Helicobacter pylori and Epstein-Barr virus infection in cell polarity alterations
Abstract The asymmetrical distribution of the cellular organelles inside the cell is maintained by a group of cell polarity proteins. The maintenance of polarity is one of the vital host defense mechanisms against pathogens, and the loss of it contributes to infection facilitation and cancer progression. Studies have suggested that infection of viruses and bacteria alters cell polarity. Helicobacter pylori and Epstein-Barr virus are group I carcinogens involved in the progression of multiple clinical conditions besides gastric cancer (GC) and Burkitt’s lymphoma, respectively. Moreover, the coinfection of both these pathogens contributes to a highly aggressive form of GC. H. pylori and EBV target the host cell polarity complexes for their pathogenesis. H. pylori–associated proteins like CagA, VacA OipA, and urease were shown to imbalance the cellular homeostasis by altering the cell polarity. Similarly, EBV-associated genes LMP1, LMP2A, LMP2B, EBNA3C, and EBNA1 also contribute to altered cell asymmetry. This review summarized all the possible mechanisms involved in cell polarity deformation in H. pylori and EBV-infected epithelial cells. We have also discussed deregulated molecular pathways like NF-κB, TGF-β/SMAD, and β-catenin in H. pylori, EBV, and their coinfection that further modulate PAR, SCRIB, or CRB polarity complexes in epithelial cells..
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2023 |
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| Erschienen: |
2023 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:69 |
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| Enthalten in: |
Folia microbiologica - 69(2023), 1 vom: 06. Sept., Seite 41-57 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Baral, Budhadev [VerfasserIn] |
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| Links: |
Volltext [lizenzpflichtig] |
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| Anmerkungen: |
© Institute of Microbiology, Academy of Sciences of the Czech Republic, v.v.i. 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. |
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| doi: |
10.1007/s12223-023-01091-7 |
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| 520 | |a Abstract The asymmetrical distribution of the cellular organelles inside the cell is maintained by a group of cell polarity proteins. The maintenance of polarity is one of the vital host defense mechanisms against pathogens, and the loss of it contributes to infection facilitation and cancer progression. Studies have suggested that infection of viruses and bacteria alters cell polarity. Helicobacter pylori and Epstein-Barr virus are group I carcinogens involved in the progression of multiple clinical conditions besides gastric cancer (GC) and Burkitt’s lymphoma, respectively. Moreover, the coinfection of both these pathogens contributes to a highly aggressive form of GC. H. pylori and EBV target the host cell polarity complexes for their pathogenesis. H. pylori–associated proteins like CagA, VacA OipA, and urease were shown to imbalance the cellular homeostasis by altering the cell polarity. Similarly, EBV-associated genes LMP1, LMP2A, LMP2B, EBNA3C, and EBNA1 also contribute to altered cell asymmetry. This review summarized all the possible mechanisms involved in cell polarity deformation in H. pylori and EBV-infected epithelial cells. We have also discussed deregulated molecular pathways like NF-κB, TGF-β/SMAD, and β-catenin in H. pylori, EBV, and their coinfection that further modulate PAR, SCRIB, or CRB polarity complexes in epithelial cells. | ||
| 650 | 4 | |a Cell polarity |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a EBV |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Coinfection |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Gastric cancer |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Kandpal, Meenakshi |4 aut | |
| 700 | 1 | |a Ray, Anushka |4 aut | |
| 700 | 1 | |a Jana, Ankit |4 aut | |
| 700 | 1 | |a Yadav, Dhirendra Singh |4 aut | |
| 700 | 1 | |a Sachin, Kumar |4 aut | |
| 700 | 1 | |a Mishra, Amit |4 aut | |
| 700 | 1 | |a Baig, Mirza S. |4 aut | |
| 700 | 1 | |a Jha, Hem Chandra |0 (orcid)0000-0002-9698-4547 |4 aut | |
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