Onkoba N, Chimbari M J, Kamau J M, Mukaratirwa S
College of Health Sciences, School of Nursing and Public Health, University of KwaZulu-Natal (UKZN), Howard Campus, Durban, South Africa; Tropical Infectious Diseases, Institute of Primate Research, Karen, Nairobi, Kenya.
College of Health Sciences, School of Nursing and Public Health, University of KwaZulu-Natal (UKZN), Howard Campus, Durban, South Africa.
Open Vet J. 2016;6(3):178-184. doi: 10.4314/ovj.v6i3.6. Epub 2016 Nov 4.
Tissue-dwelling helminths are known to induce intestinal and systemic inflammation accompanied with host compensatory mechanisms to counter balance nutritional and metabolic deficiencies. The metabolic and immune responses of the host depend on parasite species and tissues affected by the parasite. This study investigated metabolic and immuno-inflammatory responses of mice infected with tissue-dwelling larvae of and explored the relationship between infection, metabolic parameters and Th1/Th17 immune responses. Sixty (60) female BALB/c mice aged between 6 to 8 weeks old were randomly assigned into -infected and control groups. Levels of Th1 (interferon-γ) and Th17 (interleukin-17) cytokines, insulin and blood glucose were determined as well as measurements of body weight, food and water intake. Results showed that during the enteric phase of infection, insulin and IFN-γ levels were significantly higher in the infected group accompanied with a reduction in the trends of food intake and weight loss compared with the control group. During systemic larval migration, trends in food and water intake were significantly altered and this was attributed to compensatory feeding resulting in weight gain, reduced insulin levels and increased IL-17 levels. Larval migration also induced a Th1/Th17 derived inflammatory response. It was concluded that alters metabolic parameters by instigating host compensatory feeding. Furthermore, we showed for the first time that non-encapsulated parasite plays a role in immunomodulating host Th1/Th17 type responses during chronic infection.
组织内寄生蠕虫已知会引发肠道和全身性炎症,并伴有宿主的代偿机制以应对营养和代谢缺陷。宿主的代谢和免疫反应取决于寄生虫的种类以及受寄生虫影响的组织。本研究调查了感染组织内寄生幼虫的小鼠的代谢和免疫炎症反应,并探讨了感染、代谢参数与Th1/Th17免疫反应之间的关系。将60只6至8周龄的雌性BALB/c小鼠随机分为感染组和对照组。测定了Th1(干扰素-γ)和Th17(白细胞介素-17)细胞因子、胰岛素和血糖水平,以及体重、食物和水摄入量。结果显示,在感染的肠道阶段,与对照组相比,感染组的胰岛素和IFN-γ水平显著升高,同时食物摄入量和体重减轻趋势有所降低。在全身性幼虫迁移期间,食物和水摄入量的趋势发生了显著变化,这归因于代偿性进食导致体重增加、胰岛素水平降低和IL-17水平升高。幼虫迁移还诱导了Th1/Th17衍生的炎症反应。得出的结论是,通过促使宿主进行代偿性进食来改变代谢参数。此外,我们首次表明,未包囊的寄生虫在慢性感染期间对宿主Th1/Th17型反应的免疫调节中发挥作用。