The Mechanisms of the Regulation of Immune Response in Patients with Comorbidity of Chronic Obstructive Pulmonary Disease and Asthma
Background. Comorbidity of chronic obstructive pulmonary disease (COPD) and asthma (asthma COPD overlap syndrome, ACOS) is a significant problem in pulmonary practice, whose pathogenetic issues are not clarified yet. Objective. To study the features of the regulation of immune response in patients w...
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Published in | Canadian respiratory journal Vol. 2016; no. 2016; pp. 1 - 8 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Cairo, Egypt
Hindawi Publishing Corporation
01.01.2016
Hindawi Limited John Wiley & Sons, Inc Wiley |
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Abstract | Background. Comorbidity of chronic obstructive pulmonary disease (COPD) and asthma (asthma COPD overlap syndrome, ACOS) is a significant problem in pulmonary practice, whose pathogenetic issues are not clarified yet. Objective. To study the features of the regulation of immune response in patients with comorbid COPD and asthma. Methods. We assessed the levels of CD3+, CD4+, CD8+, CD4+/CD8+, CD19+, CD25+, HLA-DR, total IgE, TNF-α, IL-4, IFN-γ, TXB2, and LTB4 in patients with comorbid COPD and asthma. Results. The study involved 44 people with COPD, 39 people with asthma, and 12 people with comorbid COPD and asthma. The specific features in comorbid COPD and asthma were lymphocytosis, increased absolute count of T-helper cells, increased cytotoxic T-lymphocytes in relative and absolute count, increased relative and absolute numbers of B-lymphocytes, and high levels of total IgE. The elevated levels of TNF-α and IL-4 and inhibition of IFN-γ production were detected. The content of LTB4 was maximal; TXB2 levels were higher than in control group but lower than in COPD and asthma. Conclusion. In comorbid COPD and asthma inflammation increased even during stable period. High levels of eicosanoids, low production of Th1-type cytokines, and active synthesis of opposition IL-4, along with increased IgE, indicate the activation of Th2-type immune response. |
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AbstractList | Background. Comorbidity of chronic obstructive pulmonary disease (COPD) and asthma (asthma COPD overlap syndrome, ACOS) is a significant problem in pulmonary practice, whose pathogenetic issues are not clarified yet. Objective. To study the features of the regulation of immune response in patients with comorbid COPD and asthma. Methods. We assessed the levels of CD3+, CD4+, CD8+, CD4+/CD8+, CD19+, CD25+, HLA-DR, total IgE, TNF-α, IL-4, IFN-γ, TXB2, and LTB4 in patients with comorbid COPD and asthma. Results. The study involved 44 people with COPD, 39 people with asthma, and 12 people with comorbid COPD and asthma. The specific features in comorbid COPD and asthma were lymphocytosis, increased absolute count of T-helper cells, increased cytotoxic T-lymphocytes in relative and absolute count, increased relative and absolute numbers of B-lymphocytes, and high levels of total IgE. The elevated levels of TNF-α and IL-4 and inhibition of IFN-γ production were detected. The content of LTB4 was maximal; TXB2 levels were higher than in control group but lower than in COPD and asthma. Conclusion. In comorbid COPD and asthma inflammation increased even during stable period. High levels of eicosanoids, low production of Th1-type cytokines, and active synthesis of opposition IL-4, along with increased IgE, indicate the activation of Th2-type immune response. Background. Comorbidity of chronic obstructive pulmonary disease (COPD) and asthma (asthma COPD overlap syndrome, ACOS) is a significant problem in pulmonary practice, whose pathogenetic issues are not clarified yet. Objective. To study the features of the regulation of immune response in patients with comorbid COPD and asthma. Methods. We assessed the levels of [CD3.sup.+], [CD4.sup.+], [CD8.sup.+], [CD4.sup.+]/[CD8.sup.+], [CD19.sup.+], [CD25.sup.+], HLA-DR, total IgE, TNF-[alpha], IL-4, IFN-[gamma], [TXB.sub.2], and [LTB.sub.4] in patients with comorbid COPD and asthma. Results. The study involved 44 people with COPD, 39 people with asthma, and 12 people with comorbid COPD and asthma. The specific features in comorbid COPD and asthma were lymphocytosis, increased absolute count of T-helper cells, increased cytotoxic T-lymphocytes in relative and absolute count, increased relative and absolute numbers of B-lymphocytes, and high levels of total IgE. The elevated levels of TNF-[alpha] and IL-4 and inhibition of IFN-[gamma] production were detected. The content of LTB4 was maximal; [TXB.sub.2] levels were higher than in control group but lower than in COPD and asthma. Conclusion. In comorbid COPD and asthma inflammation increased even during stable period. High levels of eicosanoids, low production of Thl-type cytokines, and active synthesis of opposition IL-4, along with increased IgE, indicate the activation of Th2-type immune response. Background . Comorbidity of chronic obstructive pulmonary disease (COPD) and asthma (asthma COPD overlap syndrome, ACOS) is a significant problem in pulmonary practice, whose pathogenetic issues are not clarified yet. Objective . To study the features of the regulation of immune response in patients with comorbid COPD and asthma. Methods . We assessed the levels of CD3 + , CD4 + , CD8 + , CD4 + /CD8 + , CD19 + , CD25 + , HLA-DR, total IgE, TNF- α , IL-4, IFN- γ , TXB 2 , and LTB 4 in patients with comorbid COPD and asthma. Results . The study involved 44 people with COPD, 39 people with asthma, and 12 people with comorbid COPD and asthma. The specific features in comorbid COPD and asthma were lymphocytosis, increased absolute count of T-helper cells, increased cytotoxic T-lymphocytes in relative and absolute count, increased relative and absolute numbers of B-lymphocytes, and high levels of total IgE. The elevated levels of TNF- α and IL-4 and inhibition of IFN- γ production were detected. The content of LTB 4 was maximal; TXB 2 levels were higher than in control group but lower than in COPD and asthma. Conclusion . In comorbid COPD and asthma inflammation increased even during stable period. High levels of eicosanoids, low production of Th1-type cytokines, and active synthesis of opposition IL-4, along with increased IgE, indicate the activation of Th2-type immune response. . Comorbidity of chronic obstructive pulmonary disease (COPD) and asthma (asthma COPD overlap syndrome, ACOS) is a significant problem in pulmonary practice, whose pathogenetic issues are not clarified yet. . To study the features of the regulation of immune response in patients with comorbid COPD and asthma. . We assessed the levels of CD3 , CD4 , CD8 , CD4 /CD8 , CD19 , CD25 , HLA-DR, total IgE, TNF- , IL-4, IFN- , TXB , and LTB in patients with comorbid COPD and asthma. . The study involved 44 people with COPD, 39 people with asthma, and 12 people with comorbid COPD and asthma. The specific features in comorbid COPD and asthma were lymphocytosis, increased absolute count of T-helper cells, increased cytotoxic T-lymphocytes in relative and absolute count, increased relative and absolute numbers of B-lymphocytes, and high levels of total IgE. The elevated levels of TNF- and IL-4 and inhibition of IFN- production were detected. The content of LTB was maximal; TXB levels were higher than in control group but lower than in COPD and asthma. . In comorbid COPD and asthma inflammation increased even during stable period. High levels of eicosanoids, low production of Th1-type cytokines, and active synthesis of opposition IL-4, along with increased IgE, indicate the activation of Th2-type immune response. |
Audience | Academic |
Author | Vitkina, Tatyana Lobanova, Elena G. Knyshova, Vera V. Denisenko, Yulia K. Novgorodtseva, Tatyana P. Antonyuk, Marina V. Gvozdenko, Tatyana Nazarenko, Anna Kalinina, Elena P. |
AuthorAffiliation | Institute of Medical Climatology and Rehabilitation Treatment, Vladivostok Branch of Far Eastern Scientific Center of Physiology and Pathology of Respiration, 73g Russkaya St., Vladivostok 690105, Russia |
AuthorAffiliation_xml | – name: Institute of Medical Climatology and Rehabilitation Treatment, Vladivostok Branch of Far Eastern Scientific Center of Physiology and Pathology of Respiration, 73g Russkaya St., Vladivostok 690105, Russia |
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BackLink | https://www.ncbi.nlm.nih.gov/pubmed/27660519$$D View this record in MEDLINE/PubMed |
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Cites_doi | 10.3904/kjim.2015.30.4.443 10.2147/copd.s61347 10.5320/wjr.v6.i2.54 10.1378/chest.117.2_suppl.10S 10.1055/s-0035-1556063 10.1183/16000617.00009014 10.1378/chest.15-1055 10.2147/copd.s88667 10.2147/copd.s87025 |
ContentType | Journal Article |
Copyright | Copyright © 2016 Elena P. Kalinina et al. COPYRIGHT 2016 Hindawi Limited COPYRIGHT 2016 John Wiley & Sons, Inc. Copyright © 2016 Elena P. Kalinina et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Copyright © 2016 Elena P. Kalinina et al. 2016 |
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Snippet | Background. Comorbidity of chronic obstructive pulmonary disease (COPD) and asthma (asthma COPD overlap syndrome, ACOS) is a significant problem in pulmonary... . Comorbidity of chronic obstructive pulmonary disease (COPD) and asthma (asthma COPD overlap syndrome, ACOS) is a significant problem in pulmonary practice,... Background . Comorbidity of chronic obstructive pulmonary disease (COPD) and asthma (asthma COPD overlap syndrome, ACOS) is a significant problem in pulmonary... |
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SubjectTerms | Analysis Asthma Cardiovascular disease Care and treatment Chronic illnesses Chronic obstructive lung disease Chronic obstructive pulmonary disease Comorbidity Cytokines Diagnosis Disease prevention Dyspnea Family medical history Health aspects Immune response Immune system Immunoglobulin E Inflammation Laboratories Lung diseases, Obstructive Lymphocytes Patients Studies |
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Title | The Mechanisms of the Regulation of Immune Response in Patients with Comorbidity of Chronic Obstructive Pulmonary Disease and Asthma |
URI | https://search.emarefa.net/detail/BIM-1103200 https://dx.doi.org/10.1155/2016/4503267 https://www.ncbi.nlm.nih.gov/pubmed/27660519 https://www.proquest.com/docview/1818460758 https://www.proquest.com/docview/1859717223/abstract/ https://pubmed.ncbi.nlm.nih.gov/PMC5021859 https://doaj.org/article/f9d67689d9114c8ea6fe7f924a7c837e |
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