Chronic Rhinosinusitis-Microbiological Etiology, Potential Genetic Markers, and Diagnosis

Abstract

Chronic rhinosinusitis (CRS) is a significant public health problem. Bacterial colonization and impaired mucociliary clearance play a significant role in the inflammatory process. Several inflammatory pathways and host defense elements are altered in CRS, which may contribute to observed differences in the microbiome. To date, researching CRS has been difficult due to limited access to the studied tissue and a lack of available biomarkers. Ongoing scientific research is increasingly based on simple and objective analytical methods, including sensors, detection with PCR, and sequencing. Future research on microbiota and human factors should also include genomics, transcriptomics, and metabolomics approaches. This report analyzes the changes that occur in the paranasal sinuses of people with acute and chronic rhinosinusitis, the composition of the microbiota, the human genetic markers that may shed light on the predisposition to CRS, and the advantages and disadvantages of classical and molecular diagnostic methods, as well as addressing the difficulties of sinusitis treatment.

Keywords: diagnostic methods; microbiota; predisposition to CRS; probiotics; problem of susceptibility to antibiotics; sinusitis.

Figure 1

Classification of CRS based on the latest consensus (EPOS2020) [12]. (A). Classifying primary CRS taking into account endotypes and phenotypes. (B). Classifying secondary CRS taking into account endotypes and phenotypes. Legend: AFRS—allergic fungal rhinosinusitis; CRSwNP—CRS with nasal polyps; ECRS—eosinophilic chronic rhinosinusitis; CF—cystic fibrosis; PCD—primary ciliary dyskinesia; CCAD—central compartment atopic disease; GPA—granulomatosis with polyangiitis, (known as Wegener’s granulomatosis, WG); EGPA—eosinophilic granulomatosis with polyangiitis, formerly Churg-Strauss Syndrome.

Figure 2

Summary of targets and genetic markers associated with CRS susceptibility. A description of the changes for particular genes is presented in the text.

Figure 3

Promising markers for the diagnosis of CRS, obtained by genomic, proteomic and metabolomic analysis and the most commonly identified microbiota in CRS. Legend: ALOX5—arachidonate 5-lipoxygenase; ALOX5AP—arachidonate 5-lipoxygenase-activating protein; AMY-1A—amylase α1A; CFTR—cystic fibrosis transmembrane conductance regulator; CPBP—Clara cell phospholipid-binding protein; CRsNP—CRS without nasal polyps; CRwNP—CRS with nasal polyps; CYSLTR1—cysteinyl leukotriene receptor 1; GSTT1—glutathione S-transferases; HLA—human leukocyte antigen; IL22RA1—interleukin 22 receptor subunit alpha 1; IL-33—interleukin-33, IRAK4—interleukin-1 receptor-associated kinase 4; MUC1, MUC4, MUC5AC, MUC5B—mucins family; NOS2A—nitric oxide synthase gene; PARS-2—prolyl-tRNA synthetase 2; T2R38s—bitter taste receptors 38; TGFB1—transforming growth Factor Beta 1; Th1, Th2—type cytokines; TNFA—tumor necrosis factor gene.