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ArticleFrontiers in cellular and infection microbiology2020

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

Massimiliano Marazzato, Anna Maria Zicari, Marta Aleandri, Antonietta Lucia Conte, Catia Longhi, Luca Vitanza, Vanessa Bolognino, Carlo Zagaglia, Giovanna De Castro, Giulia Brindisi and 9 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular and infection microbiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

19 authors at 3 institutions in 1 country.

Massimiliano MarazzatoDepartment of Public Health and Infectious Diseases, Microbiology Section, "Sapienza" University of Rome, Rome, Italy.
Anna Maria ZicariDepartment of Pediatrics, Faculty of Medicine and Odontology, "Sapienza" University of Rome, Rome, Italy.
Marta AleandriDepartment of Public Health and Infectious Diseases, Microbiology Section, "Sapienza" University of Rome, Rome, Italy.
Antonietta Lucia ConteDepartment of Public Health and Infectious Diseases, Microbiology Section, "Sapienza" University of Rome, Rome, Italy.
Catia LonghiDepartment of Public Health and Infectious Diseases, Microbiology Section, "Sapienza" University of Rome, Rome, Italy.
Luca VitanzaDepartment of Public Health and Infectious Diseases, Microbiology Section, "Sapienza" University of Rome, Rome, Italy.
Vanessa BologninoDepartment of Public Health and Infectious Diseases, Microbiology Section, "Sapienza" University of Rome, Rome, Italy.
Carlo ZagagliaDepartment of Public Health and Infectious Diseases, Microbiology Section, "Sapienza" University of Rome, Rome, Italy.
Giovanna De CastroDepartment of Pediatrics, Faculty of Medicine and Odontology, "Sapienza" University of Rome, Rome, Italy.
Giulia BrindisiDepartment of Pediatrics, Faculty of Medicine and Odontology, "Sapienza" University of Rome, Rome, Italy.
Laura SchiaviDepartment of Pediatrics, Faculty of Medicine and Odontology, "Sapienza" University of Rome, Rome, Italy.
Valentina De VittoriDepartment of Pediatrics, Faculty of Medicine and Odontology, "Sapienza" University of Rome, Rome, Italy.
Sofia ReddelUnit of Human Microbiome, Area of Genetics and Rare Diseases, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy.
Andrea QuagliarielloUnit of Human Microbiome, Area of Genetics and Rare Diseases, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy.
Federica Del ChiericoUnit of Human Microbiome, Area of Genetics and Rare Diseases, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy.
Lorenza PutignaniUnit of Parasitology and Area of Genetics and Rare Diseases, Unit of Human Microbiome, Department of Laboratories, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy.
Marzia DuseDepartment of Pediatrics, Faculty of Medicine and Odontology, "Sapienza" University of Rome, Rome, Italy.
Anna Teresa PalamaraDepartment of Public Health and Infectious Diseases, "Sapienza" University of Rome, Laboratory Affiliated to Istituto Pasteur Italia - Fondazione Cenci Bolognetti, San Raffaele Pisana, IRCCS, Rome, Italy.
Maria Pia ConteDepartment of Public Health and Infectious Diseases, Microbiology Section, "Sapienza" University of Rome, Rome, Italy.
Sapienza University of Rome · ITBambino Gesù Children's Hospital · ITIstituto Pasteur · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

AdenoidsMicrobiotaRhinitis, AllergicChildDysbiosisHumansHypertrophyInflammationMetagenomicsRNA, Ribosomal, 16SRNA, Ribosomal, 16Sadenoid hypertrophyallergic rhinitischronic inflammationcore microbiotanasal microbiota

Identifiers

PMID32984078
PMCPMC7492700
OpenAlexW3082363383

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.