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Review
. 2020 May;40(2):251-263.
doi: 10.1016/j.iac.2019.12.009. Epub 2020 Jan 16.

The Microbiome and Chronic Rhinosinusitis

Do-Yeon Cho  1 , Ryan C Hunter  2 , Vijay R Ramakrishnan  3
Affiliations
Review

The Microbiome and Chronic Rhinosinusitis

Do-Yeon Cho et al. Immunol Allergy Clin North Am. 2020 May.

Abstract

Chronic rhinosinusitis (CRS) is persistent inflammation and/or infection of the nasal cavity and paranasal sinuses. Recent advancements in culture-independent molecular techniques have enhanced understanding of interactions between sinus microbiota and upper airway microenvironment. The dysbiosis hypothesis-alteration of microbiota associated with perturbation of the local ecological landscape-is suggested as a mechanism involved in CRS pathogenesis. This review discusses the complex role of the microbiota in health and in CRS and considerations in sinus microbiome investigation, dysbiosis of sinus microbiota in CRS, microbial interactions in CRS, and development of preclinical models. The authors conclude with future directions for CRS-associated microbiome research.

Keywords: Anaerobe; Animal model of CRS; Chronic rhinosinusitis; Microbiome; Mucin fermentation; Pseudomonas; Sinusitis.

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Figures

Figure 1.
Figure 1.. Model for the role of mucin fermenting bacteria in the progression of CF lung disease, as applied to CRS.
(A) In early life, airway surface liquid harbors a low number of bacteria. Numerous factors allow for establishment of personal local microbiota. (B) Local insult resulting in impaired mucociliary clearance and defective immune responses results in hypoxic environment ideal for expansion of anaerobes. In turn, their ability to degrade and ferment respiratory mucins further modifies the airway environment for secondary colonizers. (C) The abundance of fermentation byproducts facilitates pathogen colonization, heightened inflammation, neutrophil recruitment and further hypoxia. (D) In late stages of disease, host inflammatory responses and epithelial damage increases the abundance of pathogens, while healthy commensals are eliminated by the host and via broad spectrum antibiotic therapies. Data from Flynn JM, Niccum D, Dunitz JM, et al. Evidence and Role for Bacterial Mucin Degradation in Cystic Fibrosis Airway Disease. PLoS Pathog 2016;12(8):e1005846.
Figure 2.
Figure 2.. Concentrations of short chain fatty acids (SCFA) in human mucus samples from CRS with acute exacerbation vs healthy controls.
All 3 SCFAs were significantly higher in CRS (n = 9) compared to control (n = 6): 1) acetate = 0.89 +/− 0.19 versus 0.39 +/ 0.04 mM (p < 0.05); 2) propionate = 0.01 +/− 0.00 versus 0.0045 +/− 0.00 (p < 0.0001); 3) butyrate = 0.002 +/− 0.00 versus 0.0008 +/− 0.00 (p < 0.01).
Figure 3.
Figure 3.. Middle meatus (*) of Human (A) vs Rabbit (B) CRS.
Similar significant polypoid mucosal changes (asterisk). MT: Middle turbinate
See this image and copyright information in PMC

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