FEATURES OF REPOLARIZATION OF THE CYTOKINE PROFILE OF PATIENTS WITH CHRONIC RHINOSINUSITIS WITH COMORBID CONDITIONS

Abstract

Relevance. One of the most common diseases in otolaryngology is rhinosinusitis, which manifests itself as nasal congestion, headache, nasal discharge and other symptoms. Sometimes rhinosinusitis accompanies seasonal acute respiratory viral infections, can be a manifestation of seasonal and year-round allergies, and develops with dysfunctions of the immune system. If the symptoms of rhinosinusitis last more than 12 weeks, chronic rhinosinusitis is diagnosed. Comorbid conditions (curvature of the nasal septum, bronchial asthma, etc.) increase the manifestations of chronic rhinosinusitis

The purpose of the work: to study the features of cytokine regulation in chronic rhinosinusitis with comorbid diseases.

Materials and methods. 84 people with rhinosinusitis and 100 healthy people were examined. The study included patients with CRS (n=29), CRS and deviated septum (n=24), chronic rhinosinusitis and bronchial asthma (n=31) and a control group (n=100) consisting of practically healthy individuals. The case-control study was performed in the laboratory of clinical pathophysiology of the Research Institute of the Ministry of Railways. The materials for the study were venous blood and nasal discharge. The content of TNF-α, IFN-γ, IL-2, IL-6, IL-4, IL-10 was determined by ELISA using Vector-Best reagents (Novosibirsk) and a Muitiskan FC spectrophotometer. Statistical processing was performed using the Statistica 10.0 program. To describe samples with a distribution different from normal, the median (Me) and interquartile range (IQR), defined as the difference between the 75th (Q3) and 25th (Q1) percentiles, were used. This approach allows us to present the central tendency and measure of data dispersion, minimizing the impact of outliers (Wilcox, 2012).

Results and discussion.

All patients with CRS and comorbid conditions systemically and locally show unidirectional changes in the form of an increase in proinflammatory and anti-inflammatory cytokines, which indicates the development of immune responses by Th1/Th2 mechanisms, while the presence of comorbid conditions (curvature of the nasal septum, bronchial asthma) enhances immune responses.

Conclusions.

In comorbid conditions, the content of cytokines is statistically significantly increased relative to not only the control group, but also patients with CRS. Maximum concentrations of cytokines are detected when CRS is combined with bronchial asthma.

1. СПИСОК ЛИТЕРАТУРЫ.

2. Astaf`eva, N.G. Rinity`: immunny`e i neimmunny`e osnovy` geterogennogo sindroma / N.G. Astaf`eva // Vestnik terapevta, 2019, Vol. 2,pp. 38., URL: https://journal.therapy.school/statyi/rinity-immunnye-i-neimmunnye-osnovy-geterogennogo-sindroma/

3. Isaev, P.Yu. Citokiny` "kozhnogo okna" pri bronxial`noj astme v sochetanii s pishhevoj allergiej / P.Yu. Isaev, V.V. Klimov, V.S. Sviridova // Rossijskij immunologicheskij zhurnal, 2018, Vol.12, no. 3, pp. 317–320., URL: https://rusimmun.ru/jour/issue/view/17

4. Trushina, E.Yu. Rol` citokinov kak molekulyarny`x markerov vospaleniya pri neallergicheskoj bronxial`noj astme / E.Yu. Trushina, E.M. Kostina, N.I. Baranova // Sovremenny`e problemy` nauki i obrazovaniya, 2018,Vol. 4, pp. 79., https://science-education.ru/ru/article/view?id=27799

5. Boita M., Bucca C., Riva G., Heffler E. Release of Type 2 Cytokines by Epithelial Cells of Nasal Polyps. J. Immunol. Res., 2016, no. 2016, pp. 264-287., https://doi.org/10.1155/2016/2643297

6. Fokkens W.J., Lund, V.J., Hopkins C.; Hellings P.W., Kern, R., Reitsma, S., Toppila-Salmi, S., Bernal-Sprekelsen, M., Mullol, J., Alobid, I.. European Position Paper on Rhinosinusitis and Nasal Polyps 2020. Rhinology, 2020, no. 58, pp. 1-464., https://doi.org/10.4193/Rhin20.600.

7. Jiao J., Duan S., Meng N., Li Y., Fan E. Role of IFN-gamma, IL-13, and IL-17 on mucociliary differentiation of nasal epithelial cells in chronic rhinosinusitis with nasal polyps. Clin. Exp. Allergy, 2016, no. 46, pp. 449-460.,https://doi.org/10.1111/cea.12644.

8. Klingler A.I., Stevens W.W., Tan B.K., Peters A.T., Poposki J.A., Grammer L.C., Welch K.C., Smith S.S., Conley D.B., Kern R.C. Mechanisms and biomarkers of inflammatory endotypes in chronic rhinosinusitis without nasal polyps. J. Allergy Clin. Immunol., 2021, no. 147, pp. 1306-1317.,https://doi.org/10.1056/NEJMoa2028395.

9. Meng J., Zhou P., Liu Y., Liu F., Yi X., Liu S., Holtappels G., Bachert C., Zhang N. The development of nasal polyp disease involves early nasal mucosal inflammation and remodelling. Braz. j. otorhinolaryngol., 2013, no 1, pp. 3-39., https://doi.org/10.1016/j.bjorl.2023.01.007

10. Mueller S.K., Wendler O., Nocera A., Grundtner P. Escalation in mucus cystatin 2, pappalysin-A, and periostin levels over time predict need for recurrent surgery in chronic rhinosinusitis with nasal polyps. Int. Forum Allergy Rhinol., 2019, no. 9, 1212-219., https://doi.org/10.1002/alr.22407.

11. Nagarkar D.R., Poposki J.A., Tan B.K. Thymic stromal lymphopoietin activity is increased in nasal polyps of patients with chronic rhinosinusitis. J. Allergy Clin. Immunol, 2013, no. 132, pp. 593-600, https://doi.org/10.1016/j.jaci.2013.04.005

12. Park S.K., Jin Y.D., Park Y.K., Yeon S.H., Xu J., Han R.N., Rha K.S. IL-25-induced activation of nasal fibroblast and its association with the remodeling of chronic rhinosinusitis with nasal polyposis. PLoS ONE 2017, 12, e0181806., https://doi.org/10.1371/journal.pone.0181806

13. Soler Z.M., Yoo, F., Schlosser, R.J.; Mulligan, J., Ramakrishnan V.R., Beswick D.M., Alt J.A.; Mattos, J.L. Correlation of mucus inflammatory proteins and olfaction in chronic rhinosinusitis. Int. Forum Allergy Rhinol, 2020, no. 10, pp. 343-355., https://doi.org/doi.org/10.1016/j.jaci.2021.01.021

14. Soyka M.B., Wawrzyniak P., Eiwegger T., Holzmann D., Treis A., Wanke K. Efective epithelial barrier in chronic rhinosinusitis: The regulation of tight junctions by IFN-gamma and IL-4. J. Allergy Clin. Immunol, 2012, no. 130, pp. 1087-1096., https://doi.org/10.1016/j.jaci.2012.05.052.

15. Wise S.K., Laury A.M., Katz E.H., Den Beste, K.A. Interleukin-4 and interleukin-13 compromise the sinonasal epithelial barrier and perturb intercellular junction protein expression. Int. Forum Allergy Rhinol., 2014, no. 4, pp. 361-370., https://doi.org/10.1002/alr.21298.

16. Yan B., Lou H., Wang, Y., Li, Y., Meng Y., Qi, S. Epithelium-derived cystatin SN enhances eosinophil activation and infiltration through IL-5 in patients with chronic rhinosinusitis with nasal polyps. J. Allergy Clin. Immunol., 2019, no. 144, pp. 455-469., https://doi.org/doi.org/10.1016/j.jaci.2019.03.026