The Intersection Between Schistosoma mansoni Infection and Dyslipidemia Modulates Inflammation in the Visceral Adipose Tissue of Swiss Webster Mice.

IF 2.6 4区 医学 Q2 INFECTIOUS DISEASES
Thainá de Melo, Isadora do Monte Silveira Bruno, Luciana Brandão-Bezerra, Silvia Amaral Gonçalves da Silva, Christiane Leal Corrêa, Luciana Silva Rodrigues, José Roberto Machado-Silva, Renata Heisler Neves
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Abstract

Background: Dyslipidemia and schistosomiasis are major public health challenges, particularly in endemic regions where their coexistence may influence host metabolism and immune responses. This study aimed to evaluate visceral adipose tissue (AT) remodeling in a murine model of acute Schistosoma mansoni infection combined with diet-induced dyslipidemia. Methodology: Female Swiss Webster mice were fed either a standard or high-fat diet (HFD) for 29 weeks and infected with S. mansoni at week 20. Nine weeks after infection, biochemical, morphometric, histopathological, and immunological analyses were performed. Results: The HFD promoted weight gain and dyslipidemia, while S. mansoni infection alone did not alter lipid profiles but partially mitigated the metabolic effects of the HFD. Morphometric analysis revealed adipocyte hypertrophy and reduced cell number in HFD-fed animals. In HFD-fed infected mice, infection partially reversed hypertrophy, suggesting a modulatory effect on AT remodeling. Histopathological examinations showed that while a HFD induced mild inflammation, infection led to intense leukocyte infiltration, hyperemia, and plasma cell degeneration. Peritoneal lavage confirmed a proinflammatory immune profile. Conclusions: These findings indicate that the interaction between a HFD and S. mansoni infection exacerbates adipose tissue inflammation and metabolic alterations, highlighting the complex interplay between parasitic infection, diet, and immune-metabolic regulation.

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曼氏血吸虫感染与血脂异常的交叉调节瑞士韦氏小鼠内脏脂肪组织的炎症。
背景:血脂异常和血吸虫病是主要的公共卫生挑战,特别是在流行地区,它们的共存可能影响宿主的代谢和免疫反应。本研究旨在评估急性曼氏血吸虫感染合并饮食性血脂异常小鼠模型的内脏脂肪组织(AT)重塑。方法:雌性瑞士韦伯斯特小鼠分别饲喂标准或高脂肪饮食(HFD) 29周,并在第20周感染曼氏梭菌。感染后9周,进行生化、形态学、组织病理学和免疫学分析。结果:HFD促进体重增加和血脂异常,而曼氏梭菌感染单独不改变脂质谱,但部分减轻了HFD的代谢作用。形态计量学分析显示,饲喂hfd的动物脂肪细胞肥大,细胞数量减少。在喂食hfd的感染小鼠中,感染部分逆转了肥大,表明对AT重塑有调节作用。组织病理学检查显示,虽然HFD引起轻度炎症,但感染导致强烈的白细胞浸润,充血和浆细胞变性。腹腔灌洗证实有促炎免疫特征。结论:这些发现表明,HFD和曼氏梭菌感染之间的相互作用加剧了脂肪组织炎症和代谢改变,突出了寄生虫感染、饮食和免疫代谢调节之间的复杂相互作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Tropical Medicine and Infectious Disease
Tropical Medicine and Infectious Disease Medicine-Public Health, Environmental and Occupational Health
CiteScore
3.90
自引率
10.30%
发文量
353
审稿时长
11 weeks
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