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RISS 인기검색어
- 검색키워드
- 저자 : Nikolaos G. Papadopoulos (검색결과 4 건)
- 무료
- 기관 내 무료
- 유료
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Sylwia Moskwa,Wojciech Piotrowski,Jerzy Marczak,Małgorzata Pawełczyk,Anna Lewandowska-Polak,Marzanna Jarzębska,Małgorzata Brauncajs,Anna Głobińska,Paweł Górski,Nikolaos G. Papadopoulos,Michael R. Edwa 대한천식알레르기학회 2018 Allergy, Asthma & Immunology Research Vol.10 No.2
Purpose: In order to gain an insight into determinants of reported variability in immune responses to respiratory viruses in human bronchial epithelial cells (HBECs) from asthmatics, the responses of HBEC to viral infections were evaluated in HBECs from phenotypically heterogeneous groups of asthmatics and in healthy controls. Methods: HBECs were obtained during bronchoscopy from 10 patients with asthma (6 atopic and 4 non-atopic) and from healthy controls (n=9) and grown as undifferentiated cultures. HBECs were infected with parainfluenza virus (PIV)-3 (MOI 0.1) and rhinovirus (RV)-1B (MOI 0.1), or treated with medium alone. The cell supernatants were harvested at 8, 24, and 48 hours. IFN-α, CXCL10 (IP-10), and RANTES (CCL5) were analyzed by using Cytometric Bead Array (CBA), and interferon (IFN)-β and IFN-λ1 by ELISA. Gene expression of IFNs, chemokines, and IFN-regulatory factors (IRF-3 and IRF-7) was determined by using quantitative PCR. Results: PIV3 and RV1B infections increased IFN-λ1 mRNA expression in HBECs from asthmatics and healthy controls to a similar extent, and virus-induced IFN-λ1 expression correlated positively with IRF-7 expression. Following PIV3 infection, IP-10 protein release and mRNA expression were significantly higher in asthmatics compared to healthy controls (median 36.03-fold). No differences in the release or expression of RANTES, IFN-λ1 protein and mRNA, or IFN-α and IFN-β mRNA between asthmatics and healthy controls were observed. However, when asthmatics were divided according to their atopic status, HBECs from atopic asthmatics (n=6) generated significantly more IFN-λ1 protein and demonstrated higher IFN-α, IFN-β, and IRF-7 mRNA expressions in response to PIV3 compared to non-atopic asthmatics (n=4) and healthy controls (n=9). In response to RV1B infection, IFN-β mRNA expression was lower (12.39-fold at 24 hours and 19.37-fold at 48 hours) in non-atopic asthmatics compared to atopic asthmatics. Conclusions: The immune response of HBECs to virus infections may not be deficient in asthmatics, but seems to be modified by atopic status.
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Viral Agents Involved in Wheezing and Asthma in Children
( Nikolaos G. Papadopoulos ),( Kalliopi M. Kouloufakou Gratsia ),( Ioannis Christodoulou ) 대한천식알레르기학회 2008 천식 및 알레르기 Vol.28 No.1
The role of respiratory viral infections in the development of childhood asthma remains under intense investigation. There is a plethora of viral agents (rhinoviruses [RV], enteroviruses, respiratory syncytial virus [RSV], metapneumovirus [MPV], adenoviruses, influenza and parainfluenza [PIV] viruses, bocavirus [hBoV], coronaviruses etc) which are associated with asthma exacerbation. Viral infections are also closely linked to infantile wheezing. Severe wheezing infections, such as bronchiolitis, in early infancy may predispose to chronic childhood asthma. The current review focuses on the latest epidemiological reports of asthma exacerbation and wheezing and tries to delineate the associations with viral agents detected during the course of the disease. According to these studies, RV infection is likely the major trigger, initially affecting asthma in school-age children while RSV is associated with severe bronchiolitis. Both agents may contribute to later asthma. Newly discovered agents such as MPV and hBoV have also been suggested as viruses with a propensity to induce wheeze and asthma exacerbations, but more studies are required to evaluate their importance. The prevention or early treatment of respiratory viral infections in children may be an important strategy to improve quality of life for patients who suffered from asthma exacerbations. (Korean J Asthma Allergy Clin Immunol 2008;28:1-9)
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MicroRNAs in Asthma and Respiratory Infections: Identifying Common Pathways
Styliani Taka,Panayiota Tzani-Tzanopoulou,Hannah Wanstall,Nikolaos G. Papadopoulos 대한천식알레르기학회 2020 Allergy, Asthma & Immunology Research Vol.12 No.1
MicroRNAs (miRs) are single-stranded RNAs of 18-25 nucleotides. These molecules regulate gene expression at the post-transcriptional level; several of these are differentially expressed in asthma as well as in viral acute respiratory infections (ARIs), the main triggers of acute asthma exacerbations. In recent years, miRs have been studied in order to discover drug targets as well as biomarkers for diagnosis, disease severity and prognosis. We describe recent findings on miR expression and function in asthma and their role in the regulation of viral ARIs, according to cell tissue specificity and asthma severity. By combining the above information, we identify miRs that may be important in virus-induced asthma exacerbations. This is the first attempt to link miR profiles of asthmatic patients and ARI-induced miRs, addressing the question of whether there might be a specific miR deficit in asthmatic subjects that make them more susceptible and/or reactive to infection.
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Stanciu, Luminita A,Roberts, Kevan,Papadopoulos, Nikolaos G,Cho, Sang-Heon,Holgate, Stephen T,Coyle, Anthony J,Johnston, Sebastian L BioMed Central 2005 Respiratory research Vol.6 No.-
<P><B>Background</B></P><P>Virus infections are the major cause of asthma exacerbations. CD8<SUP>+ </SUP>T cells have an important role in antiviral immune responses and animal studies suggest a role for CD8<SUP>+ </SUP>T cells in the pathogenesis of virus-induced asthma exacerbations. We have previously shown that the presence of IL-4 during stimulation increases the frequency of IL-5-positive cells and CD30 surface staining in CD8<SUP>+ </SUP>T cells from healthy, normal subjects. In this study, we investigated whether excess IL-4 during repeated TCR/CD3 stimulation of CD8<SUP>+ </SUP>T cells from atopic asthmatic subjects alters the balance of type 1/type 2 cytokine production in favour of the latter.</P><P><B>Methods</B></P><P>Peripheral blood CD8<SUP>+ </SUP>T cells from mild atopic asthmatic subjects were stimulated <I>in vitro </I>with anti-CD3 and IL-2 ± excess IL-4 and the expression of activation and adhesion molecules and type 1 and type 2 cytokine production were assessed.</P><P><B>Results</B></P><P>Surface expression of very late antigen-4 [VLA-4] and LFA-1 was decreased and the production of the type 2 cytokines IL-5 and IL-13 was augmented by the presence of IL-4 during stimulation of CD8<SUP>+ </SUP>T cells from mild atopic asthmatics.</P><P><B>Conclusion</B></P><P>These data suggest that during a respiratory virus infection activated CD8<SUP>+ </SUP>T cells from asthmatic subjects may produce excess type 2 cytokines and may contribute to asthma exacerbation by augmenting allergic inflammation.</P>
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