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Features of lymphocytes during programmed cell death in patients with atopic bronchial asthma
- Authors: Pinchuk YV1, Vodunon AC1, Mustafin IG2, Abramova ZI1
-
Affiliations:
- Kazan State University
- Kazan State Medical University
- Issue: Vol 7, No 4 (2010)
- Pages: 32-39
- Section: Articles
- URL: https://rusalljournal.ru/raj/article/view/870
- DOI: https://doi.org/10.36691/RJA870
- ID: 870
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Abstract
Background. To establish features of programmed cell death of lymphocytes depending on disease severity
score.
Methods. The morphology of lymphocytes was investigated with a method of electronic microscopy. Apoptotic
cells were defined by flow cytometry.
Results. We have revealed lymphocytes morphological difference between asthmatics and normal donors. Also
we found out the difference between number of cells during the incubation process.
Conclusion. These findings can promote deeper understanding of the disease pathogenesis.
score.
Methods. The morphology of lymphocytes was investigated with a method of electronic microscopy. Apoptotic
cells were defined by flow cytometry.
Results. We have revealed lymphocytes morphological difference between asthmatics and normal donors. Also
we found out the difference between number of cells during the incubation process.
Conclusion. These findings can promote deeper understanding of the disease pathogenesis.
Keywords
About the authors
Y V Pinchuk
Kazan State UniversityKazan State University
A C Vodunon
Kazan State UniversityKazan State University
I G Mustafin
Kazan State Medical UniversityKazan State Medical University
Z I Abramova
Kazan State University
Email: zina.abramova@mail.ru
Kazan State University
References
- Шапорова Н.Л., Петрова М.А., Трофимов В.И. Бронхиальная астма тяжелого течения: особенности патогенеза и лечения. Пульмонология. 2003, № 6, с. 108-113.
- Огородова Л.М., Петровская Ю.А., Камалтынова Е.М. и соавт. Тяжелая бронхиальная астма у детей: факторы риска, течения. Пульмонология. 2002, № 1, с. 68-71.
- Stirling R.G., Chung K.F. Severe asthma: definition and mechanisms. Allergy. 2001, v. 56, p. 825-840.
- Манских В.Н. Пути гибели клетки и их биологическое значение. Цитология. 2007, т. 49 (11), с. 909-915.
- Бойчук СВ., Мустафин И.Г. Fas-рецептор и его роль при атопических заболеваниях. Иммунология. 2001, № 3, с. 24-28.
- Vignola A.M., Chiappara G., Gagliardo R. Apoptosis and airway inflammation in asthma. Apoptosis. 2000, v. 5, № 5, p. 473-485.
- Patel D., Rubbi СР., Rickwood D. Separation of T and В lymphocytes from human peripheral blood mononuclear cells using density perturbation methods. Clin. Chim. Acta. 1995, v. 240, p. 187-193.
- MelisM., Siena L. Fluticasone induces apoptosis in peripheral T-lymphocytes: a comparison between asthmatic and normal subjects. Eur. Respir. J. 2002, v. 19, p. 257-266.
- Mower D.A, Peckhman D.W et al. 1994. Decreased membrane phospholipid packing and decreased cell size precede DNA cleavage in mature mouse В cell apoptosis. J. Immunol, v. 152, p. 4832-4842.
- Nicoletti I., Migliorati G. Rapid and simple method of measurement of nuclear apoptosis. J. Immunol. Meth. 1991, p. 271-279.
- Urbonien D., Skalauskas R., Sitkauskiene B. Autoimmunity in pathogenesis of chronic obstructive pulmonary disease. Medicina (Kaunas). 2005, v. 41, № 3, p. 190-195.
- Райхлин Н.Т., Райхлин А.Н. Регуляция и проявления апоптоза в физиологических условиях и в опухолях. Вопросы онкологии. 2002, т. 48, с. 159-171.
- Мамонтова Т.В., Кайдашев И.П. Новые аспекты апоптоза мононуклеарных клеток в патогенезе атопической бронхиальной астмы. Аллергология. 2005, № 4, с. 15-23.
- Бойчук С.В., Мустафин И.Г., Фассахов Р.С. Механизмы дексаметазон-индуцированного апоптоза лимфоцитов при атопической бронхиальной астме. Пульмонология. 2003, №2, с. 10-16.
- Погорелов В.М., Козинец Г.И. Морфология апоптоза при нормальном и патологическом гемопоэзе. Гематол. и трансфузиол. 1995, № 5, с. 21-25.
- Degenhardt К., Mathew R., Beaudoin В., Chen G. et al. Autophagy promotes tumor cell survival and restricts necrosis, inflammation, and tumorigenesis. Cancer Cell. 2006, № 10, p. 51-64.
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