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16S 宏基因组学揭示了慢性鼻炎症儿童鼻腔核心微生物群的失调:腺样体肥大和过敏性鼻炎的作用。

16S Metagenomics Reveals Dysbiosis of Nasal Core Microbiota in Children With Chronic Nasal Inflammation: Role of Adenoid Hypertrophy and Allergic Rhinitis.

机构信息

Department of Public Health and Infectious Diseases, Microbiology Section, "Sapienza" University of Rome, Rome, Italy.

Department of Pediatrics, Faculty of Medicine and Odontology, "Sapienza" University of Rome, Rome, Italy.

出版信息

Front Cell Infect Microbiol. 2020 Sep 2;10:458. doi: 10.3389/fcimb.2020.00458. eCollection 2020.


DOI:10.3389/fcimb.2020.00458
PMID:32984078
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7492700/
Abstract

Allergic rhinitis (AR) and adenoid hypertrophy (AH) are, in children, the main cause of partial or complete upper airway obstruction and reduction in airflow. However, limited data exist about the impact of the increased resistance to airflow, on the nasal microbial composition of children with AR end AH. Allergic rhinitis (AR) as well as adenoid hypertrophy (AH), represent extremely common pathologies in this population. Their known inflammatory obstruction is amplified when both pathologies coexist. In our study, the microbiota of anterior nares of 75 pediatric subjects with AR, AH or both conditions, was explored by 16S rRNA-based metagenomic approach. Our data show for the first time, that in children, the inflammatory state is associated to similar changes in the microbiota composition of AR and AH subjects respect to the healthy condition. Together with such alterations, we observed a reduced variability in the between-subject biodiversity on the other hand, these same alterations resulted amplified by the nasal obstruction that could constitute a secondary risk factor for dysbiosis. Significant differences in the relative abundance of specific microbial groups were found between diseased phenotypes and the controls. Most of these taxa belonged to a stable and quantitatively dominating component of the nasal microbiota and showed marked potentials in discriminating the controls from diseased subjects. A pauperization of the nasal microbial network was observed in diseased status in respect to the number of involved taxa and connectivity. Finally, while stable co-occurrence relationships were observed within both control- and diseases-associated microbial groups, only negative correlations were present between them, suggesting that microbial subgroups potentially act as maintainer of the eubiosis state in the nasal ecosystem. In the nasal ecosystem, inflammation-associated shifts seem to impact the more intimate component of the microbiota rather than representing the mere loss of microbial diversity. The discriminatory potential showed by differentially abundant taxa provide a starting point for future research with the potential to improve patient outcomes. Overall, our results underline the association of AH and AR with the impairment of the microbial interplay leading to unbalanced ecosystems.

摘要

变应性鼻炎(AR)和腺样体肥大(AH)是儿童上气道部分或完全阻塞及气流减少的主要原因。然而,目前关于气流阻力增加对 AR 合并 AH 儿童鼻腔微生物组成的影响的数据有限。变应性鼻炎(AR)和腺样体肥大(AH)在该人群中是极为常见的疾病。当这两种疾病同时存在时,已知的炎症阻塞会加剧。在我们的研究中,通过基于 16S rRNA 的宏基因组方法探索了 75 名 AR、AH 或同时存在两种疾病的儿童前鼻孔的微生物群。我们的数据首次表明,在儿童中,炎症状态与 AR 和 AH 患者的微生物群组成的相似变化相关,而与健康状况相关。除了这些变化,我们还观察到在个体间生物多样性的变异性降低,另一方面,这种变化被鼻腔阻塞放大,这可能构成了微生态失调的次要风险因素。在疾病表型与对照组之间发现了特定微生物群的相对丰度存在显著差异。这些分类群中的大多数属于鼻腔微生物群的稳定和定量主导成分,并具有从对照组中区分疾病患者的显著潜力。与所涉及的分类群数量和连通性相比,在疾病状态下观察到鼻腔微生物网络的贫困化。最后,虽然在对照组和疾病相关的微生物群内观察到稳定的共现关系,但它们之间仅存在负相关,这表明微生物亚群可能作为鼻腔生态系统中内稳态状态的维持者发挥作用。在鼻腔生态系统中,与炎症相关的变化似乎影响了微生物群的更亲密组成部分,而不仅仅是微生物多样性的丧失。差异丰度分类群显示出的区分潜力为未来的研究提供了一个起点,有望改善患者的预后。总的来说,我们的结果强调了 AH 和 AR 与微生物相互作用的损害有关,导致生态系统失衡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1640/7492700/9de39afb5227/fcimb-10-00458-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1640/7492700/f4390eeaa14e/fcimb-10-00458-g0001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1640/7492700/b7748e9bb13e/fcimb-10-00458-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1640/7492700/c2c48a73217b/fcimb-10-00458-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1640/7492700/281da72a98b4/fcimb-10-00458-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1640/7492700/9de39afb5227/fcimb-10-00458-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1640/7492700/f4390eeaa14e/fcimb-10-00458-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1640/7492700/e4ebce1ff551/fcimb-10-00458-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1640/7492700/b7748e9bb13e/fcimb-10-00458-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1640/7492700/c2c48a73217b/fcimb-10-00458-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1640/7492700/281da72a98b4/fcimb-10-00458-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1640/7492700/9de39afb5227/fcimb-10-00458-g0006.jpg

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