Dataset Information

Antibiotic-Dependent Relationships Between the Nasal Microbiome and Secreted Proteome in Nasal Polyps.

ABSTRACT:

Purpose

Chronic rhinosinusitis (CRS) is a heterogeneous chronic inflammatory condition of the paranasal sinuses and nasal passages. Although antibiotics are used to reduce inflammation or to treat an episode of acute rhinosinusitis, their effects on the nasal environment and host response in CRS is unclear.

Methods

We analyzed the effects of antibiotics on the nasal microbiome and secreted proteome in CRS using multi-omic analysis. Nasal secretions were collected from 29 controls, 30 CRS patients without nasal polyps (NP), and 40 CRS patients with NP. A total of 99 subjects were divided into 2 groups that included subjects who had taken antibiotics 3 months prior to sampling and those who had not. We performed 16S ribosomal DNA sequence analyses and Orbitrap mass spectrometry-based proteomic analyses. Spearman correlation was used to assess the correlations between the nasal microbiome and secreted proteome.

Results

The associations between the nasal microbiome and secreted proteome were noted in subjects who had used antibiotics. Antibiotics could have stronger effects on their associations in patients with CRS with NP than in those without. It remains unknown whether these holistic changes caused by antibiotics are beneficial or harmful to CRS, however, the associations could be differentially affected by disease severity.

Conclusion

These findings provide new insight into the nasal environment and the host response in CRS.

SUBMITTER: Kim YS

PROVIDER: S-EPMC8255347 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:ObjectivesPrevious research has suggested connections between specific inflammatory cytokines and nasal conditions, including Allergic Rhinitis (AR), Chronic Rhinosinusitis (CRS), and Nasal Polyps (NP). However, a lack of robust research establishing the causal underpinnings of them. This Mendelian Randomization (MR) study aims to evaluate the causal relationships between 41 inflammatory cytokines and the incidence of AR, CRS and NP.MethodsThis study employed a two-sample MR design, harnessing genetic variations derived from publicly accessible genome-wide association studies (GWAS) datasets. AR data was sourced from a GWAS with 25,486 cases and 87,097 controls (identifier: ukb-b-7178). CRS data originated from a GWAS encompassing 1,179 cases and 360,015 controls (identifier: ukb-d-J32). NP data was extracted from a GWAS involving 1,637 cases and 335,562 controls (identifier: ukb-a-541). The data for 41 inflammatory cytokines were obtained from an independent GWAS encompassing 8,293 participants. Inverse variance weighted (IVW), MR Egger regression and Weighted median were used to evaluate the causalities of exposures and outcomes. A range of sensitivity analyses were implemented to assess the robustness of the results.ResultsThe results revealed significant associations between elevated circulating levels of MIP-1α (odds ratio, OR: 1.01798, 95% confidence interval, CI: 1.00217-1.03404, p = 0.02570) and TNF-α (OR: 1.01478, 95% CI: 1.00225-1.02746, p = 0.02067) with an augmented risk of AR in the IVW approach. Heightened levels of circulating IL-2 exhibited a positive correlation with an increased susceptibility to NP in the IVW approach (OR: 1.00129, 95% CI: 1.00017-1.00242, p = 0.02434), whereas elevated levels of circulating PDGF-BB demonstrated a decreased risk of NP (OR: 0.99920, 95% CI: 0.99841-0.99999, p = 0.047610). The MR analysis between levels of 41 inflammatory cytokines and the incidence of CRS yielded no positive outcomes.ConclusionThis investigation proposes a potential causal association between elevated levels of MIP-1α and TNF-α with an elevated risk of AR, as well as an increased risk of NP linked to elevated IL-2 levels. Furthermore, there appears to be a potential association between increased levels of circulating PDGF-BB and a reduced risk of NP.