The intersection of host in vivo metabolism and immune responses to infection with kinetoplastid and apicomplexan parasites.
Autor: | Ewald S; Department of Microbiology, Immunology, and Cancer Biology at the Carter Immunology Center, University of Virginia School of Medicine, Charlottesville, Virginia, USA., Nasuhidehnavi A; Department of Chemistry and Biochemistry, University of Oklahoma, Norman, Oklahoma, USA., Feng T-Y; Department of Microbiology, Immunology, and Cancer Biology at the Carter Immunology Center, University of Virginia School of Medicine, Charlottesville, Virginia, USA., Lesani M; Department of Microbiology and Plant Biology, University of Oklahoma, Norman, Oklahoma, USA., McCall L-I; Department of Chemistry and Biochemistry, University of Oklahoma, Norman, Oklahoma, USA.; Department of Microbiology and Plant Biology, University of Oklahoma, Norman, Oklahoma, USA.; Laboratories of Molecular Anthropology and Microbiome Research, University of Oklahoma, Norman, Oklahoma, USA.; Department of Chemistry and Biochemistry, San Diego State University, San Diego, California, USA. |
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Jazyk: | angličtina |
Zdroj: | Microbiology and molecular biology reviews : MMBR [Microbiol Mol Biol Rev] 2024 Mar 27; Vol. 88 (1), pp. e0016422. Date of Electronic Publication: 2024 Feb 01. |
DOI: | 10.1128/mmbr.00164-22 |
Abstrakt: | 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. Competing Interests: The authors declare no conflict of interest. |
Databáze: | MEDLINE |
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