The intersection of host in vivo metabolism and immune responses to infection with kinetoplastid and apicomplexan parasites
SUMMARYProtozoan parasite infection dramatically alters host metabolism, driven by immunological demand and parasite manipulation strategies. Immunometabolic checkpoints are often exploited by kinetoplastid and protozoan parasites to establish chronic infection, which can significantly impair host metabolic homeostasis. The recent growth of tools to analyze metabolism is expanding our understanding of these questions. Here, we review and contrast host metabolic alterations that occur in vivo during infection with Leishmania, trypanosomes, Toxoplasma, Plasmodium, and Cryptosporidium. Although genetically divergent, there are commonalities among these pathogens in terms of metabolic needs, induction of the type I immune responses required for clearance, and the potential for sustained host metabolic dysbiosis. Comparing these pathogens provides an opportunity to explore how transmission strategy, nutritional demand, and host cell and tissue tropism drive similarities and unique aspects in host response and infection outcome and to design new strategies to treat disease.
Medienart: |
E-Artikel |
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Erscheinungsjahr: |
2024 |
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Erschienen: |
2024 |
Enthalten in: |
Zur Gesamtaufnahme - volume:88 |
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Enthalten in: |
Microbiology and molecular biology reviews : MMBR - 88(2024), 1 vom: 27. März, Seite e0016422 |
Sprache: |
Englisch |
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Beteiligte Personen: |
Ewald, Sarah [VerfasserIn] |
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Links: |
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Themen: |
Apicomplexan |
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Anmerkungen: |
Date Completed 28.03.2024 Date Revised 29.03.2024 published: Print-Electronic Citation Status MEDLINE |
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doi: |
10.1128/mmbr.00164-22 |
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funding: |
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Förderinstitution / Projekttitel: |
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PPN (Katalog-ID): |
NLM367891387 |
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520 | |a SUMMARYProtozoan parasite infection dramatically alters host metabolism, driven by immunological demand and parasite manipulation strategies. Immunometabolic checkpoints are often exploited by kinetoplastid and protozoan parasites to establish chronic infection, which can significantly impair host metabolic homeostasis. The recent growth of tools to analyze metabolism is expanding our understanding of these questions. Here, we review and contrast host metabolic alterations that occur in vivo during infection with Leishmania, trypanosomes, Toxoplasma, Plasmodium, and Cryptosporidium. Although genetically divergent, there are commonalities among these pathogens in terms of metabolic needs, induction of the type I immune responses required for clearance, and the potential for sustained host metabolic dysbiosis. Comparing these pathogens provides an opportunity to explore how transmission strategy, nutritional demand, and host cell and tissue tropism drive similarities and unique aspects in host response and infection outcome and to design new strategies to treat disease | ||
650 | 4 | |a Journal Article | |
650 | 4 | |a Review | |
650 | 4 | |a Cryptosporidium | |
650 | 4 | |a Leishmania | |
650 | 4 | |a Plasmodium | |
650 | 4 | |a Toxoplasma gondii | |
650 | 4 | |a Trypanosoma | |
650 | 4 | |a apicomplexan | |
650 | 4 | |a host-parasite relationship | |
650 | 4 | |a immunity | |
650 | 4 | |a kinetoplastida | |
650 | 4 | |a metabolism | |
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700 | 1 | |a Nasuhidehnavi, Azadeh |e verfasserin |4 aut | |
700 | 1 | |a Feng, Tzu-Yu |e verfasserin |4 aut | |
700 | 1 | |a Lesani, Mahbobeh |e verfasserin |4 aut | |
700 | 1 | |a McCall, Laura-Isobel |e verfasserin |4 aut | |
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