TY  - JOUR
AB  - The global emergence of clinical diseases caused by enterohemorrhagic Escherichia coli (EHEC) is an issue of great concern. EHEC release Shiga toxins (Stxs) as their key virulence factors, and investigations on the cell-damaging mechanisms toward target cells are inevitable for the development of novel mitigation strategies. Stx-mediated hemolytic uremic syndrome (HUS), characterized by the triad of microangiopathic hemolytic anemia, thrombocytopenia, and acute renal injury, is the most severe outcome of an EHEC infection. Hemolytic anemia during HUS is defined as the loss of erythrocytes by mechanical disruption when passing through narrowed microvessels. The formation of thrombi in the microvasculature is considered an indirect effect of Stx-mediated injury mainly of the renal microvascular endothelial cells, resulting in obstructions of vessels. In this review, we summarize and discuss recent data providing evidence that HUS-associated hemolytic anemia may arise not only from intravascular rupture of erythrocytes, but also from the extravascular impairment of erythropoiesis, the development of red blood cells in the bone marrow, via direct Stx-mediated damage of maturing erythrocytes, leading to "non-hemolytic" anemia.
AU  - Detzner, Johanna
AU  - Pohlentz, Gottfried
AU  - Müthing, Johannes
DA  - 2020-06-04
DO  - 10.17879/54049576452
KW  - AB5 toxin
KW  - red blood cells
KW  - developing erythrocytes
KW  - EHEC
KW  - erythropoiesis
KW  - Gb3Cer
KW  - Gb4Cer
KW  - glycosphingolipids
KW  - hemolytic anemia
LA  - eng
N1  - Toxins 12 (2020) 6, 373, 1-53
N1  - Finanziert durch den Open-Access-Publikationsfonds der Westfälischen Wilhelms-Universität Münster (WWU Münster).
N1  - Förderer: Deutsche Forschungsgemeinschaft / Projektnummer: 404813761
N1  - Funding organisation: Deutsche Forschungsgemeinschaft / Project number: 404813761
PY  - 2020-06-04
TI  - Valid Presumption of Shiga Toxin-Mediated Damage of Developing Erythrocytes in EHEC-Associated Hemolytic Uremic Syndrome
UR  - https://nbn-resolving.org/urn:nbn:de:hbz:6-54049574307
Y2  - 2024-11-21T18:11:14
ER  -