Fischer David D, Kandasamy Sukumar, Paim Francine C, Langel Stephanie N, Alhamo Moyasar A, Shao Lulu, Chepngeno Juliet, Miyazaki Ayako, Huang Huang-Chi, Kumar Anand, Rajashekara Gireesh, Saif Linda J, Vlasova Anastasia N
Department of Veterinary Preventive Medicine Department, Food Animal Health Research Program (FAHRP), The Ohio Agricultural Research and Development Center (OARDC), The Ohio State University, Wooster, Ohio, USA.
Department of Veterinary Preventive Medicine Department, Food Animal Health Research Program (FAHRP), The Ohio Agricultural Research and Development Center (OARDC), The Ohio State University, Wooster, Ohio, USA
Clin Vaccine Immunol. 2017 Aug 4;24(8). doi: 10.1128/CVI.00172-17. Print 2017 Aug.
Malnutrition leads to increased morbidity and is evident in almost half of all deaths in children under the age of 5 years. Mortality due to rotavirus diarrhea is common in developing countries where malnutrition is prevalent; however, the relationship between malnutrition and rotavirus infection remains unclear. In this study, gnotobiotic pigs transplanted with the fecal microbiota of a healthy 2-month-old infant were fed protein-sufficient or -deficient diets and infected with virulent human rotavirus (HRV). After human rotavirus infection, protein-deficient pigs had decreased human rotavirus antibody titers and total IgA concentrations, systemic T helper (CD3 CD4) and cytotoxic T (CD3 CD8) lymphocyte frequencies, and serum tryptophan and angiotensin I-converting enzyme 2. Additionally, deficient-diet pigs had impaired tryptophan catabolism postinfection compared with sufficient-diet pigs. Tryptophan supplementation was tested as an intervention in additional groups of fecal microbiota-transplanted, rotavirus-infected, sufficient- and deficient-diet pigs. Tryptophan supplementation increased the frequencies of regulatory (CD4 or CD8 CD25 FoxP3) T cells in pigs on both the sufficient and the deficient diets. These results suggest that a protein-deficient diet impairs activation of the adaptive immune response following HRV infection and alters tryptophan homeostasis.
营养不良会导致发病率上升，并且在5岁以下儿童几乎一半的死亡案例中都很明显。在营养不良普遍存在的发展中国家，轮状病毒腹泻导致的死亡率很高；然而，营养不良与轮状病毒感染之间的关系仍不清楚。在这项研究中，将健康2个月大婴儿的粪便微生物群移植到无菌猪体内，分别给它们喂食蛋白质充足或缺乏的饮食，然后感染强毒性人轮状病毒（HRV）。感染人轮状病毒后，蛋白质缺乏的猪的人轮状病毒抗体滴度和总IgA浓度、全身辅助性T细胞（CD3 CD4）和细胞毒性T细胞（CD3 CD8）频率以及血清色氨酸和血管紧张素I转换酶2均下降。此外，与蛋白质充足饮食的猪相比，蛋白质缺乏饮食的猪在感染后色氨酸分解代谢受损。在另外几组粪便微生物群移植、感染轮状病毒、饮食充足和缺乏的猪中，测试了补充色氨酸作为一种干预措施。补充色氨酸增加了饮食充足和缺乏的猪体内调节性（CD4或CD8 CD25 FoxP3）T细胞的频率。这些结果表明，蛋白质缺乏饮食会损害HRV感染后适应性免疫反应的激活，并改变色氨酸稳态。
