Ali Munwar, Xu Chang, Wang Mingyue, Hina Qazal, Ji Yaru, Anwar Subiha, Lu Sijia, He Qing, Qiu Yawei, Li Kun
College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095, China.
MOE Joint International Research Laboratory of Animal Health and Food Safety, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095, China.
Vet Sci. 2025 Jan 23;12(2):85. doi: 10.3390/vetsci12020085.
Cryptosporidiosis is a zoonotic protozoan parasite-born disease, equally significant in both animals and humans, especially affecting immunocompromised individuals (e.g., AIDS patients) and neonates. The prime concerns of this review article are to demonstrate the disruption of the intestinal barrier and variations in the gut microbiome during cryptosporidiosis, and to explore host gut-parasite interactions that can lead to the development of novel therapeutics. The review concluded that the enteric barrier is particularly maintained by tight junction proteins (e.g., occludin, claudin, and ZO-1, etc.) and mucosal immunity, both of which are severely compromised during spp. infections, resulting in increased intestinal barrier permeability, inflammatory responses, diarrhea, and ultimately death in severe cases. -induced dysbiosis is characterized by reduced microbial diversity and richness, a shift from commensal to pathogenic bacteria, as evidenced by increased pro-inflammatory taxa like Proteobacteria, and reduced proportions of beneficial SCFAs producing bacteria, e.g., Firmicutes. Recent investigations have highlighted the interrelations between gut microbiota and epithelial barrier integrity, especially during cryptosporidiosis, demonstrating the modulations regarding tight junctions (TJs), immune reactions, and SCFA production, all of which are main players in alleviating this protozoal parasitic infection. This review comprehensively describes the fine details underlying these impairments, including autophagy-mediated TJs' degradation, inflammasome activation, and gut microbiome-driven alterations in metabolic pathways, providing the latest relevant, and well-organized piece of knowledge regarding intestinal barrier alterations and microbial shifts during cryptosporidiosis. This work emphasizes the future need for longitudinal studies and advanced sequencing techniques to understand host gut microbiota-parasite interactions, aiming to formulate innovative strategies to mitigate cryptosporidiosis.
隐孢子虫病是一种人畜共患的原生动物寄生虫病,对动物和人类都具有同等重要意义,尤其会影响免疫功能低下的个体(如艾滋病患者)和新生儿。这篇综述文章的主要关注点在于展示隐孢子虫病期间肠道屏障的破坏以及肠道微生物群的变化,并探索可能导致新型疗法开发的宿主肠道与寄生虫的相互作用。综述得出结论,肠道屏障尤其由紧密连接蛋白(如闭合蛋白、claudin和ZO-1等)和黏膜免疫维持,而在隐孢子虫感染期间这两者都会受到严重损害,导致肠道屏障通透性增加、炎症反应、腹泻,严重时最终会导致死亡。隐孢子虫感染引起的生态失调的特征是微生物多样性和丰富度降低,从共生菌向病原菌转变,如变形菌门等促炎类群增加,而产生有益短链脂肪酸的细菌(如厚壁菌门)比例降低就证明了这一点。最近的研究突出了肠道微生物群与上皮屏障完整性之间的相互关系,尤其是在隐孢子虫病期间,展示了紧密连接、免疫反应和短链脂肪酸产生方面的调节,所有这些都是减轻这种原生动物寄生虫感染的主要因素。这篇综述全面描述了这些损伤背后的详细情况,包括自噬介导的紧密连接降解、炎性小体激活以及肠道微生物群驱动的代谢途径改变,提供了有关隐孢子虫病期间肠道屏障改变和微生物变化的最新、相关且条理清晰的知识。这项工作强调了未来需要进行纵向研究和先进的测序技术,以了解宿主肠道微生物群与寄生虫的相互作用,旨在制定减轻隐孢子虫病的创新策略。