Helicobacter pylori Affects the Antigen Presentation Activity of Macrophages Modulating the Expression of the Immune Receptor CD300E through miR-4270
(Hp) is a Gram-negative bacterium that infects the human gastric mucosa, leading to chronic inflammation. If not eradicated with antibiotic treatment, the bacterium persists in the human stomach for decades increasing the risk to develop chronic gastritis, gastroduodenal ulcer, and gastric adenocarc...
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| Vydané v: | Frontiers in immunology Ročník 8; s. 1288 |
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| Hlavní autori: | , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | English |
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Frontiers Media S.A
12.10.2017
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| ISSN: | 1664-3224, 1664-3224 |
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| Abstract | (Hp) is a Gram-negative bacterium that infects the human gastric mucosa, leading to chronic inflammation. If not eradicated with antibiotic treatment, the bacterium persists in the human stomach for decades increasing the risk to develop chronic gastritis, gastroduodenal ulcer, and gastric adenocarcinoma. The lifelong persistence of Hp in the human stomach suggests that the host response fails to clear the infection. It has been recently shown that during Hp infection phagocytic cells promote high Hp loads rather than contributing to bacterial clearance. Within these cells Hp survives in "megasomes," large structures arising from homotypic fusion of phagosomes, but the mechanism that Hp employs to avoid phagocytic killing is not completely understood. Here, we show that Hp infection induces the downregulation of specific microRNAs involved in the regulation of transcripts codifying for inflammatory proteins. miR-4270 targets the most upregulated gene: the immune receptor
, whose expression is strictly dependent on Hp infection. CD300E engagement enhances the pro-inflammatory potential of macrophages, but in parallel it affects their ability to express and expose MHC class II molecules on the plasma membrane, without altering phagocytosis. This effect compromises the possibility for effector T cells to recognize and activate the killing potential of macrophages, which, in turn would become a survival niche for the bacterium. Taken together, our data add another piece to the complicate puzzle represented by the long-life coexistence between Hp and the human host and contribute with new insights toward understanding the regulation and function of the immune receptor CD300E. |
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| AbstractList | Helicobacter pylori (Hp) is a Gram-negative bacterium that infects the human gastric mucosa, leading to chronic inflammation. If not eradicated with antibiotic treatment, the bacterium persists in the human stomach for decades increasing the risk to develop chronic gastritis, gastroduodenal ulcer, and gastric adenocarcinoma. The lifelong persistence of Hp in the human stomach suggests that the host response fails to clear the infection. It has been recently shown that during Hp infection phagocytic cells promote high Hp loads rather than contributing to bacterial clearance. Within these cells Hp survives in “megasomes,” large structures arising from homotypic fusion of phagosomes, but the mechanism that Hp employs to avoid phagocytic killing is not completely understood. Here, we show that Hp infection induces the downregulation of specific microRNAs involved in the regulation of transcripts codifying for inflammatory proteins. miR-4270 targets the most upregulated gene: the immune receptor CD300E, whose expression is strictly dependent on Hp infection. CD300E engagement enhances the pro-inflammatory potential of macrophages, but in parallel it affects their ability to express and expose MHC class II molecules on the plasma membrane, without altering phagocytosis. This effect compromises the possibility for effector T cells to recognize and activate the killing potential of macrophages, which, in turn would become a survival niche for the bacterium. Taken together, our data add another piece to the complicate puzzle represented by the long-life coexistence between Hp and the human host and contribute with new insights toward understanding the regulation and function of the immune receptor CD300E. (Hp) is a Gram-negative bacterium that infects the human gastric mucosa, leading to chronic inflammation. If not eradicated with antibiotic treatment, the bacterium persists in the human stomach for decades increasing the risk to develop chronic gastritis, gastroduodenal ulcer, and gastric adenocarcinoma. The lifelong persistence of Hp in the human stomach suggests that the host response fails to clear the infection. It has been recently shown that during Hp infection phagocytic cells promote high Hp loads rather than contributing to bacterial clearance. Within these cells Hp survives in "megasomes," large structures arising from homotypic fusion of phagosomes, but the mechanism that Hp employs to avoid phagocytic killing is not completely understood. Here, we show that Hp infection induces the downregulation of specific microRNAs involved in the regulation of transcripts codifying for inflammatory proteins. miR-4270 targets the most upregulated gene: the immune receptor , whose expression is strictly dependent on Hp infection. CD300E engagement enhances the pro-inflammatory potential of macrophages, but in parallel it affects their ability to express and expose MHC class II molecules on the plasma membrane, without altering phagocytosis. This effect compromises the possibility for effector T cells to recognize and activate the killing potential of macrophages, which, in turn would become a survival niche for the bacterium. Taken together, our data add another piece to the complicate puzzle represented by the long-life coexistence between Hp and the human host and contribute with new insights toward understanding the regulation and function of the immune receptor CD300E. Helicobacter pylori (Hp) is a Gram-negative bacterium that infects the human gastric mucosa, leading to chronic inflammation. If not eradicated with antibiotic treatment, the bacterium persists in the human stomach for decades increasing the risk to develop chronic gastritis, gastroduodenal ulcer, and gastric adenocarcinoma. The lifelong persistence of Hp in the human stomach suggests that the host response fails to clear the infection. It has been recently shown that during Hp infection phagocytic cells promote high Hp loads rather than contributing to bacterial clearance. Within these cells Hp survives in "megasomes," large structures arising from homotypic fusion of phagosomes, but the mechanism that Hp employs to avoid phagocytic killing is not completely understood. Here, we show that Hp infection induces the downregulation of specific microRNAs involved in the regulation of transcripts codifying for inflammatory proteins. miR-4270 targets the most upregulated gene: the immune receptor CD300E, whose expression is strictly dependent on Hp infection. CD300E engagement enhances the pro-inflammatory potential of macrophages, but in parallel it affects their ability to express and expose MHC class II molecules on the plasma membrane, without altering phagocytosis. This effect compromises the possibility for effector T cells to recognize and activate the killing potential of macrophages, which, in turn would become a survival niche for the bacterium. Taken together, our data add another piece to the complicate puzzle represented by the long-life coexistence between Hp and the human host and contribute with new insights toward understanding the regulation and function of the immune receptor CD300E.Helicobacter pylori (Hp) is a Gram-negative bacterium that infects the human gastric mucosa, leading to chronic inflammation. If not eradicated with antibiotic treatment, the bacterium persists in the human stomach for decades increasing the risk to develop chronic gastritis, gastroduodenal ulcer, and gastric adenocarcinoma. The lifelong persistence of Hp in the human stomach suggests that the host response fails to clear the infection. It has been recently shown that during Hp infection phagocytic cells promote high Hp loads rather than contributing to bacterial clearance. Within these cells Hp survives in "megasomes," large structures arising from homotypic fusion of phagosomes, but the mechanism that Hp employs to avoid phagocytic killing is not completely understood. Here, we show that Hp infection induces the downregulation of specific microRNAs involved in the regulation of transcripts codifying for inflammatory proteins. miR-4270 targets the most upregulated gene: the immune receptor CD300E, whose expression is strictly dependent on Hp infection. CD300E engagement enhances the pro-inflammatory potential of macrophages, but in parallel it affects their ability to express and expose MHC class II molecules on the plasma membrane, without altering phagocytosis. This effect compromises the possibility for effector T cells to recognize and activate the killing potential of macrophages, which, in turn would become a survival niche for the bacterium. Taken together, our data add another piece to the complicate puzzle represented by the long-life coexistence between Hp and the human host and contribute with new insights toward understanding the regulation and function of the immune receptor CD300E. |
| Author | Chemello, Francesco Millino, Caterina Della Bella, Chiara Pagliari, Matteo Fassan, Matteo de Bernard, Marina Pacchioni, Beniamina Codolo, Gaia Toffoletto, Marta Lonardi, Silvia Vermi, William Munari, Fabio Cagnin, Stefano |
| AuthorAffiliation | 1 Department of Biology, University of Padua , Padua , Italy 4 CRIBI Biotechnology Center, University of Padua , Padua , Italy 3 Department of Molecular and Translational Medicine, Section of Pathology, University of Brescia , Brescia , Italy 5 Department of Medicine, University of Padua , Padua , Italy 2 Department of Biomedical Sciences, University of Padua, Venetian Institute of Molecular Medicine (VIMM) , Padua , Italy |
| AuthorAffiliation_xml | – name: 3 Department of Molecular and Translational Medicine, Section of Pathology, University of Brescia , Brescia , Italy – name: 2 Department of Biomedical Sciences, University of Padua, Venetian Institute of Molecular Medicine (VIMM) , Padua , Italy – name: 5 Department of Medicine, University of Padua , Padua , Italy – name: 4 CRIBI Biotechnology Center, University of Padua , Padua , Italy – name: 1 Department of Biology, University of Padua , Padua , Italy |
| Author_xml | – sequence: 1 givenname: Matteo surname: Pagliari fullname: Pagliari, Matteo – sequence: 2 givenname: Fabio surname: Munari fullname: Munari, Fabio – sequence: 3 givenname: Marta surname: Toffoletto fullname: Toffoletto, Marta – sequence: 4 givenname: Silvia surname: Lonardi fullname: Lonardi, Silvia – sequence: 5 givenname: Francesco surname: Chemello fullname: Chemello, Francesco – sequence: 6 givenname: Gaia surname: Codolo fullname: Codolo, Gaia – sequence: 7 givenname: Caterina surname: Millino fullname: Millino, Caterina – sequence: 8 givenname: Chiara surname: Della Bella fullname: Della Bella, Chiara – sequence: 9 givenname: Beniamina surname: Pacchioni fullname: Pacchioni, Beniamina – sequence: 10 givenname: William surname: Vermi fullname: Vermi, William – sequence: 11 givenname: Matteo surname: Fassan fullname: Fassan, Matteo – sequence: 12 givenname: Marina surname: de Bernard fullname: de Bernard, Marina – sequence: 13 givenname: Stefano surname: Cagnin fullname: Cagnin, Stefano |
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| Copyright | Copyright © 2017 Pagliari, Munari, Toffoletto, Lonardi, Chemello, Codolo, Millino, Della Bella, Pacchioni, Vermi, Fassan, de Bernard and Cagnin. 2017 Pagliari, Munari, Toffoletto, Lonardi, Chemello, Codolo, Millino, Della Bella, Pacchioni, Vermi, Fassan, de Bernard and Cagnin |
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| Keywords | microRNAs CD300E macrophages major histocompatibility complex class II Helicobacter pylori chronic inflammation |
| Language | English |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Edited by: Hao Shen, University of Pennsylvania, United States Reviewed by: Mario M. D’Elios, University of Florence, Italy; Elsa Anes, Faculdade de Farmácia, Universidade de Lisboa, Portugal; Laurence C. Eisenlohr, University of Pennsylvania, United States Co-first authors. Specialty section: This article was submitted to Microbial Immunology, a section of the journal Frontiers in Immunology |
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| Title | Helicobacter pylori Affects the Antigen Presentation Activity of Macrophages Modulating the Expression of the Immune Receptor CD300E through miR-4270 |
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