生物
免疫系统
寄主(生物学)
疟原虫(生命周期)
向性
利什曼原虫
免疫学
微生物学
寄生虫寄主
生态学
计算机科学
万维网
病毒
作者
Sarah E. Ewald,Azadeh Nasuhidehnavi,Tzu-Yu Feng,Mahbobeh Lesani,Laura‐Isobel McCall
标识
DOI:10.1128/mmbr.00164-22
摘要
SUMMARY Protozoan 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.
科研通智能强力驱动
Strongly Powered by AbleSci AI