Pathophysiology of Typical Hemolytic Uremic Syndrome

被引：52

作者：

Karpman, Diana ^{[1
]}

Sartz, Lisa ^{[1
]}

Johnson, Sally ^{[2
]}

机构：

[1] Lund Univ, Dept Pediat, Lund, Sweden

[2] Birmingham Childrens Hosp, Dept Paediat Nephrol, Birmingham, W Midlands, England

来源：

SEMINARS IN THROMBOSIS AND HEMOSTASIS | 2010年 / 36卷 / 06期

基金：

瑞典研究理事会;

关键词：

Hemolytic uremic syndrome; Shiga toxin; enterohemorrhagic Escherichia coli; thrombotic microangiopathy; kidney; ENTEROHEMORRHAGIC ESCHERICHIA-COLI; SHIGA-LIKE TOXIN; MICROVASCULAR ENDOTHELIAL-CELLS; INTESTINAL EPITHELIAL-CELLS; CYTOLETHAL DISTENDING TOXIN; TISSUE FACTOR EXPRESSION; NITRIC-OXIDE SYNTHASE; TUMOR-NECROSIS-FACTOR; UP-REGULATION; TNF-ALPHA;

D O I：

10.1055/s-0030-1262879

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

The typical form of hemolytic uremic syndrome (HUS) is associated with enterohemorrhagic Escherichia coli (EHEC) infection. The disease process is initiated and perpetuated by interactions between the pathogen or its virulence factors and host cells, as well as the host response. During EHEC-associated HUS, alterations occurring at the intestinal mucosal barrier and in the circulation, as well as on endothelial cells and other target-organ cells, lead to cell activation and/or cytotoxicity, and trigger a prothrombotic state. This review summarizes current knowledge regarding the interactions of the pathogen and its virulence factors with cells in the intestine, bloodstream, kidney, and brain. Mechanisms of bacterial colonization, toxin circulation, and induction of target organ damage are discussed.

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收藏

页码：575 / 585

页数：11

相关论文

共 140 条

[1] Relative nephroprotection during Escherichia coli O157:H7 infections:: Association with intravenous volume expansion [J].

Ake, JA ;

Jelacic, S ;

Ciol, MA ;

Watkins, SL ;

Murray, KF ;

Christie, DL ;

Klein, EJ ;

Tarr, PI .

PEDIATRICS, 2005, 115 (06) :E673-E680

[2] Hemolysin from Shiga toxin-negative Escherichia coli O26 strains injures microvascular endothelium [J].

Aldick, Thomas ;

Bielaszewska, Martina ;

Zhang, Wenlan ;

Brockmeyer, Jens ;

Schmidt, Herbert ;

Friedrich, Alexander W. ;

Kim, Kwang S. ;

Schmidt, M. Alexander ;

Karch, Helge .

MICROBES AND INFECTION, 2007, 9 (03) :282-290

[3] Putative Adhesins of Enteropathogenic and Enterohemorrhagic Escherichia coli of Serogroup O26 Isolated from Humans and Cattle [J].

Bardiau, Marjorie ;

Labrozzo, Sabrina ;

Mainil, Jacques G. .

JOURNAL OF CLINICAL MICROBIOLOGY, 2009, 47 (07) :2090-2096

[4] Enterohemorrhagic Escherichia coli suppresses inflammatory response to cytokines and its own toxin [J].

Bellmeyer, Amy ;

Cotton, Cynthia ;

Kanteti, Rajani ;

Koutsouris, Athanasia ;

Viswanathan, V. K. ;

Hecht, Gail .

AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY, 2009, 297 (03) :G576-G581

[5] Consequences of enterohaemorrhagic Escherichia coli infection for the vascular endothelium [J].

Bielaszewska, M ;

Karch, H .

THROMBOSIS AND HAEMOSTASIS, 2005, 94 (02) :312-318

[6] Cytolethal distending toxin from Shiga toxin-producing Escherichia coli O157 causes irreversible G2/M arrest, inhibition of proliferation, and death of human endothelial cells [J].

Bielaszewska, M ;

Sinha, B ;

Kuczius, T ;

Karch, H .

INFECTION AND IMMUNITY, 2005, 73 (01) :552-562

[7] Shiga toxin activatable by intestinal mucus in Escherichia coli isolated from humans:: Predictor for a severe clinical outcome [J].

Bielaszewska, Martina ;

Friedrich, Alexander W. ;

Aldick, Thomas ;

Schuerk-Bulgrin, Robin ;

Karch, Helge .

CLINICAL INFECTIOUS DISEASES, 2006, 43 (09) :1160-1167

[8] Verotoxin (Shiga toxin) sensitizes renal epithelial cells to increased heme toxicity: Possible implications for the hemolytic uremic syndrome [J].

Bitzan, M ;

Bickford, BB ;

Foster, GH .

JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY, 2004, 15 (09) :2334-2343

[9] Verotoxin and ricin have novel effects on preproendothelin-1 expression but fail to modify nitric oxide synthase (ecNOS) expression and NO production in vascular endothelium [J].

Bitzan, MM ;

Wang, Y ;

Lin, J ;

Marsden, PA .

JOURNAL OF CLINICAL INVESTIGATION, 1998, 101 (02) :372-382

[10] Intracerebroventricular administration of Shiga toxin type 2 altered the expression levels of neuronal nitric oxide synthase and glial fibrillary acidic protein in rat brains [J].

Boccoli, Javier ;

Loidl, C. Fabian ;

Lopez-Costa, Juan Jose ;

Pistone Creydt, Virginia ;

Ibarra, Cristina ;

Goldstein, Jorge .

BRAIN RESEARCH, 2008, 1230 :320-333

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