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美国的病原体负荷与白细胞端粒长度

Pathogen burden and leukocyte telomere length in the United States.

作者信息

Noppert Grace A, Feinstein Lydia, Dowd Jennifer B, Stebbins Rebecca C, Zang Emma, Needham Belinda L, Meier Helen C S, Simanek Amanda, Aiello Allison E

机构信息

Social Environment and Health, Survey Research Center, Institute for Social Research, University of Michigan, Ann Arbor, MI, USA.

Carolina Population Center, University of North Carolina at Chapel Hill, 123 West Franklin St., Chapel Hill, NC, 27516, USA.

出版信息

Immun Ageing. 2020 Nov 19;17(1):36. doi: 10.1186/s12979-020-00206-9.

DOI:10.1186/s12979-020-00206-9
PMID:33292353
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7677839/
Abstract

BACKGROUND

Prior studies in humans have suggested that telomere shortening may be accelerated by infection, but research on multiple pathogens and use of large population-based study samples has been limited. We estimated cross-sectional associations between seropositivity to five persistent pathogens (Herpes Simplex Virus Type-1 (HSV-1), Herpes Simplex Virus Type-2 (HSV-2), cytomegalovirus (CMV), Helicobacter pylori (H.pylori), and Hepatitis B) as well as total pathogen burden and leukocyte telomere length. Data were derived from the National Health and Nutrition Examination Survey (1999-2000) for individuals 20-49 years of age, N = 1708. We analyzed the influence of each pathogen separately, a pathogen count score and a latent class model of pathogen burden on log telomere length using linear regression models, adjusted for covariates.

RESULTS

Individuals in a latent pathogen burden class characterized by high probabilities of infection with HSV-1, CMV, and H. pylori, had significantly decreased log telomere length (- 0.30 [95% CI: - 0.36, - 0.24]) compared to those in a latent class characterized by low probabilities of all five infections. There were limited significant associations using other pathogen measures.

CONCLUSIONS

These results suggest that infection with specific combinations of pathogens may be one mechanism contributing to accelerated cellular senescence with possible origins early in the life course.

摘要

背景

先前针对人类的研究表明,感染可能会加速端粒缩短,但关于多种病原体以及使用基于大样本人群的研究样本的研究有限。我们估计了血清学阳性反应与五种持续性病原体(1型单纯疱疹病毒(HSV-1)、2型单纯疱疹病毒(HSV-2)、巨细胞病毒(CMV)、幽门螺杆菌(H.pylori)和乙型肝炎)之间的横断面关联,以及总病原体负担与白细胞端粒长度之间的关联。数据来源于针对20至49岁个体的国家健康与营养检查调查(1999 - 2000年),样本量N = 1708。我们使用线性回归模型分别分析了每种病原体、病原体计数得分以及病原体负担的潜在类别模型对对数端粒长度的影响,并对协变量进行了调整。

结果

与所有五种感染概率均较低的潜在类别个体相比,以HSV-1、CMV和幽门螺杆菌感染概率较高为特征的潜在病原体负担类别个体的对数端粒长度显著缩短(-0.30 [95%置信区间:-0.36,-0.24])。使用其他病原体测量方法时,显著关联有限。

结论

这些结果表明,特定病原体组合的感染可能是导致细胞衰老加速的一种机制,其起源可能在生命早期。

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