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肥胖和哮喘患者气道微生物群和免疫介质相关性存在差异

2023/02/01

   摘要
   背景:哮喘和肥胖症都是以慢性炎症为特征的复杂疾病,肥胖相关的严重哮喘与微生物组的差异有关。然而,肥胖者与非严重哮喘患者之间的气道微生物组和微生物群免疫反应关系是否不同,目前尚无定论。
   目的:本研究旨在比较肥胖和非肥胖受试者(有和无轻度中度哮喘)的气道微生物组和微生物群免疫介质之间的相关性。
   方法:本研究采用16S核糖体RNA基因和内部转录间隔区测序对气道(诱导痰液)微生物组和血液及痰液中的细胞因子进行横断面分析,以确定细菌和真菌的分布,并进行多重免疫测定。分析工具包括QIIME 2、线性判别分析效果大小(即LEfSe)、Piphillin和用于生态关联推断的稀疏逆协方差估计(即SPIEC-EASI)。
   结果:无论哮喘状况如何,肥胖都与痰液细菌群落结构和组成的显著差异相关(未加权UniFrac排列方差分析,P=0.02),其中普雷沃氏菌、吉姆菌和链球菌物种的相对丰度较高。在哮喘受试者中,肥胖和非肥胖个体在痰液细菌组成和真菌丰富度方面存在额外差异。相关网络分析表明,肥胖和非肥胖哮喘之间的细胞因子之间的关系存在差异,这些介质与涉及血液PAI-1、痰液IL-1β、GM-CSF、IL-8、TNF-α和几种普雷沃氏菌的特定气道细菌之间的关系也存在差异。
   结论:肥胖本身与痰液微生物组的改变相关,这在轻中度哮喘患者中变化更大。肥胖哮喘患者气道微生物群和免疫标志物关系的显著差异表明,气道微生物可能参与肥胖哮喘的发病机制或结果。

 
(中日友好医院呼吸与危重症医学科 张婧媛 摘译 林江涛 审校)
(Allergy Clin Immunol. 2022 Dec 23:S0091-6749(22)02534-9. doi: 10.1016/j.jaci.2022.11.024.)

 

 
Airway microbiota and immune mediator relationships differ in obesity and asthma.
 
Kozik AJ, Begley LA, Lugogo N, Baptist A, Erb-Downward J, Opron K, Huang YJ. J
 
Abstract
BACKGROUND:Asthma and obesity are both complex conditions characterized by chronic inflammation, and obesity-related severe asthma has been associated with differences in the microbiome. However, whether the airway microbiome and microbiota-immune response relationships differ between obese persons with or without nonsevere asthma is unestablished.
OBJECTIVES: We compared the airway microbiome and microbiota-immune mediator relationships between obese and nonobese subjects, with and without mild-moderate asthma.
METHODS:We performed cross-sectional analyses of the airway (induced sputum) microbiome and cytokine profiles from blood and sputum using 16S ribosomal RNA gene and internal transcribed spacer region sequencing to profile bacteria and fungi, and multiplex immunoassays. Analysis tools included QIIME 2, linear discriminant analysis effect size (aka LEfSe), Piphillin, and Sparse inverse covariance estimation for ecological association inference (aka SPIEC-EASI).
RESULTS:Obesity, irrespective of asthma status, was associated with significant differences in sputum bacterial community structure and composition (unweighted UniFrac permutational analysis of variance, P = .02), including a higher relative abundance of Prevotella, Gemella, and Streptococcus species. Among subjects with asthma, additional differences in sputum bacterial composition and fungal richness were identified between obese and nonobese individuals. Correlation network analyses demonstrated differences between obese and nonobese asthma in relationships between cytokine mediators, and these together with specific airway bacteria involving blood PAI-1, sputum IL-1β, GM-CSF, IL-8, TNF-α, and several Prevotella species.
CONCLUSIONS:Obesity itself is associated with an altered sputum microbiome, which further differs in those with mild-moderate asthma. The distinct differences in airway microbiota and immune marker relationships in obese asthma suggest potential involvement of airway microbes that may affect mechanisms or outcomes of obese asthma.




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