Valid Presumption of Shiga Toxin-Mediated Damage of Developing Erythrocytes in EHEC-Associated Hemolytic Uremic Syndrome
The global emergence of clinical diseases caused by enterohemorrhagic <i>Escherichia coli</i> (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 th...
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| Format: | Article |
| Language: | English |
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MDPI AG
2020-06-01
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| Series: | Toxins |
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| Online Access: | https://www.mdpi.com/2072-6651/12/6/373 |
| _version_ | 1827715589413535744 |
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| author | Johanna Detzner Gottfried Pohlentz Johannes Müthing |
| author_facet | Johanna Detzner Gottfried Pohlentz Johannes Müthing |
| author_sort | Johanna Detzner |
| collection | DOAJ |
| description | The global emergence of clinical diseases caused by enterohemorrhagic <i>Escherichia coli</i> (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. |
| first_indexed | 2024-03-10T19:22:03Z |
| format | Article |
| id | doaj.art-ac9daf851b404365973eb3939d00f94a |
| institution | Directory Open Access Journal |
| issn | 2072-6651 |
| language | English |
| last_indexed | 2024-03-10T19:22:03Z |
| publishDate | 2020-06-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Toxins |
| spelling | doaj.art-ac9daf851b404365973eb3939d00f94a2023-11-20T02:53:26ZengMDPI AGToxins2072-66512020-06-0112637310.3390/toxins12060373Valid Presumption of Shiga Toxin-Mediated Damage of Developing Erythrocytes in EHEC-Associated Hemolytic Uremic SyndromeJohanna Detzner0Gottfried Pohlentz1Johannes Müthing2Institute of Hygiene, University of Münster, 48149 Münster, GermanyInstitute of Hygiene, University of Münster, 48149 Münster, GermanyInstitute of Hygiene, University of Münster, 48149 Münster, GermanyThe global emergence of clinical diseases caused by enterohemorrhagic <i>Escherichia coli</i> (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.https://www.mdpi.com/2072-6651/12/6/373AB<sub>5</sub> toxinred blood cellsdeveloping erythrocytesEHECerythropoiesisGb3Cer |
| spellingShingle | Johanna Detzner Gottfried Pohlentz Johannes Müthing Valid Presumption of Shiga Toxin-Mediated Damage of Developing Erythrocytes in EHEC-Associated Hemolytic Uremic Syndrome Toxins AB<sub>5</sub> toxin red blood cells developing erythrocytes EHEC erythropoiesis Gb3Cer |
| title | Valid Presumption of Shiga Toxin-Mediated Damage of Developing Erythrocytes in EHEC-Associated Hemolytic Uremic Syndrome |
| title_full | Valid Presumption of Shiga Toxin-Mediated Damage of Developing Erythrocytes in EHEC-Associated Hemolytic Uremic Syndrome |
| title_fullStr | Valid Presumption of Shiga Toxin-Mediated Damage of Developing Erythrocytes in EHEC-Associated Hemolytic Uremic Syndrome |
| title_full_unstemmed | Valid Presumption of Shiga Toxin-Mediated Damage of Developing Erythrocytes in EHEC-Associated Hemolytic Uremic Syndrome |
| title_short | Valid Presumption of Shiga Toxin-Mediated Damage of Developing Erythrocytes in EHEC-Associated Hemolytic Uremic Syndrome |
| title_sort | valid presumption of shiga toxin mediated damage of developing erythrocytes in ehec associated hemolytic uremic syndrome |
| topic | AB<sub>5</sub> toxin red blood cells developing erythrocytes EHEC erythropoiesis Gb3Cer |
| url | https://www.mdpi.com/2072-6651/12/6/373 |
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