Obesity and ancylostomiasis are considered public health problems. Recent studies have shown that infection by intestinal helminths in obese individuals can ameliorate metabolic disorder and improve glucose tolerance by decreasing both insulin resistance and low-intensity inflammation. However, few helminth species have been studied in this context, and some modulation mechanisms still require deeper investigation. Therefore, the present work aimed to investigate the role of experimental infection with Ancylostoma ceylanicum in the modulation of the immune response in an obese experimental model. Four groups of hamsters were used as follows: two groups were submitted to a hyperlipidic and hypercaloric diet capable of inducing obesity, one infected and the other uninfected; and two normonourished control groups, one infected and one uninfected by A. ceylanicum. Biochemical, haematological, parasitological and immunological parameters were evaluated. The results demonstrated that A. ceylanicum infection accentuated weight loss in obese animals compared to normonourished animals. However, obesity reduced the recovery of worms and oviposition of the females, and both infected groups showed decreased levels of haemoglobin, albumin, iron and erythrocytes. Significant relations were observed for pathogenesis in the following cases: infection interfered in lipid metabolism, which increased levels of total cholesterol and triglycerides in the obese group, and caused a decrease in HDL levels in both groups. Obesity led to an increase in glucose levels, and the infection exacerbated this parameter in both the normonourished and obese groups. Inflammation was intensified in obese animals that showed elevated macrophage and neutrophil activation in adipose tissue, enlargement of the spleen and accumulation of lipids in the liver and faeces. Despite the decrease in IFN-γ levels, the infection did not potentiated the expression of the Foxp3, IL-10 and IL-2 transcription factor for any of the infected groups, markers that could positively compensate the host from the damage caused by obesity.

肥胖和尿道脱口被认为是公共卫生问题。最近的研究表明，肥胖个体中肠道蠕虫感染可通过降低胰岛素抵抗和低强度炎症来改善代谢紊乱并改善葡萄糖耐量。但是，在这种情况下，很少研究蠕虫种类，并且某些调节机制仍需要更深入的研究。因此，本研究旨在调查实验性头孢小锥虫感染的作用。在肥胖的实验模型中调节免疫反应。使用四组仓鼠，如下：两组接受能够诱发肥胖的高脂和高热量饮食，一种感染而另一种未感染。和两个normonourished对照组，一个感染者和一个由未感染A. ceylanicum。评估了生化，血液学，寄生虫学和免疫学参数。结果表明，A。ceylanicum与正常动物相比，肥胖动物的感染加剧了体重减轻。然而，肥胖减少了蠕虫的恢复和雌性的产卵，并且两个感染组均显示血红蛋白，白蛋白，铁和红细胞的水平降低。在以下情况下，观察到了发病机理的重要关系：感染干扰了脂质代谢，肥胖组中总胆固醇和甘油三酯的水平增加，而两组中HDL的水平降低。肥胖导致葡萄糖水平升高，并且在正常饮食和肥胖人群中，感染都会加剧该参数。肥胖动物的炎症加剧，在脂肪组织中巨噬细胞和嗜中性粒细胞活化升高，脾脏肿大，肝脏和粪便中脂质堆积。