment[J].Infection,2018,46(6):751-760.[31]Yoseph BP,Klingensmith NJ,Liang Z,et al.Mechanisms of intestinal barrier dysfunction in sepsis[J].Shock,2016,46(1):52-59.[32]Klingensmith NJ,Coopersmith CM.The gut as the motor of multiple organ dysfunction in critical illness[J].Crit Care Clin,2016,32(2):203-212.[33]Guh AY,Mu YI,Winston LG,et al.ClostridioidesdifficileTrends in U.S. Burden of Infection and Outcomes[J].The New England Journal of Medicine,2020,382(14):1320-1330.[34]Price R,MacLennan G,Glen J,et al.Selective digestive or oropharyngeal decontamination and topical oropharyngeal chlorhexidine for prevention of death in general intensive care: systematic review and network meta-analysis[J].BMJ,2014(348):g2197.[35]Raymond SL,Holden DC,Mira JC,et al.Microbial recognition and danger signals in sepsis and trauma[J].Biochim Biophys Acta Mol Basis Dis,2017,1863(10 PtB):2564-2573.[36]Cao X.Self-regulation and cross-regulation of pattern-recognition receptor signalling in health and disease[J].Nat Rev Immunol,2016,16(1):35-50.[37]Hazeldine J,Dinsdale RJ,Harrison P,et al.Traumatic injury and exposure to mitochondrial-derived damage associated molecular patterns suppresses neutrophil extracellular trap formation[J].Front Immunol,2019(10):685.[38]Lord JM,Midwinter MJ,Chen YF,et al.The systemic immune response to trauma: an overview of pathophysiology and treatment[J].Lancet,2014,384(9952):1455-1465.[39]Levy RM,Mollen KP,Prince JM,et al.Systemic inflammation and remote organ injury following trauma require HMGB1[J].Am J Physiol Regul Integr Comp Physiol,2007,293(4):R1538-R1544.[40]Sodhi CP,Jia HP,Yamaguchi Y,et al.Intestinal epithelial TLR-4 activation is required for the development of acute lung injury after trauma/hemorrhagic shock via the release of HMGB1 from the gut[J].J Immunol,2015,194(10):4931-4939.[41]Reino DC,Palange D,Feketeova E,et al.Activation of toll-like receptor 4 is necessary for trauma hemorrhagic shock-induced gut injury and polymorphonuclear neutrophil priming[J].Shock,2012,38(1):107-114.[42]Yang RK,Harada T,Mollen KP,et al.Anti-HMGB1 neutralizing antibody ameliorates gut barrier dysfunction and improves survival after hemorrhagic shock[J].Mol Med,2006,12(4-6):105-114.[43]Andersson U,Yang H,Harris H.High-mobility group box 1 protein (HMGB1) operates as an alarmin outside as well as inside cells[J].Semin Immunol,2018(38):40-48.[44]Gould TJ,Lysov Z,Liaw PC.Extracellular DNA and histones:double-edged swords in immunothrombosis[J].J Thromb Haemost,2015,13(Suppl1):S82-S91.[45]Fuchs TA,Bhandari AA,Wagner DD.Histones induce rapid and profound thrombocytopenia in mice[J].Blood,2011,118(13):3708-3714.[46]Alhamdi Y,Abrams ST,Lane S,et al.Histone-associated thrombocytopenia in patients who are critically ill[J].JAMA,2016,315(8):817-819.[47]Lam FW,Cruz MA,Parikh K,et al.Histones stimulate von Willebrand factor release in vitro and in vivo[J].Haematologica,2016,101(7):e277-e279.[48]McDonald B,Davis RP,Kim SJ,et al.Platelets and neutrophil extracellular traps collaborate to promote intravascular coagulation during sepsis in mice[J].Blood,2017,129(10):1357-1367.[49]王昕,吴松,郑曙云,等.细胞外组蛋白对损伤小鼠肠黏膜屏障的影响及在脓毒症发生发展中的作用[J].中华创伤杂志,2016,32(10):882-886.[50]Abrams ST,Zhang N,Manson J,et al.Circulating histones are mediators of trauma-associated lung injury[J].Am J Respir Crit Care Med,2013,187(2):160-169.[51]Xu J,Zhang XM,Monestier M,et al.Extracellular histones are mediators of death through TLR2 and TLR4 in mouse fatal liver injury[J].J Immunol,2011,187(5):2626-2631.[52]Villalba N,Baby S,Cha BJ,et al.Site-specific opening of the blood-brain barrier by extracellular histones[J].J Neuroinflammation,2020,17(1):281.[53]Iba T,Hashiguchi N,Nagaoka I,et al.Heparins attenuated histone-mediated cytotoxicity in vitro and improved the survival in a rat model of histone-induced organ dysfunction[J].Intensive Care Med Exp,2015,3(1):36.[54]Wygrecka M,Kosanovic D,Wujak L,et al.Antihistoneproperties of C1 esterase inhibitor protect against lung injury[J].Am J Respir Crit Care Med,2017,196(2):186-199.[55]Marks PA,Richon VM,Miller T,et al.Histone deacetylase inhibitors[J].A Adv Cancer Res,2004(91):137-168.[56]Boyapati RK,Tamborska A,Dorward DA,et al.Advances in the understanding of mitochondrial DNA as a pathogenic factor in inflammatory diseases[J].F1000Research,2017(6):169.[57]Itagaki K,Kaczmarek E,Kwon WY,et al.Formyl peptide receptor-1 blockade prevents receptor regulation by mitochondrial danger-associated molecular patterns and preserves neutrophil function after trauma[J].Crit Care Med,2020,48(2):e123-e132.[58]Fensterheim BA,Young JD,Luan LM,et al.The TLR4 agonist monophosphoryllipid A drives broad resistance to infection via dynamic reprogramming of macrophage metabolism[J].J Immunol,2018,200(11):3777-3789.[59]Hernandez A,Luan LM,Stothers CL,et al.Phosphorylated hexa-acyl disaccharides augment host resistance against common nosocomial pathogens[J].Crit Care Med,2019,47(11):e930-e938.[60]O’Dea KP,Porter JR,Tirlapur N,et al.Circulating microvesiclesare elevated acutely following major burns injury and associated with clinical severity[J].PLoS One,2016,11(12):e0167801.[61]Ogura H,Kawasaki T,Tanaka H,et al.Activated platelets enhance microparticle formation and platelet-leukocyte interaction in severe trauma and sepsis[J].J Trauma,2001,50(5):801-809.[62]Lehner GF,Harler U,Haller VM,et al.Characterization of microvesicles in septic shock using high-sensitivity flow cytometry[J].Shock,2016,46(4):373-381.

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更新日期/Last Update: 1900-01-01