85 -9 (71) 2024 - F.M.Khamidova, M.B.Zhovlieva - MORPHOLOGICAL MARKERS OF REMODELING OF THE BRONCHIAL MUCOSA IN A MODEL OF BRONCHIECTACTIC DISEASE

MORPHOLOGICAL MARKERS OF REMODELING OF THE BRONCHIAL MUCOSA IN A MODEL OF BRONCHIECTACTIC DISEASE

F.M.Khamidova - Samarkand State Medical University Uzbekistan

M.B.Zhovlieva - Samarkand State Medical University Uzbekistan

Zh.M.Ismoilov - Samarkand State Medical University Uzbekistan

Resume

Introduction. The study of lung tissue in bronchiectasis under experimental conditions in animals is necessary for a deeper understanding of the cellular and molecular mechanisms of chronic respiratory diseases and the development of new approaches to their diagnosis and therapy. The purpose of the study -The aim of the study was to study the morphological and immunohistochemical characteristics of bronchi and lungs on a model of bronchiectactic disease Materials and methods: 70 male white outbred rabbits were used in the work. The control group included intact animals, 10 rabbits were included. The main group - animals with a model of chronic pneumonia, included 60 rabbits: 10 animals each were removed from the experiment 7, 8, 9, 10, 11 and 12 months after reproducing the pathology model. The resulting micropreparations of lung tissue were stained with hematoxylin and eosin, picrofuchsin according to Van Gieson, and resorcinol-fuchsin according to Weigert. Immunohistochemical studies of lung micropreparations were performed using antibodies to Ki-67, Bcl-2, CD3, CD20, CD163, CK5/6 and CK8/18. Results. Over time, after 7-12 months in a model of chronic pneumonia, signs of inflammatory and destructive processes are observed, as well as a persistent increase in the thickness of all layers of the bronchial wall. There is an increase in the number of CD-3, CD-20, CD-163, Bcl-2 and Ki-67 positive cells over the course of observation, reaching the highest values at the 12th month of the experiment. The expression level of the macrophage marker CD-163 increased by the 9th month of observation. Conclusion. A comprehensive histological and immunohistochemical characterization of the lung tissue of rabbits with a model of chronic pulmonary inflammation was carried out. In the dynamics from 7 to 12 months of observation in the pathology model, the progression of chronic inflammation with activation of the T- and B-dependent components of the adaptive immune response, associated with remodeling of the bronchial wall, was noted, and data were obtained in favor of the development of metaplasia of the bronchial epithelium.

Key words: bronchi, lungs, chronic inflammation, mucous membrane, rabbit

First page

482

Last page

493

For citation:F.M.Khamidova, M.B.Zhovlieva, Zh.M.Ismoilov - MORPHOLOGICAL MARKERS OF REMODELING OF THE BRONCHIAL MUCOSA IN A MODEL OF BRONCHIECTACTIC DISEASE//New Day in Medicine 9(71)2024 482-493 https://newdayworldmedicine.com/en/new_day_medicine/9-71-2024

List of References

  1. Gupta A.K., Lodha R., Kabra S.K. Non Cystic Fibrosis Bronchiectasis. //Indian J Pediatr 2015;82(10):938-44. DOI: 10.1007/s12098-015- 1866-4,
  2. Zaid A.A., Elnazir B., Greally P. A decade of non-cystic fibrosis bronchiectasis 1996– 2016. IrMed J 2016;103:77-79.
  3. Viegi G., Maio, S., Fasola, S., & Baldacci, S. (2020). Global burden of chronic respiratory diseases. //Journal of aerosol medicine and pulmonary drug delivery, 2020;33(4):171-177.
  4. Сатвалдиева Э.А., Юсупов А.С., Урумбаев Р.М., Муродова М.С., Коллас Е.В. Клинический случай интенсивной терапии ребенка 2-х лет с бронхоэктатической болезнью (поздняя диагностика) Евросиё педиатрия ахборотномаси 2021;2(9):34-40.
  5. Murray P.J., Wynn T.A. Protective and pathogenic functions of macrophage subsets. Nat. Rev. Immunol. 2011;11:723-737. doi: 10.1038/nri3073. [PMC free article] [PubMed] [CrossRef] [Google Scholar
  6. Strengert M., Knaus U.G. Analysis of epithelial barrier integrity in polarized lung epithelial cells. //Methods Mol. Biol. 2011;763:195-206. doi: 10.1007/978-1-61779-191-8_13. [PubMed] [CrossRef] [Google Scholar
  7. Murray P.J., Wynn T.A. Protective and pathogenic functions of macrophage subsets. //Nat. Rev. Immunol. 2011;11:723-737. doi: 10.1038/nri3073. [PMC free article] [PubMed] [CrossRef] [Google Scholar].
  8. Pollard J.W. Trophic macrophages in development and disease. //Nat. Rev. Immunol. 2009;9:259-270. doi: 10.1038/nri2528. [PMC free article] [PubMed] [CrossRef] [Google Scholar].
  9. Miyata R., Van Eeden S.F. The innate and adaptive immune response induced by alveolar macrophages exposed to ambient particulate matter. //Toxicol. Appl. Pharmacol. 2011;257:209-226. doi: 10.1016/j.taap.2011.09.007. [PubMed] [CrossRef] [Google Scholar]
  10. Lanyu Z., Feilong H. Emerging role of extracellular vesicles in lung injury and inflammation. Biomed.Pharmacother. 2019;113:108748.doi: 10.1016/j.biopha.2019.108748. [PubMed] [CrossRef] [Google Scholar]
  11. Luyts K., Napierska D., Dinsdale D., Klein S.G., Serchi T., Hoet P.H. A coculture model of the lung–blood barrier: The role of activated phagocytic cells. Toxicol. In Vitro. 2015;29:234–241. doi: 10.1016/j.tiv.2014.10.024. [PubMed] [CrossRef] [Google Scholar]
  12. Hiemstra P.S., McCray P.B., Jr., Bals R. The innate immune function of airway epithelial cells in inflammatory lung disease. //Eur. Respir. J. 2015;45:1150–1162. doi: 10.1183/09031936.00141514. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
  13. Galasso R., Gruppo di lavoro Sentieri SENTIERI/Quinto Rapporto—Studio Epidemiologico Na-zionale dei Territori e degli Insediamenti Esposti a Rischio da Inquinamento. Valutazione della evidenza epidemiologica. Epidemiol. Prev. 2019;43((Suppl. 2–3)):1–208. doi: 10.19191/EP19.2-3.S1.032. [CrossRef] [Google Scholar]
  14. Jairaman A., Maguire C.H., Schleimer R.P., Prakriya M. Allergens stimulate store-operated calci-um entry and cytokine production in airway epithelial cells. Sci. Rep. 2016;6:32311. doi: 10.1038/srep32311. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
  15. Osterlund C., Grönlund H., Polovic N., Sundström S., Gafvelin G., Bucht A. The Non-Proteolytic House Dust Mite Allergen Der p 2 Induce NF-kappaB and MAPK Dependent Activation of Bronchial Epithelial Cells. Clin. Exp. Allergy. 2009;39:1199–1208. doi: 10.1111/j.1365-2222.2009.03284.x. [PubMed] [CrossRef] [Google Scholar]
  16. Usmani S.M., von Einem J., Frick M., Miklavc P., Mayenburg M., Husmann M., Dietl P., Wittekindt O.H. Molecular basis of early epithelial response to strep-tococcal exotoxin: Role of STIM1 and Orai1 proteins. Cell Microbiol. 2012;14:299–315. doi: 10.1111/j.1462-5822.2011.01724.x. [PubMed] [CrossRef] [Google Scholar]
  17. Takizawa H., Ohtoshi T., Kikutani T., Okazaki H., Akiyama N., Sato M., Shoji S., Ito K. Histamine activates bronchial epithelial cells to re-lease inflammatory cytokines in vitro. Int Arch. Allergy Immunol. 1995;108:260–267. doi: 10.1159/000237162. [PubMed] [CrossRef] [Google Scholar]
  18. Farias R., Rousseau S. The TAK1 → IKKβ → TPL2 → MKK1/MKK2 signaling cascade regulates IL-33 expression in cystic fibrosis airway epithelial cells following infection by Pseudomonas Aeruginosa. Front. Cell Dev. Biol. 2016;3:87. doi: 10.3389/fcell.2015.00087. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
  19. Heyen L., Müller U., Siegemund S., Schulze B., Protschka M., Alber G., Piehler D. Lung epithelium is the major source of IL-33 and is regulated by IL-33-dependent and IL-33-independent mechanisms in pulmonary cryptococ-cosis. Pathog. Dis. 2016;74:ftw086. doi: 10.1093/femspd/ftw086. [PubMed] [CrossRef] [Google Scholar]
  20. Hristova M., Habibovic A., Veith C., Janssen-Heininger Y.M., Dixon A.E., Geiszt M., van der Vliet A. Airway epithelial dual oxidase 1 mediates allergen-induced IL-33 secretion and activation of type 2 immune responses. J. Allergy Clin. Immunol. 2016;137:1545–1556.e11. doi: 10.1016/j.jaci.2015.10.003. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

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