http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
( Pureun-haneul Lee ),( An-soo Jang ),( Byeong-gon Kim ),( Jisu Hong ),( Yun-ki Lee ),( June-hyuck Lee ),( Sung- Woo Park ),( Do-jin Kim ) 대한결핵 및 호흡기학회 2019 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.127 No.-
Background: Air pollutants induce or incite respiratory diseases such as asthma and COPD. Whether junctional proteins can contribute to development or exacerbations of airway diseases remain to be clarified. Objective: The aim of this study was to observe the effect of diesel exhaust particulates (DEP) on junctional proteins of both nose and lung in a mouse model. Methods: Mice were treatment with saline (Sham) and exposed to 100 μg/m3 DEPs 1 hour a day for 5 days a week for 4 weeks and 8 weeks in a closed-system chamber attached to a ultrasonic nebulizer. Airway hyperresponsiveness (AHR) was measured and bronchoalveolar lavage fluid, lung and nasal tissue were collected. The effects of DEP on junctional proteins such as claudin (CLND) 4, CLND 5, and CLND 17 were estimated using Western blot, immunohistochemical stain in nasal and lung tissue. Results: AHR and inflammatory cells in the airway were higher in DEP exposure group than in control group and were higher in 4 and 8 weeks group than in control group. The expression of CLND4, CLND 5, and CLND 17 in both lung and nasal tissue were significantly increased in DEP exposure group than in the control group. Conclusion: These results suggesting that air pollutants can change CLDNs and disintegrate cell barriers, causing to airway inflammation of both nose and lung.
The Impact of Environmental Pollutants on Barrier Dysfunction in Respiratory Disease
Lee Pureun-Haneul,Park Shinhee,Lee Yun-Gi,Choi Seon-Muk,An Min-Hyeok,Jang An-Soo 대한천식알레르기학회 2021 Allergy, Asthma & Immunology Research Vol.13 No.6
Respiratory epithelial cells form a selective barrier between the outside environment and underlying tissues. Epithelial cells are polarized and form specialized cell-cell junctions, known as the apical junctional complex (AJC). Assembly and disassembly of the AJC regulates epithelial morphogenesis and remodeling processes. The AJC consists of tight and adherens junctions, functions as a barrier and boundary, and plays a role in signal transduction. Endothelial junction proteins play important roles in tissue integrity and vascular permeability, leukocyte extravasation, and angiogenesis. Air pollutants such as particulate matter, ozone, and biologic contaminants penetrate deep into the airways, reaching the bronchioles and alveoli before entering the bloodstream to trigger airway inflammation. Pollutants accumulating in the lungs exacerbate the symptoms of respiratory diseases, including asthma and chronic obstructive lung disease. Biological contaminants include bacteria, viruses, animal dander and cat saliva, house dust mites, cockroaches, and pollen. Allergic inflammation develops in tissues such as the lung and skin with large epithelial surface areas exposed to the environment. Barrier dysfunction in the lung allows allergens and environmental pollutants to activate the epithelium and produce cytokines that promote the induction and development of immune responses. In this article, we review the impact of environmental pollutants on the cell barrier in respiratory diseases.
Alteration in Claudin-4 Contributes to Airway Inflammation and Responsiveness in Asthma
Lee, Pureun-Haneul,Kim, Byeong-Gon,Lee, Sun-Hye,Lee, June-Hyuck,Park, Sung-Woo,Kim, Do-Jin,Park, Choon-Sik,Leikauf, George D.,Jang, An-Soo The Korean Academy of Asthma, Allergy and Clinical 2018 Allergy, Asthma & Immunology Research Vol.10 No.1
<P><B>Purpose</B></P><P>Claudin-4 has been reported to function as a paracellular sodium barrier and is one of the 3 major claudins expressed in lung alveolar epithelial cells. However, the possible role of claudin-4 in bronchial asthma has not yet been fully studied. In this study, we aimed to elucidate the role of claudin-4 in the pathogenesis of bronchial asthma.</P><P><B>Methods</B></P><P>We determined claudin-4 levels in blood from asthmatic patients. Moreover, using mice sensitized and challenged with OVA, as well as sensitized and challenged with saline, we investigated whether claudin-4 is involved in the pathogenesis of bronchial asthma. Der p1 induced the inflammatory cytokines in NHBE cells.</P><P><B>Results</B></P><P>We found that claudin-4 in blood from asthmatic patients was increased compared with that from healthy control subjects. Plasma claudin-4 levels were significantly higher in exacerbated patients than in control patients with bronchial asthma. The plasma claudin-4 level was correlated with eosinophils, total IgE, FEV1% pred, and FEV1/FVC. Moreover, lung tissues from the OVA-OVA mice showed significant increases in transcripts and proteins of claudin-4 as well as in TJ breaks and the densities of claudin-4 staining. When claudin-4 was knocked down by transfecting its siRNA, inflammatory cytokine expressions, which were induced by Der p1 treatment, were significantly increased.</P><P><B>Conclusions</B></P><P>These findings thus raise the possibility that regulation of lung epithelial barrier proteins may constitute a therapeutic approach for asthma.</P>
Kim, Byeong-Gon,Lee, Pureun-Haneul,Lee, Sun-Hye,Baek, Ae-Rin,Park, Jong-Sook,Lee, Junehyuk,Park, Sung-Woo,Kim, Do-Jin,Park, Choon-Sik,Jang, An-Soo The Korean Academy of Asthma, Allergy and Clinical 2018 Allergy, Asthma & Immunology Research Vol.10 No.5
<P><B>Purpose</B></P><P>The tight junction protein claudin-5 (CLDN5) is critical to the control of endothelial cellular polarity and pericellular permeability. The role of CLDN5 in chronic obstructive pulmonary disease (COPD) remains unclear. The aim of this study was to investigate the association between CLDN5 levels and clinical variables in patients with COPD.</P><P><B>Methods</B></P><P>In total, 30 patients with COPD and 30 healthy controls were enrolled in the study. The plasma CLDN5 level was checked in patients with stable or exacerbated COPD and in healthy controls.</P><P><B>Results</B></P><P>The mean plasma CLDN5 level of patients with COPD was 0.63 ± 0.05 ng/mL and that of healthy controls was 6.9 ± 0.78 ng/mL (<I>P</I> = 0.001). The mean plasma CLDN5 level was 0.71 ± 0.05 ng/mL in exacerbated COPD patients and 0.63 ± 0.04 ng/mL in patients with stable COPD (<I>P</I> < 0.05). The plasma CLDN5 level among COPD subjects was correlated with the smoking amount (<I>r</I> = −0.530, <I>P</I> = 0.001). The plasma CLDN5 level in stable COPD patients was correlated with forced expiratory volume in one second (FEV1, %pred.) (<I>r</I> = −0.481, <I>P</I> = 0.037).</P><P><B>Conclusions</B></P><P>The plasma CLDN5 level was not correlated with age. CLDN5 may be involved in the pathogenesis of COPD. Further studies having a larger sample size will be needed to clarify CLDN5 in COPD.</P>
( An Soo Jang ),( Pureun Haneul Lee ),( Kuk Young Moon ),( Sung Woo Park ),( Choon Sik Park ) 대한내과학회 2014 대한내과학회 추계학술대회 Vol.2014 No.1
Background: The tight junction (TJ) protein, claudin 5 (CLN5) is a critical regulator of TJ. But its clinical significance and therapeutic trial of the molecular mechanisms underlying CLN5 in bronchial asthma remain unresolved. To identify the role and regulator of the endothelial tight junction protein CLN5 in a mouse model of asthma. Methods: Using mice sensitized with ovalbumin (OVA) and challenged with OVA (OVA mice) as well as mice sensitized with saline and challenged with air (sham mice), we investigated potential links of CLN5 and bronchial asthma using RT-PCR, ELISA, immunoblotting, and confocal imaging. Results: In OVA mice, inflammatory cytokine levels, airway inflammation, and bronchial hyperresponsiveness were increased than in sham mice. Lung CLN5 transcript and protein level were increased in OVA mice than in sham mice. Lung endothelial cells integrity was disrupted in OVA mice compared with sham mice. Dexamethasone treatment recovered disrupted CLDN5 Conclusions: These results indicate that CLN5 be implicated in the pathogenesis of bronchial asthma and represent a potential target for therapeutic intervention.
( Hyun-jung Seo ),( Pureun-haneul Lee ),( Byeong-gon Kim ),( Sun-hye Lee ),( Jong-sook Park ),( Junehyuck Lee ),( Sung-woo Park ),( Do-jin Kim ),( Choon-sik Park ),( An-soo Jang ) 대한내과학회 2018 The Korean Journal of Internal Medicine Vol.33 No.4
Background/Aims: The methacholine bronchial provocation test (MBPT) is used to detect and quantify airway hyper-responsiveness (AHR). Since improvements in the severity of asthma are associated with improvements in AHR, clinical studies of asthma therapies routinely use the change of airway responsiveness as an objective outcome. The aim of this study was to assess the relationship between serial MBPT and clinical profiles in patients with asthma. Methods: A total of 323 asthma patients were included in this study. The MBPT was performed on all patients beginning at their initial diagnosis until asthma was considered controlled based on the Global Initiative for Asthma guidelines. A responder was defined by a decrease in AHR while all other patients were considered non-responders. Results: A total of 213 patients (66%) were responders, while 110 patients (34%) were non-responders. The responder group had a lower initial PC<sub>20</sub> (provocative concentration of methacholine required to decrease the forced expiratory volume in 1 second by 20%) and longer duration compared to the non-responder group. Members of the responder group also had superior qualities of life, compared to members of the non-responder group. Whole blood cell counts were not related to differences in PC<sub>20</sub>; however, eosinophil concentration was. No differences in sex, age, body mass index, smoking history, serum immunoglobulin E, or frequency of acute exacerbation were observed between responders and non-responders. Conclusions: The initial PC<sub>20</sub>, the duration of asthma, eosinophil concentrations, and quality-of-life may be useful variables to identify improvements in AHR in asthma patients.
Angulin-1/lipolysis-stimulated Lipoprotein Receptor in Asthma
( Da Yeon Hwang ),( Min-hyeok An ),( Pureun-haneul Lee ),( Jung-hyun Kim ),( Yunha Nam ),( Shinhee Park ),( Ae-rin Baek ),( June Hyuck Lee ),( Do Jin Kim ),( Sung Woo Park ),( An Soo Jang ) 대한결핵 및 호흡기학회 2023 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.136 No.0
SOX18 as a potential biomarker in asthma
( Jisu Hong ),( An-soo Jang ),( Pureun-haneul Lee ),( Yun-ki Lee ),( June-hyuck Lee ),( Sung-woo Park ) 대한결핵 및 호흡기학회 2019 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.127 No.-
Background: Asthma characterized by airway hyperresponsiveness, increased inflammatory cells, and fibrosis and angiogenesis. SRY-related HMG-box 18 (SOX18) is an important transcription factor involved in the development of cardiovascular and lymphatic vessels during embryonic development and wound-healing processes. SOX18 remains to be clarified in asthma. Objective: In this study we aimed to elucidate the role of SOX18 in the pathogenesis of bronchial asthma. Methods: Using an established mouse model of ovalbumin (OVA)-induced chronic allergic asthma, we investigated whether SOX18 is involved in pathogenesis of asthma. Airway hyperresponsiveness (AHR) was measured and bronchoalveolar lavage fluid was collected, lung tissue was processed for protein and RNA, and hematoxylin and eosin stain. Collagen was measured by trichrome stain and sircol assay. SOX18 level checked in lung human microvascular endothelial cells (HMVEC-L) and normal human bronchial epithelial (NHBE) cells treated with house dust mite (HDM). Moreover, we observed SOX18 levels in blood from asthmatic patients between stable and exacerbated state. Results: The chronic asthma mice showed that SOX18, PROX1, COUP-TFII, mucous gland hyperplasia and collagen deposition in lung tissue were significantly increased after OVA challenge. SOX18 protein in HMVEC-L and NHBE cells was increased following HDM treatment. PROX1 and COUP-TFII protein in HMVEC-L were decreased and increased in NHBE cells following HDM treatment. SOX18 in blood from exacerbated asthmatics was increased compared with those from stable asthmatics. Conclusion: These results suggesting that SOX18 may be associated with asthma exacerbation and can be a biomarker for asthma.
( Shinhee Park ),( An-soo Jang ),( Pureun-haneul Lee ),( Ae-rin Baek ),( Jong-sook Park ),( June-hyuk Lee ),( Sung-Woo Park ),( Do-jin Kim ) 대한결핵 및 호흡기학회 2021 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.129 No.-
Objectives Chronic obstructive pulmonary disease (COPD) imposes a major healthcare burden. A tight junction protein, claudin-4 (CLDN4), may play a protective role in acute lung injury, but its role in COPD is unclear. To investigate the relationship between CLDN4 and COPD, we evaluated the association of CLDN4 with the clinical parameters of COPD, including exacerbations. Methods We analyzed a cohort of 30 patients with COPD and 25 healthy controls, and evaluated their clinical parameters, including lung function. The plasma CLDN4 level in stable and exacerbated COPD was measured. Results The COPD patients were all males, and predominantly smokers; their initial lung function was poorer than the healthy controls. The mean CLDN4 plasma level was 0.0219 ± 0.0205 ng/mg in the control group, 0.0086 ± 0.0158 ng/mg in the stable COPD group (COPD-ST) and 0.0917 ± 0.0871 ng/mg in the exacerbated COPD (COPD-EXA) group. The plasma CLDN4 level was significantly lower in the COPD-ST than control group, but was significantly elevated in the COPD-EXA group. The plasma CLDN4 level was inversely correlated with FVC and FEV1 in the COPD-EXA group (r = 0.506, P = 0.001 and r = 0.527, P < 0.001, respectively). Conclusions The plasma CLDN4 level is closely correlated with COPD exacerbations and decreased lung function. This suggests that CLDN4 has potential as a severity marker for COPD.