Saftawy Enas El, Alghamdi Mansour, Aboulhoda Basma Emad
Department of Medical Parasitology, Faculty of Medicine, Cairo University, Cairo, Egypt.
Department of Medical Parasitology, Armed Forces College of Medicine, Cairo, Egypt.
Nutr Metab (Lond). 2025 Sep 15;22(1):105. doi: 10.1186/s12986-025-00972-7.
Parasitic infections possess comparable risk factors to obesity. In addition, obesity impairs innate and adaptive immunity subsequently increasing vulnerability to infectious diseases.
The study investigated the leptin/leptin receptors, obesity-parasites mutual relationship and the effect of parasitic infections on immune metabolism, microbiota, and tumorigenesis in the context of obesity.
To implement the current review, articles were gathered using the Egyptian Knowledge Bank (EKB), Web of Science, PubMed, and Google Scholar.
Leptin enhances anti-parasitic immunity. Obesity favors intestinal colonization of Blastocystis sp., Dientamoeba fragilis, Entamoeba coli, and Giardia intestinalis. Adipocytes act as a niche and a food source for Trypanosoma cruzi, Trypanosoma brucei, and Plasmodium. In addition, Toxoplasma gondii relies on the circulatory cholesterol to thrive. Obesity provokes low-grade chronic inflammation and metabolic syndrome. Yet, Nippostrongylus brasiliensis and Fasciola hepatica attempted to alleviate inflammation and metabolic syndrome. Hookworm improves insulin resistance. However, parasites such as Schistosoma mansoni, Trichuris suis, Taenia pisiformis, Entamoeba histolytica, Trypanosoma cruzi, and Trypanosoma brucei, and Toxoplasma aggravated metabolic immune metabolic syndrome. Obesity hampered immunity against Leishmania sp.. and Plasmodium sp. is diabetogenic. Giardia infection and Heligmosoides polygyrus infections induce dysbiosis in obesity. Obesity and parasites like Trichomonas vaginalis, S. haematobium, S. mansoni, Clonorchis sinensis, Opishorchis viverrini showed similar cancer types. Yet, Toxoplasma gondii and Echinococcus granulosus have anti-tumorigenic effects. Obesity/high-fat diet hinders Schistosoma mansoni, Trichuris muris, and Entamoeba histolytica infections. Also, Blastocystis sp., Dientamoeba fragilis, Giardia intestinalis, Trichinella spiralis, and Schistosoma appeared to have ameliorative effects in obesity.
寄生虫感染与肥胖具有相似的风险因素。此外，肥胖会损害先天性和适应性免疫，从而增加对传染病的易感性。
本研究在肥胖背景下，调查了瘦素/瘦素受体、肥胖与寄生虫的相互关系以及寄生虫感染对免疫代谢、微生物群和肿瘤发生的影响。
为进行本综述，通过埃及知识库（EKB）、科学网、PubMed和谷歌学术收集文章。
瘦素增强抗寄生虫免疫。肥胖有利于芽囊原虫、脆弱双核阿米巴、结肠内阿米巴和肠道贾第虫在肠道定殖。脂肪细胞是克氏锥虫、布氏锥虫和疟原虫的生存场所和食物来源。此外，刚地弓形虫依靠循环胆固醇生长。肥胖引发低度慢性炎症和代谢综合征。然而，巴西日圆线虫和肝片吸虫试图减轻炎症和代谢综合征。钩虫可改善胰岛素抵抗。然而，曼氏血吸虫、猪鞭虫、豆状带绦虫、溶组织内阿米巴、克氏锥虫、布氏锥虫和刚地弓形虫等寄生虫会加重代谢性免疫代谢综合征。肥胖会阻碍对利什曼原虫属的免疫。疟原虫属具有致糖尿病作用。贾第虫感染和多枝单睾线虫感染会在肥胖状态下导致微生物群失调。肥胖与阴道毛滴虫、埃及血吸虫、曼氏血吸虫、华支睾吸虫、麝猫后睾吸虫等寄生虫表现出相似的癌症类型。然而，刚地弓形虫和细粒棘球绦虫具有抗肿瘤作用。肥胖/高脂饮食会阻碍曼氏血吸虫、鼠鞭虫和溶组织内阿米巴的感染。此外，芽囊原虫、脆弱双核阿米巴、肠道贾第虫、旋毛虫和血吸虫似乎对肥胖有改善作用。
