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Chronic rhinosinusitis (CRS) is a disease caused by inflammation of the paranasal sinuses and its mucous membrane lasting for more than 4 weeks continuously. The aim of our study was to examine the main pathophysiological features of chronic IgE-mediated rhinosinusitis of bacterial etiology according to publications in the Russian Federation and in the world. A search was made through English- and Russian-language literature sources using the following databases: PubMed, MedLine, Web of Science, Russian Science Citation Index, Springer, Scopus, Scientific Research, Google Scholar, Crossref, eLibrary. The epidemiological features of CRS in the Russian Federation, bacterial pathogens and pathophysiological characteristics of CRS were analyzed. A 2-fold increase in the prevalence of CRS was registered over the past 20 years. Prevalence of the disease increases at longer age ranges. Chronic rhinosinusitis ranks first among all chronic diseases in the field of otorhinolaryngology. Allergic rhinitis, asthma, bronchiectasia, immunodeficiencies, cystic fibrosis, primary ciliary dyskinesia and autoimmune diseases are associated with CRS. The most common bacterial pathogens are S. aureus, Staphylococcus epidermidis and Propionibacterium acnes, Prevotella, Streptococcus and Veillonella, and some Gram-negative bacteria, e.g., Pseudomonas aeruginosa (P. aeruginosa), Proteus mirabilis and Klebsiella pneumoniae. Staphylococcus aureus (S. aureus) is involved in pathogenesis of nasal polyps. The colonizing bacteria may contribute to pathogenesis of CRS through the formation of biofilms. Alterations in the sino-nasal microbiome may also contribute to the development of CRS. An association of the CRS and CFTR gene mutations plays a significant role in the pathogenesis of chronic rhinosinusitis. An “immune barrier hypothesis” has been proposed as potential mechanism of CRS. Reduced expression of SPINK5, impaired STAT3 signaling, and T2R38 bitter taste receptor polymorphism have been identified in the pathogenesis of CRS. The T2R38 gene stimulates epithelial cells to produce nitrous oxide with a bactericidal effect, promotes mucociliary elimination of pathogens and prevention of upper respiratory tract infections, the polymorphism of this gene predisposes patients to gram-negative infectious diseases, and therefore is a risk factor for the development of CRS. In addition, antibody deficiency is the most common primary immunodeficiency associated with CRS.Hence, the pathogenesis of chronic IgE-mediated rhinosinusitis of bacterial etiology is associated with defects in innate immunity and mucociliary clearance, influence of the sinonasal microbiome, allergies, and genetic factors. A comprehensive assessment of these factors is necessary for the development of new preventive and therapeutic options for the correction of CRS.
Chronic rhinosinusitis (CRS) is a disease caused by inflammation of the paranasal sinuses and its mucous membrane lasting for more than 4 weeks continuously. The aim of our study was to examine the main pathophysiological features of chronic IgE-mediated rhinosinusitis of bacterial etiology according to publications in the Russian Federation and in the world. A search was made through English- and Russian-language literature sources using the following databases: PubMed, MedLine, Web of Science, Russian Science Citation Index, Springer, Scopus, Scientific Research, Google Scholar, Crossref, eLibrary. The epidemiological features of CRS in the Russian Federation, bacterial pathogens and pathophysiological characteristics of CRS were analyzed. A 2-fold increase in the prevalence of CRS was registered over the past 20 years. Prevalence of the disease increases at longer age ranges. Chronic rhinosinusitis ranks first among all chronic diseases in the field of otorhinolaryngology. Allergic rhinitis, asthma, bronchiectasia, immunodeficiencies, cystic fibrosis, primary ciliary dyskinesia and autoimmune diseases are associated with CRS. The most common bacterial pathogens are S. aureus, Staphylococcus epidermidis and Propionibacterium acnes, Prevotella, Streptococcus and Veillonella, and some Gram-negative bacteria, e.g., Pseudomonas aeruginosa (P. aeruginosa), Proteus mirabilis and Klebsiella pneumoniae. Staphylococcus aureus (S. aureus) is involved in pathogenesis of nasal polyps. The colonizing bacteria may contribute to pathogenesis of CRS through the formation of biofilms. Alterations in the sino-nasal microbiome may also contribute to the development of CRS. An association of the CRS and CFTR gene mutations plays a significant role in the pathogenesis of chronic rhinosinusitis. An “immune barrier hypothesis” has been proposed as potential mechanism of CRS. Reduced expression of SPINK5, impaired STAT3 signaling, and T2R38 bitter taste receptor polymorphism have been identified in the pathogenesis of CRS. The T2R38 gene stimulates epithelial cells to produce nitrous oxide with a bactericidal effect, promotes mucociliary elimination of pathogens and prevention of upper respiratory tract infections, the polymorphism of this gene predisposes patients to gram-negative infectious diseases, and therefore is a risk factor for the development of CRS. In addition, antibody deficiency is the most common primary immunodeficiency associated with CRS.Hence, the pathogenesis of chronic IgE-mediated rhinosinusitis of bacterial etiology is associated with defects in innate immunity and mucociliary clearance, influence of the sinonasal microbiome, allergies, and genetic factors. A comprehensive assessment of these factors is necessary for the development of new preventive and therapeutic options for the correction of CRS.
Background. Chronic polyposis rhinosinusitis is characterized by an immune-dependent type of polyp formation with a defect in local protective factors. The use of local immunomodulators will improve immune protection in the nasal cavity. Aim. To study cytokine levels in nasal secretion and blood serum in patients with chronic polyposis rhinosinusitis after therapy with interferon gamma. Material and methods. To study immunological indices, 32 patients with chronic polyposis rhinosinusitis, who were treated with intranasal interferon gamma, and 30 healthy people (control group) were examined. In the group of patients with the disease, the levels of interleukins-4, -10 and -18, tumor necrosis factor , and secretory immunoglobulin A were determined in the nasal secretion and blood serum before treatment and 1 month after it. Statistical analysis of the results was performed using the Statistica 12.0 software package. The test for normality of distribution in the sample was carried out using the ShapiroWilk test. Most of the parameters did not have a normal distribution; therefore, nonparametric statistical methods were used for further analysis. The description of the results obtained in the study was carried out by calculating the median (Me) and the interquantile range in the form of the 25th and 75th percentiles (Q0.25 and Q0.75). Comparative analysis of quantitative signs in independent groups was performed according to the MannWhitney test, in dependent groups using the Wilcoxon method. Differences were considered significant at p 0.05. Results. Clinical efficacy was assessed according to a 4-point scale: excellent treatment result, good result, satisfactory and unsatisfactory. A good effect of the therapy was 78.1% (25 patients). Unsatisfactory effect was registered in 7 (21.9%) patients. After treatment, a decrease in the content of interleukin-4 (p2=0.000034), interleukin-18 (p2=0.000075), an increase in the level of interleukin-10 (p2=0.033), a decrease in the amount of secretory immunoglobulin A in the nasal secretion (p2=0.0001) took place. The levels of tumor necrosis factor in blood serum were reduced both before treatment compared with the control group (p1=0.005) and after therapy (p2=0.000075). Conclusion. An increase in the content of interleukin-10 in the nasal secretion and a decrease in the level of proinflammatory cytokines interleukin-18, tumor necrosis factor and interleukin-4 in the blood serum after treatment with interferon gamma in patients with chronic polyposis rhinosinusitis may indicate a decrease in the activity of immune inflammation in the nasal cavity.
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