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

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.

Airway Microbiome and Serum Metabolomics Analysis Identify Differential Candidate Biomarkers in Allergic Rhinitis

“…), and Actinobacteria (e.g., Corynebacterium spp.) ( 33 , 34 ). The increase of the phyla Actinobacteria and the genera Klebsiella , Prevotella and Staphylococcus in the upper respiratory tract of AR patients may be related to the enlargement of the inferior turbinates during the allergic state, increasing epithelial permeability, allowing the presence of abnormal fluid accumulation on the airway surface and affecting the balance of the commensal microbiota in the nasal mucosa.…”

“…Thus, the dietary modulation of gut microbiota was suggested to be involved in allergy processes ( 41 , 42 ) and to influence the microbiota alterations in the airway and gut. Not only adults, but also children with chronic rhinitis have been shown to have significant differences in the relative abundance of specific microbiota compared to children with healthy conditions ( 34 , 43 ). These results support our findings that the IgE mediated inflammatory response characteristic of AR may influence the airway microbiota.…”

IL-32 exacerbates adenoid hypertrophy via activating NLRP3-mediated cell pyroptosis, which promotes inflammation

“…The inflammatory response has been extensively reported to contribute to the occurrence and progression of AH ( 7 , 25 ). The present study aimed to analyze the association between the pro-inflammatory cytokine IL-32 and AH.…”

“…The inflammatory stimulation of epithelial cells on the surface of adenoids can directly or indirectly cause rhinitis and sinusitis ( 6 ). Inflammatory products that invade the eustachian tube on both sides can cause otitis media ( 7 ). However, the related underlying mechanisms of adenoid epithelial cell hypertrophy have not been fully elucidated.…”

Effects of Heat-Killed Lactococcus lactis Strain Plasma on Skin Homeostasis-Related Genes and the Skin Microbiome among Healthy Adults: A Randomized Controlled Double-Blind Study

“…In the LEfSe analysis, more genera and species were identified as the candidates most likely to explain differences between 0 W and 8 W in the placebo group than in the LC-plasma group. Most of these candidates accounted for less than 0.1% of total microbiota and are not listed in Tables S2 and S3; however, several have been reported to be more abundant in the mucus membrane of head tissues, including Dolosigranulum in sinus [26], Cloacibacterium in laryngeal [27], and Cedecea in nasal membranes [28]. In addition, such microbiota have also been reported as important markers of disease or lifestyle, such as chronic rhinosinusitis, smoking, and adenoid hypertrophy.…”