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寄生虫感染调节与 2 型糖尿病发病机制相关的系统性促炎细胞因子和趋化因子。

Helminth infection modulates systemic pro-inflammatory cytokines and chemokines implicated in type 2 diabetes mellitus pathogenesis.

机构信息

National Institute of Health-NIRT-International Center for Excellence in Research, Chennai, India.

National Institute for Research in Tuberculosis, Chennai, India.

出版信息

PLoS Negl Trop Dis. 2020 Mar 3;14(3):e0008101. doi: 10.1371/journal.pntd.0008101. eCollection 2020 Mar.

Abstract

BACKGROUND

The prevalence of helminth infections exhibits an inverse association with the prevalence of Type 2 diabetes mellitus (T2DM), and helminths are postulated to mediate a protective effect against T2DM. However, the biological mechanism behind this effect is not known.

AIMS/METHODS: We postulated that helminth infections act by modulating the pro-inflammatory cytokine and chemokine milieu that is characteristic of T2DM. To examine the association of cytokines and chemokines in helminth-diabetes co-morbidity, we measured the plasma levels of a panel of pro-inflammatory cytokines and chemokines in individuals with Strongyloides stercoralis infection (Ss+) and T2DM at the time of Ss diagnosis and then 6 months after definitive anthelmintic treatment along with uninfected control individuals with T2DM alone (Ss-).

PRINCIPAL FINDINGS

Ss+ individuals exhibited significantly diminished levels of the pro-inflammatory cytokines-IL-1α, IL-1β, IL-6, IL-12, IL-18, IL-23, IL-27, G-CSF and GM-CSF and chemokines-CCL1, CCL2, CCL3, CCL11, CXCL1, CXCL2, CXCL8, CXCL9, CXCL10 and CXCL11. In contrast, Ss+ individuals exhibited significantly elevated levels of IL-1Ra. Anthelmintic treatment resulted in increased levels of all of the cytokines and chemokines.

CONCLUSIONS

Thus, helminth infections alleviate and anthelmintic therapy partially restores the plasma cytokine and chemokine levels in helminth-diabetes co-morbidity. Our data therefore offer a plausible biological mechanism for the protective effect of helminth infections against T2DM.

摘要

背景

寄生虫感染的流行与 2 型糖尿病(T2DM)的流行呈负相关,寄生虫被认为对 T2DM 具有保护作用。然而,这种作用的生物学机制尚不清楚。

目的/方法:我们推测,寄生虫感染通过调节 T2DM 特征性的促炎细胞因子和趋化因子环境来发挥作用。为了研究寄生虫感染与糖尿病合并症之间细胞因子和趋化因子的相关性,我们在诊断为 Strongyloides stercoralis 感染(Ss+)和 T2DM 的个体中测量了一组促炎细胞因子和趋化因子的血浆水平,然后在明确驱虫治疗后 6 个月进行了测量,同时测量了未感染的单独患有 T2DM 的个体(Ss-)的血浆水平。

主要发现

Ss+个体表现出明显降低的促炎细胞因子-IL-1α、IL-1β、IL-6、IL-12、IL-18、IL-23、IL-27、G-CSF 和 GM-CSF 以及趋化因子-CCL1、CCL2、CCL3、CCL11、CXCL1、CXCL2、CXCL8、CXCL9、CXCL10 和 CXCL11 的水平。相比之下,Ss+个体表现出明显升高的 IL-1Ra 水平。驱虫治疗导致所有细胞因子和趋化因子水平增加。

结论

因此,寄生虫感染减轻,驱虫治疗部分恢复了寄生虫感染合并糖尿病的血浆细胞因子和趋化因子水平。因此,我们的数据为寄生虫感染对 T2DM 的保护作用提供了一个合理的生物学机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aae2/7069638/f03a323be251/pntd.0008101.g001.jpg

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