Enas El Saftawy, Mansour Alghamdi, Basma Emad Aboulhoda
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引用次数: 0
摘要
背景：寄生虫感染具有与肥胖相当的危险因素。此外，肥胖损害先天和适应性免疫，从而增加对传染病的易感性。目的：研究肥胖背景下瘦素/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。方法学：为实施本次综述，文章收集使用埃及知识库（EKB）、Web of Science、PubMed和谷歌Scholar。结论：瘦素增强抗寄生虫免疫。肥胖有利于囊虫、脆弱地阿米巴、大肠内阿米巴和肠贾第虫的肠道定植。脂肪细胞是克氏锥虫、布鲁氏锥虫和疟原虫的生态位和食物来源。此外，刚地弓形虫依靠循环胆固醇繁殖。肥胖会引起低度慢性炎症和代谢综合征。然而，巴西尼波圆线虫和肝片吸虫试图减轻炎症和代谢综合征。钩虫改善胰岛素抵抗。然而，寄生虫如曼氏血吸虫、猪毛虫、梨形带绦虫、溶组织内阿米巴、克氏锥虫、布鲁氏锥虫和弓形虫加重了代谢免疫代谢综合征。肥胖阻碍了对利什曼原虫的免疫。而疟原虫可致糖尿病。贾第鞭毛虫感染和多回Heligmosoides感染引起肥胖患者的生态失调。肥胖与阴道毛滴虫、血单胞菌、曼氏单胞菌、华支支睾吸虫、活弧菌等寄生虫的癌症类型相似。而刚地弓形虫和细粒棘球绦虫具有抗肿瘤作用。肥胖/高脂肪饮食会阻碍曼氏血吸虫、毛线虫和溶组织内阿米巴的感染。此外，囊虫、脆弱地阿米巴、肠贾第鞭毛虫、旋毛虫和血吸虫似乎对肥胖有改善作用。
Interplay of obesity and parasitic infection: current evidence of immunogenesis, tumorigenesis and leptin receptor involvement.
Background: Parasitic infections possess comparable risk factors to obesity. In addition, obesity impairs innate and adaptive immunity subsequently increasing vulnerability to infectious diseases.
Aim: 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.
Methodology: To implement the current review, articles were gathered using the Egyptian Knowledge Bank (EKB), Web of Science, PubMed, and Google Scholar.
Conclusion: 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.
期刊介绍：
Nutrition & Metabolism publishes studies with a clear focus on nutrition and metabolism with applications ranging from nutrition needs, exercise physiology, clinical and population studies, as well as the underlying mechanisms in these aspects.
The areas of interest for Nutrition & Metabolism encompass studies in molecular nutrition in the context of obesity, diabetes, lipedemias, metabolic syndrome and exercise physiology. Manuscripts related to molecular, cellular and human metabolism, nutrient sensing and nutrient–gene interactions are also in interest, as are submissions that have employed new and innovative strategies like metabolomics/lipidomics or other omic-based biomarkers to predict nutritional status and metabolic diseases.
Key areas we wish to encourage submissions from include:
-how diet and specific nutrients interact with genes, proteins or metabolites to influence metabolic phenotypes and disease outcomes;
-the role of epigenetic factors and the microbiome in the pathogenesis of metabolic diseases and their influence on metabolic responses to diet and food components;
-how diet and other environmental factors affect epigenetics and microbiota; the extent to which genetic and nongenetic factors modify personal metabolic responses to diet and food compositions and the mechanisms involved;
-how specific biologic networks and nutrient sensing mechanisms attribute to metabolic variability.
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