• 제목/요약/키워드: Chronic airway disease

검색결과 167건 처리시간 0.026초

Multiple Small Nodular Lung Lesions with Severe Dyspnea (심한 호흡곤란을 보인 다발성 소결절성 폐질환)

  • Yang, Suck-Chul;Lee, Kyung-Sang;Yoon, Ho-Joo;Shin, Dong-Ho;Park, Sung-Soo;Lee, Jung-Hee;Hahm, Shee-Young;Lee, Chul-Burm
    • Tuberculosis and Respiratory Diseases
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    • 제43권2호
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    • pp.285-290
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    • 1996
  • Diffuse panbronchiolitis is a chronic inflammatory lung disease of unknown etiology which is characterized by chronic airflow limitation and airway inflammation, predominantly localized in the respiratory bronchioles with infiltration of inflammatory cells, and has typical clinical, radiological and pathological features. Obstructive respiratory functional impairment, occasional symptoms of wheezing, and also cough and sputum resemble the feature of emphysema, bronchial asthma, or chronic bronchitis, respectively. We experienced a case of pathologically proven advanced diffuse panbronchiolitis in a 55-year-old man with productive cough and exertional dyspnea. The chest radiography showed multiple tiny nodular densities on whole lung fields. It was confirmed by thoracoscopy-guided lung biopsy and the patient was improved after initiation of treatment with low-dose erythromycin.

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A Study the Effects of Three Preparations of Hirudo on the Expression of Pro-inflammatory Cytokines in Human Bronchial Epithelial Cells Line BEAS-2B (수질(水蛭)의 제법(制法)에 따른 BEAS-2B 인간(人間) 기관지상피세포(氣管支上皮細胞)의 염증유발성(炎症誘發性) Cytokines 발현(發顯)에 미치는 영향(影響))

  • Jung, Hee-Jae;Jung, Sung-Ki;Rhee, Hyung-Koo;Han, Dong-Ha
    • The Journal of Internal Korean Medicine
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    • 제25권4호
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    • pp.260-273
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    • 2004
  • Backgrounds : In recent years, asthma has become recognized as a chronic inflammatory disease associated pathologically with airway epithelial inflammation and airway remodeling. Objectives : To evaluate the different effects of Hirudo depending upon pharmaceutical manufactures on the expression and the activities of IL-6 and GM-CSF in airway epithelial cells, samples of Hirudo(水蛭), Hirudo toasted with Talcum(水蛭滑石炒) and Hirudo toasted with Ephedrae Herba(水蛭麻黃炒) were tested. Methods : After inducing enhanced messenger RNA(mRNA) expression and secretion of each cytokine by tumor necrosis factor-alpha(10 ng/ml) treatment, cultured human bronchial epithelial cell line BEAS-2B was added to each sample$(l,\;10,\;100\;&\;1000\;{\mu}g/ml)$. Subsequently, DNA activities were analyzed. Specifically mRNA expression and culture supernatants(protein levels) of IL-6 and GM-CSF from BEAS-2B cells, were analyzed using luciferase reporter gene assay, reverse transcription-polymerase chain reaction(RT-PCR) analysis and enzyme-linked immunosorbent assay. Results : Hirudo toasted with Ephedrae Herba(水蛭麻黃炒) and Hirudo(水蛭) inhibited IL-6 activities in BEAS-2B cells remarkably, and inhibited mRNA expression levels and protein levels in supernatant of IL-6 and GM-CSF at various concentrations, significantly(p<0.05). However, Hirudo toasted with Talcum(水蛭滑石炒) had no effect on mRNA expression levels and showed a slight inhibitory effect on GM-CSF protein levels in supernatant of culture medium. Conclusions : These results strongly suggest that Hirudo toasted with Ephedrae Herba(水蛭麻黃炒) and Hirudo(水蛭) would be serve as effective medicaments in the treatment of airway inflammation and remodeling of asthmatic patients.

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Polymorphisms of Angiotensin-converting Enzyme Gene Associated in Patients with COPD with or without Bronchial Hyperresponsiveness (만성폐쇄성폐질환에서 ACE 유전자 다형성과 기관지 과민성의 연관성)

  • Kim, Seung Soo;Choi, Eu Gene;Park, Seoung Ju;Lee, Heung Bum;Lee, Yong Chul;Rhee, Yang Keun
    • Tuberculosis and Respiratory Diseases
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    • 제58권1호
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    • pp.25-30
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    • 2005
  • Background : An insertion-deletion polymorphism of angiotensin converting enzyme (ACE) gene has been shown to be associated with enzyme activity levels of ACE. Reported results that have been mutually contradictory about asthmatic hypersensitiveness and occurrence according to ACE gene insertion (I)/deletion (D) polymorphism. Also, the involvement of the ACE genes as the genetic basis of bronchial asthma is currently controversy. We investigated whether there was any association between polymorphisms of the ACE genes and airway hyper-responsiveness in chronic obstructive pulmonary disease (COPD). Methods : A total of 100 patients with COPD were enrolled in this study. The ACE genotypes were determined in all subjects by polymerase chain reaction. Pulmonary function test including bronchodilator response (BDR), methacholine bronchial provocation test (MBPT) were done in those patients. Airway hyper-responsiveness include any findings of positive BDR or MBPT. Results : In COPD patients, the ACE genotype distribution did not differ significantly among groups of patients with severities of COPD, and with or without airway hyper-responsiveness. Conclusions : These results suggest that polymorphisms of the ACE gene may not be associated with airway hyper-responsiveness, development and severity of COPD.

Effects of Macrolide and Corticosteroid in Neutrophilic Asthma Mouse Model

  • An, Tai Joon;Rhee, Chin Kook;Kim, Ji Hye;Lee, Young Rong;Chon, Jin Young;Park, Chan Kwon;Yoon, Hyoung Kyu
    • Tuberculosis and Respiratory Diseases
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    • 제81권1호
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    • pp.80-87
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    • 2018
  • Background: Asthma is a disease of chronic airway inflammation with heterogeneous features. Neutrophilic asthma is corticosteroid-insensitive asthma related to absence or suppression of $T_H2$ process and increased $T_H1$ and/or $T_H17$ process. Macrolides are immunomodulatory drug that reduce airway inflammation, but their role in asthma is not fully known. The purpose of this study was to evaluate the role of macrolides in neutrophilic asthma and compare their effects with those of corticosteroids. Methods: C57BL/6 female mice were sensitized with ovalbumin (OVA) and lipopolysaccharides (LPS). Clarithromycin (CAM) and/or dexamethasone (DXM) were administered at days 14, 15, 21, 22, and 23. At day 24, the mice were sacrificed. Results: Airway resistance in the OVA+LPS exposed mice was elevated but was more attenuated after treatment with CAM+DXM compared with the monotherapy group (p<0.05 and p<0.01). In bronchoalveolar lavage fluid study, total cells and neutrophil counts in OVA+LPS mice were elevated but decreased after CAM+DXM treatment. In hematoxylin and eosin stain, the CAM+DXM-treated group showed less inflammation additively than the monotherapy group. There was less total protein, interleukin 17 (IL-17), interferon ${\gamma}$, and tumor necrosis factor ${\alpha}$ in the CAM+DXM group than in the monotherapy group (p<0.001, p<0.05, and p<0.001). More histone deacetylase 2 (HDAC2) activity was recovered in the DXM and CAM+DXM challenged groups than in the control group (p<0.05). Conclusion: Decreased IL-17 and recovered relative HDAC2 activity correlated with airway resistance and inflammation in a neutrophilic asthma mouse model. This result suggests macrolides as a potential corticosteroid-sparing agent in neutrophilic asthma.

15-Hydroxyeicosatetraenoic Acid Inhibits Phorbol-12-Myristate-13-Acetate-Induced MUC5AC Expression in NCI-H292 Respiratory Epithelial Cells

  • Song, Yong-Seok;Kim, Man Sub;Lee, Dong Hun;Oh, Doek-Kun;Yoon, Do-Young
    • Journal of Microbiology and Biotechnology
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    • 제25권5호
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    • pp.589-597
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    • 2015
  • It has been reported that overexpression of MUC5AC induced by excessive inflammation leads to airway obstruction in respiratory diseases such as chronic obstructive pulmonary disease and asthma. 15-Hydroxyeicosatetraenoic acid (15-HETE) has been reported to have anti-inflammatory effects, but the role of 15-HETE in respiratory inflammation has not been determined. Therefore, the aim of this study was to investigate the effects of 15-HETE on MUC5AC expression and related pathways. In this study, phorbol-12-myristate-13-acetate (PMA) was used to stimulate NCI-H292 bronchial epithelial cells in order to examine the effects of 15-HETE. 15-HETE inhibited PMA-induced expression of MUC5AC mRNA and secretion of MUC5AC protein. Moreover, 15-HETE regulated matrix metallopeptidase 9 (MMP-9), mitogen-activated protein kinase kinase (MEK), and extracellular signal-regulated kinase (ERK). In addition, 15-HETE decreased the nuclear translocation of specificity protein-1 (Sp-1) transcription factor and nuclear factor κB (NF-κB). Furthermore, 15-HETE enhanced the transcriptional activity of peroxisome proliferator-activated receptor gamma (PPARγ) as a PPARγ agonist. This activity reduced the phosphorylation of protein kinase B (PΚB/Akt) by increasing the expression of phosphatase and tensin homolog (PTEN). In conclusion, 15-HETE regulated MUC5AC expression via modulating MMP-9, MEK/ERK/Sp-1, and PPARγ/PTEN/Akt signaling pathways in PMA-treated respiratory epithelial cells.

Elevated C-reactive Protein Levels are a Sign of Pulmonary Arterial Hypertension in AECOPD (만성 폐쇄성 폐질환 급성 악화 시 C-반응단백과 폐동맥 고혈압의 관계)

  • Kim, So Ri;Choe, Yeong Hun;Lee, Ka Young;Min, Kyung Hoon;Park, Seoung Ju;Lee, Heung Bum;Lee, Yong Chul;Rhee, Yang Keun
    • Tuberculosis and Respiratory Diseases
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    • 제64권2호
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    • pp.125-132
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    • 2008
  • Background: In chronic obstructive pulmonary disease (COPD) patients, the serum levels of C-reactive protein (CRP) are elevated and an increase of CRP is more exaggerated in the acute exacerbation form of COPD (AECOPD) than in stable COPD. Pulmonary arterial hypertension is a common complication of COPD. An increased level of CRP is known to be associated with the risk of systemic cardio-vascular disorders. However, few findings are available on the potential role of CRP in pulmonary arterial hypertension due to COPD. Methods: This study was performed prospectively and the study population was composed of 72 patients that were hospitalized due to AECOPD. After receiving acute management for AECOPD, serum CRP levels were evaluated, arterial oxygen pressure ($PaO_2$), was measured, and the existence of pulmonary arterial hypertension under room air inhalation was determined in the patients. Results: The number of patients with pulmonary arterial hypertension was 47 (65.3%)., There was an increased prevalence of pulmonary arterial hypertension and an increase of serum CRP levels in patients with the higher stages of COPD (e.g., patients with stage 3 and stage 4 disease; P<0.05). The mean serum CRP levels of patients with pulmonary arterial hypertension and without pulmonary arterial hypertension were $37.6{\pm}7.4mg/L$ and $19.9{\pm}6.6mg/L$, respectively (P<0.05). However, there was no significant difference of the mean values of $PaO_2$ between patients with pulmonary arterial hypertension and without pulmonary arterial hypertension statistically ($77.8{\pm}3.6mmHg$ versus $87.2{\pm}6.0mmHg). Conclusion: We conclude that higher serum levels of CRP can be a sign for pulmonary arterial hypertension in AECOPD patients.

Study on the Prevalence of Non-respiratory Comorbidities in Asthma Patients: A Nationwide Cohort Study (천식환자의 비호흡기 동반질환 유병률 분석연구: 전국민 코호트 연구)

  • Su-Jin Kang;Kiyon Rhew
    • Korean Journal of Clinical Pharmacy
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    • 제34권3호
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    • pp.194-201
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    • 2024
  • Background: Asthma is a chronic inflammatory airway disease associated with systemic inflammation and increased prevalence of various comorbid conditions. This study investigates the prevalence of non-respiratory comorbidities among adult asthma patients in South Korea, aiming to elucidate potential correlations and impacts of asthma on overall health, thereby affecting patients' quality of life and healthcare systems. Methods: This retrospective cohort study utilized the National Health Insurance Service data (HIRA-NPS-2020) and included adults diagnosed with asthma. Non-respiratory diseases were identified using the Korean Standard Disease Classification (KCD-8) codes, with exclusions applied for other respiratory conditions. The prevalence of comorbidities was analyzed and compared between asthma and non-asthma patients, adjusting for confounders such as age, gender, and insurance status through inverse probability treatment weighting (IPTW). Results: The analysis revealed that asthma patients exhibit significantly higher rates of cardiovascular diseases, metabolic disorders, gastrointestinal conditions, and mental health issues compared to the control group. Notably, conditions such as heart failure, gastroesophageal reflux disease, and anxiety were more prevalent, with odds ratios (OR) ranging from 1.18 to 3.90. These results demonstrate a substantial burden of comorbidities associated with asthma, indicating a broad impact on health beyond the respiratory system. Conclusion: The findings highlight the systemic nature of asthma and the interconnectedness of inflammatory processes across different organ systems. This comprehensive analysis confirms previous research linking asthma with an increased risk of various non-respiratory diseases, providing insights into the multifaceted impact of asthma on patient health.

Clinical characteristics and treatment plan for patients with snoring and obstructive sleep apnea (코골이와 수면무호흡증 환자의 임상적 특징과 치료계획)

  • Jung, Jae-Kwang;Kim, Ki-Rim;Byun, Jin-Seok;Choi, Jae-Kap
    • The Journal of the Korean dental association
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    • 제53권4호
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    • pp.249-258
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    • 2015
  • Snoring and obstructive sleep apnea are the representative sleep disordered breathings, caused by the temporary and repetitive constriction or obstruction of upper airway during sleep. They present with excessively vibratory noise and repetitive cease of respiration. These disorders commonly result in sleep disturbance and the subsequent daytime sleepiness, chronic fatigue. Furthermore, they can cause the serious and extensive complications including increased risk of hypertension, cardiac arrhythmia, cardiovascular disease, cerebrovascular accident, neurocognitive disturbance, traffic and occupational accidents, type II diabetes, childhood growth interruption, awakening headache and finally, relatively increased mortality rate. Because appropriate therapeutic intervention is best way for patients to relieve their symptoms and prevent their possible complications, it is very important for dentists to recognize their own role and responsibility in diagnosis and treatment of these disorders. For this, the present article provides the understanding of the clinical features, possible complications, various treatment modalities, and suitable treatment strategies for snoring and obstructive sleep apnea.

The Therapeutic Effects of Optimal Dose of Mesenchymal Stem Cells in a Murine Model of an Elastase Induced-Emphysema

  • Kim, You-Sun;Kim, Ji-Young;Huh, Jin Won;Lee, Sei Won;Choi, Soo Jin;Oh, Yeon-Mok
    • Tuberculosis and Respiratory Diseases
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    • 제78권3호
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    • pp.239-245
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    • 2015
  • Background: Chronic obstructive pulmonary disease is characterized by emphysema, chronic bronchitis, and small airway remodeling. The alveolar destruction associated with emphysema cannot be repaired by current clinical practices. Stem cell therapy has been successfully used in animal models of cigarette smoke- and elastase-induced emphysema. However, the optimal dose of mesenchymal stem cells (MSCs) for the most effective therapy has not yet been determined. It is vital to determine the optimal dose of MSCs for clinical application in emphysema cases. Methods: In the present study, we evaluated the therapeutic effects of various doses of MSCs on elastase-induced emphysema in mice. When 3 different doses of MSCs were intravenously injected into mice treated with elastase, only $5{\times}10^4$ MSCs showed a significant effect on the emphysematous mouse lung. We also identified action mechanisms of MSCs based on apoptosis, lung regeneration, and protease/antiprotease imbalance. Results: The MSCs were not related with caspase-3/7 dependent apoptosis. But activity of matrix metalloproteinase 9 increased by emphysematous lung was decreased by intravenously injected MSCs. Vascular endothelial growth factor were also increased in lung from MSC injected mice, as compared to un-injected mice. Conclusion: This is the first study on the optimal dose of MSCs as a therapeutic candidate. This data may provide important basic data for determining dosage in clinical application of MSCs in emphysema patients.

Inhibition of Inducible Nitric Oxide Synthase and Cyclooxygenase-2 by Gamijihwang-tang Via Suppression of Nuclear Factor-B Activation in RAW 264.7 cells

  • Jang Du-Hyun;Kim Ji-Young;Han Eun-Hee;Park Hee-Ok;Kim Dong-Hee;Jeong Hye-Gwang;Yoo Dong-Yeol
    • Journal of Physiology & Pathology in Korean Medicine
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    • 제19권5호
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    • pp.1405-1410
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    • 2005
  • Asthma is recognized today as an inflammatory disease of the lung characterized by acute non-specific airway hypersensitiveness in association with chronic pulmonary inflammation. Gamijihwang-tang(GJT), a fortified prescription of YMJHT, is applied for the treatments of chronic coughing and asthma, and post-delivery coughing and asthma in the gynecology. Also in the clinical practice, GJT is known to be very effective for controlling coughing and asthma as a cold sequoia. In this study, we investigated the effects of GJT on the lipopolysaccharide (LPS)-induced nitric oxide (NO) and prostaglandin $E_2$ ($PGE_2$) production, and on the level of inducible nitric oxide synthase (iNOS) and Cyclooxygenase-2 expression in murine macrophage RAW 264.7 cells. We found that GJT inhibited LPS-induced NO and $PGE_2$ production in a dose dependent manner. Furthermore, GJT inhibited the expression of LPS-induced iNOS and COX-2 protein and mRNA expression in RAW 264.7 macrophages. Treatment with GJT of RAW 264.7 cells transfected with a reporter construct indicated a reduced level of LPS-induced nuclear factor-KB (NF-kB) activity and effectively lowered NF-kB binding as measured by transient transfection assay. These results suggest that the main inhibitory mechanism of the GJT may be the reduction of iNOS and COX-2 gene expression through blocking of NF-kB activation.