Рецепт. 2020; : 289-298
Система антиоксидантной защиты и цитокиновое звено иммунитета в течении и прогрессировании гастроэзофагеальной рефлюксной болезни у лиц молодого возраста с аутоиммунным воспалением
https://doi.org/10.34883/PI.2020.2.2.037Аннотация
Цель. Определить состояние антиоксидантной системы и провоспалительного звена цитокиновой сети при развитии воспалительной реакции различной степени выраженности в слизистой пищевода у лиц молодого возраста с гастроэзофагеальной рефлюксной болезнью (ГЭРБ), которая протекает на фоне аутоиммунного тиреоидита (АИТ). Материалы. Обследовано 207 пациентов – студентов в возрасте от 18 до 25 лет и с длительностью анамнеза по изучаемым нозологиям до 3 лет. Определены три группы исследуемых: 120 пациентов с коморбидностью ГЭРБ и АИТ, 45 – с изолированной ГЭРБ и 42 с изолированным АИТ. Проведено изучение провоспалительных цитокинов – каспазы-1 и ИЛ-18, а также показателей антиоксидантной системы (АОС) – общей антиоксидантной активности (АОА) и митохондриального фермента второй фазы АОС (супероксиддисмутазы 2 (СОД2)). Результаты. Установлено, что при всех нозологических формах у лиц молодого возраста наблюдается увеличение синтеза каспазы-1 и ИЛ-18 – маркеров воспалительного процесса и аутоиммунных реакций (ИЛ-18). Причем у пациентов с АИТ в большей степени наблюдались изменения в синтезе ИЛ-18 (латентный процесс аутоиммунного характера), в то время как при ГЭРБ – каспазы-1 (банальная воспалительная реакция). Показано, что на уровень провоспалительных цитокинов оказывали влияние морфологические изменения слизистой пищевода: максимальные их величины регистрировались при эрозивной форме заболевания. Течение ГЭРБ и АИТ у лиц молодого возраста происходило на фоне снижения показателя общей АОА и повышения синтеза митохондриального фермента СОД2, что подтверждает переход контроля над образованием продуктов окислительного стресса на вторую фазу антиоксидантной системы. Полученные результаты можно использовать для характеристики течения ГЭРБ и АИТ, а также контроля лечебных мероприятий.
Список литературы
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14. Jung J.H., Song G.G., Kim J.H., Choi S.J. (2016) Association of Interleukin 10 Gene Polymorphisms with Autoimmune Thyroid Disease: Meta- Analysis Scand. J. Immunol. vol. 84, no 5, pp. 272–277.
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19. Luty J., Ruckemann-Dziurdzińska K., Witkowski J.M., Bryl E. (2019) Immunological aspects of autoimmune thyroid disease – Complex interplay between cells and cytokines Cytokine, vol. 116, pp. 128–133. Available at: https://doi.org/10.1016/j.cyto.2019.01.003
20. Islam M.O., Bacchetti T., Ferretti G. (2019). Alterations of Antioxidant Enzymes and Biomarkers of Nitro-oxidative Stress in Tissues of Bladder Cancer. Oxidative medicine and cellular longevity, vol.2019, 2730896. Available at: https://doi.org/10.1155/2019/2730896).
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22. Boucher D., Monteleone M., Coll R.C. (2018) Caspase-1 self-cleavage is an intrinsic mechanism to terminate inflammasome activity. J Exp Med, vol. 215, no 3, pp. 827–840. doi: https://doi.org/10.1084/jem.20172222
23. Yasuda K., Nakanishi K., & Tsutsui H. (2019). Interleukin-18 in Health and Disease. International journal of molecular sciences, vol. 20, no 3, pp. 649.https://doi.org/10.3390/ijms20030649.
24. Boraschi D., & Dinarello C. (2007). IL-18 in autoimmunity: Review. European cytokine network. vol. 17, pp. 224–252.
25. Solodenova M.E. (2009) Clinical features of lipid peroxidation and the function of antioxidant protection in patients with various types of gastroesophageal reflux disease: dis. PhD. Sib. State Medical University.
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Recipe. 2020; : 289-298
System of Antioxidant Protection and Cytokine Link of Immunity in the Course and Progression of Gastroesophageal Reflux Disease in Young People with Autoimmune Inflammation
https://doi.org/10.34883/PI.2020.2.2.037Abstract
References
1. Chaplin D.D. (2010) Overview of the immune response. The Journal of allergy and clinical immunology, vol. 125, no 2, pp. 3–23. Available at: https://doi.org/10.1016/j.jaci.2009.12.980
2. Hanaa Ali Hassan Mostafa Abd El-Aal (2012). Lipid Peroxidation End-Products as a Key of Oxidative Stress: Effect of Antioxidant on Their Production and Transfer of Free Radicals. Lipid Peroxidation, Angel Catala, IntechOpen. doi: 10.5772/45944.
3. Borza C., Muntean D., Dehelean C. (2013) Oxidative Stress and Lipid Peroxidation – A Lipid Metabolism Dysfunction, Lipid Metabolism, Rodrigo Valenzuela Baez, IntechOpen. doi: 10.5772/51627
4. Justiz Vaillant A.A., Jan A. (2020) Physiology, Immune Response. [Updated 2019 Mar 21]. StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing, Jan. Available at: https://www.ncbi.nlm.nih.gov/books/NBK539801/
5. José Luis Muñoz Carrillo, Flor Pamela Castro García, Oscar Gutiérrez Coronado, María Alejandra Moreno García and Juan Francisco Contreras Cordero (2017). Physiology and Pathology of Innate Immune Response Against Pathogens, Physiology and Pathology of Immunology. Nima Rezaei, IntechOpen. doi: 10.5772/intechopen.70556.
6. Willadsen T.G., Bebe A., Køster-Rasmussen R. (2016). The role of diseases, risk factors and symptoms in the definition of multimorbidity – a systematic review. Scandinavian journal of primary health care, vol. 34, no 2, pp. 112–121. Available at: https://doi.org/10.3109/02813432. 2016.1153242)
7. World Health Organisation (2009). Global health risks: Mortality and burden of disease attributable to selected major risks. Geneva: World Health Organization. Available at: http://www.who.int/healthinfo/global_burden_disease/global_health_risks/en/
8. Australian Institute of Health and Welfare (2015). Risk factors to health. Retrieved June 23, 2015. Available at: http://www.aihw.gov.au/risk-factors/
9. Taub D.D. (2008). Neuroendocrine interactions in the immune system. Cellular immunology, vol. 252, no 1–2, pp. 1–6. Available at: https://doi. org/10.1016/j.cellimm.2008.05.006
10. Tomer Y., & Huber A. (2009). The etiology of autoimmune thyroid disease: a story of genes and environment. Journal of autoimmunity, vol. 32, no 3–4, pp. 231–239. Available at: https://doi.org/10.1016/j.jaut.2009.02.007
11. Gryaznova M.A., Khamnueva L.Yu. (2017). The specific feature of cytokines regulation by pathology of thyroid disease (review) Health and Education Millennium, vol. 19, no 7, pp. 33–39.
12. Salvi M., Pedrazzoni M., Girasole G. (2000). Serum concentrations of proinflammatory cytokines in Graves’ disease: Effect of treatment, thyroid function, ophthalmopathy and cigarette smoking. European journal of endocrinology/European Federation of Endocrine Societies, vol. 143, pp. 197–202. 10.1530/eje.0.1430197.
13. Nikitin Y.P., Rymar O.D., Maksimov,V.N. (2009). Polymorphism G(-308)A gene TNF, association with susceptibility to autoimmune thyroid disease in population of Novosibirsk. Siberian Scientific Medical Journal, vol. 1, pp. 69–73.
14. Jung J.H., Song G.G., Kim J.H., Choi S.J. (2016) Association of Interleukin 10 Gene Polymorphisms with Autoimmune Thyroid Disease: Meta- Analysis Scand. J. Immunol. vol. 84, no 5, pp. 272–277.
15. Ganesh B.B., Bhattacharya P., Gopisetty A., & Prabhakar B.S. (2011). Role of cytokines in the pathogenesis and suppression of thyroid autoimmunity. Journal of interferon & cytokine research: the official journal of the International Society for Interferon and Cytokine Research, vol. 31, no 10, pp. 721–731. Available at: https://doi.org/10.1089/jir.2011.0049
16. Brent G.A. (2008) Graves’ disease. N. Engl. J. Med., vol. 358, no 24, pp. 2594–2605.
17. Eusebi L.H., Ratnakumaran R., Yuan Y. (2018) Global prevalence of, and risk factors for, gastro-oesophageal reflux symptoms: a meta-analysis. Gut., vol. 67, no 3, pp. 430–440. doi:10.1136/gutjnl-2016–313589.
18. Mikoś H, Mikoś M, Obara-Moszyńska M, Niedziela M (2014) The role of the immune system and cytokines involved in the pathogenesis of autoimmune thyroid disease (AITD). Endokrynol Pol., vol. 65, no 2, pp. 150–155. doi: 10.5603/EP.2014.0021.
19. Luty J., Ruckemann-Dziurdzińska K., Witkowski J.M., Bryl E. (2019) Immunological aspects of autoimmune thyroid disease – Complex interplay between cells and cytokines Cytokine, vol. 116, pp. 128–133. Available at: https://doi.org/10.1016/j.cyto.2019.01.003
20. Islam M.O., Bacchetti T., Ferretti G. (2019). Alterations of Antioxidant Enzymes and Biomarkers of Nitro-oxidative Stress in Tissues of Bladder Cancer. Oxidative medicine and cellular longevity, vol.2019, 2730896. Available at: https://doi.org/10.1155/2019/2730896).
21. Birben E., Sahiner U., Sackesen C., Erzurum S., Kalayci O. (2012). Oxidative Stress and Antioxidant Defense. World Allergy Organization Journal., vol. 5, pp. 9–19. 10.1097/WOX.0b013e3182439613.
22. Boucher D., Monteleone M., Coll R.C. (2018) Caspase-1 self-cleavage is an intrinsic mechanism to terminate inflammasome activity. J Exp Med, vol. 215, no 3, pp. 827–840. doi: https://doi.org/10.1084/jem.20172222
23. Yasuda K., Nakanishi K., & Tsutsui H. (2019). Interleukin-18 in Health and Disease. International journal of molecular sciences, vol. 20, no 3, pp. 649.https://doi.org/10.3390/ijms20030649.
24. Boraschi D., & Dinarello C. (2007). IL-18 in autoimmunity: Review. European cytokine network. vol. 17, pp. 224–252.
25. Solodenova M.E. (2009) Clinical features of lipid peroxidation and the function of antioxidant protection in patients with various types of gastroesophageal reflux disease: dis. PhD. Sib. State Medical University.
26. Solodyenova M.E., Luzina E.V., Suvorova T.V. (2008) Function of thyroid gland in patients with gastroesophageal reflux disease. Far Eastern Medical Journal, vol. 2, pp. 21–24.
