• Tuberculosis and Respiratory Diseases
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• 제67권6호
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• pp.512-516
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• 2009

Background: Pulmonary paragonimiasis is a subacute to chronic inflammatory disease of the lung caused by lung flukes that result in prolonged inflammation and mechanical injury to the bronchi. However, there are few reports on the bronchoscopic findings of pulmonary paragonimiasis. This report describes the bronchoscopic findings of pulmonary paragonimiasis. Methods: The bronchosocpic findings of 30 patients (20 males, median age 50 years) with pulmonary paragonimiasis between May 1995 and December 2007 were reviewed retrospectively. Results: The diagnoses were based on a positive serologic test results for Paragonimus-specific antibodies in 13 patients (43%), or the detection of Paragonimus eggs in the sputum, bronchial washing fluid, or lung biopsy specimens in 17 patients (57%). The bronchoscopic examinations revealed endobronchial lesions in 17 patients (57%), which were located within the segmental bronchi in 10 patients (59%), lobar bronchi in 6 patients (35%) and main bronchi in 1 patient (6%). The bronchoscopic characteristics of endobronchial lesions were edematous swelling of the mucosa (16/17, 94%) and mucosal nodularity (4/17, 24%), accompanied by bronchial stenosis in 16 patients (94%). Paragonimus eggs were detected in the bronchial washing fluid of 9 out of the 17 patients with endobronchial lesions. The bronchial mucosal biopsy specimens showed evidence of chronic inflammation with eosinophilic infiltration in 6 out of 11 patients (55%). However, no adult fluke or ova were found in the bronchial tissue. Conclusion: Bronchial stenosis with mucosal changes including edematous swelling and mucosal nodularity is the most common bronchoscopic finding of pulmonary paragonimiasis.

• Tuberculosis and Respiratory Diseases
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• 제78권4호
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• pp.440-444
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• 2015

Gastric mucosal damage by iron pills is often reported. However, iron pill aspiration is uncommon. Oxidation of the impacted iron pill causes bronchial mucosal damage that progresses to chronic bronchial inflammation, necrosis, endobronchial stenosis and rarely, perforation. We reported a case of a 92-year-old woman with chronic productive cough and significant left-sided atelectasis. Bronchoscopy revealed substantial luminal narrowing with exudative inflammation of the left main bronchus. Bronchial washing cytology showed necroinflammatory exudate and a small amount of brown material. Mucosal biopsy showed diffuse brown pigments indicative of ferrous pigments, crystal deposition, and marked tissue degeneration. After vigorous coughing, she expectorated dark sediments and her symptoms and radiological abnormalities improved. There are a few such reports worldwide; however, this was the first case reported in Korea. Careful observation of aspiration-prone patients and early detection of iron pill aspiration may prevent iron pill-induced bronchial injury.

• 한국산업보건학회지
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• 제29권2호
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• pp.251-258
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• 2019

Objective: Chronic obstructive pulmonary disease(COPD) is characterized by persistent airflow limitations associated with chronic inflammatory response due to noxious particles or gases in the lung. Inflammation and oxidative stress are associated with COPD. The aim of this study was to evaluate the relationship among inflammation, oxidative stress, and airflow limitation severity in retired miners with COPD. Methods: The levels of serum high-sensitivity C-reactive protein(hsCRP) as a biomarker for inflammation, degree of reactive oxygen metabolites(dROMs) and biological antioxidants potential(BAP) in plasma as biomarkers for oxidative stress were measured in 211 male subjects with COPD. Degree of airflow limitation severity as determined by spirometry was divided into three grades grouped according to the classification of the Global Initiatives for Obstructive Lung Disease(GOLD)(1, mild; 2, moderate; $3{\leq}$, severe or more) using a fixed ratio, post- bronchodilator $FEV_1/FVC$ < 0.7. Results: Mean levels of dROMs significantly increased in relation to airflow limitation severity(GOLD 1, 317.8 U.CARR vs. GOLD 2, 320.3 U.CARR vs. GOLD $3{\leq}$, 350.9 U.CARR, p=0.047) and dROMs levels were correlated with serum hsCRP levels(r=0.514, p<0.001). Mean levels of hsCRP were higher in current smokers(non-smoker, 1.47 mg/L vs. smoker, 2.34 mg/L, p=0.006), and tended to increase with degree of airflow limitation severity(p=0.071). Mean levels of BAP were lower in current smokers(non-smoker, $1873{\mu}mol/L$ vs. smoker, $1754{\mu}mol/L$, p=0.006). Conclusions: These results suggest that inflammation and oxidative stress are related to airflow limitation severity in retired miners with COPD, and there was a correlation between inflammation and oxidative stress.

• Tuberculosis and Respiratory Diseases
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• 제83권1호
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• pp.42-50
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• 2020

Background: Fractional exhaled nitric oxide (FeNO) is regarded as a potential biomarker for identifying eosinophilic inflammation. We aimed to evaluate the clinical implication of FeNO and its influence on inhaled corticosteroids (ICS) prescription rate in Korean chronic obstructive pulmonary disease (COPD) patients. Methods: FeNO level and its association with clinical features were analyzed. Changes in the prescription rate of ICS before and after FeNO measurement were identified. Results: A total of 160 COPD patients were divided into increased (≥25 parts per billion [ppb], n=74) and normal (<25 ppb, n=86) FeNO groups according to the recommendations from the American Thoracic Society. Compared with the normal FeNO group, the adjusted odds ratio for having history of asthma without wheezing and with wheezing in the increased FeNO group were 2.96 (95% confidence interval [CI], 1.40-6.29) and 4.24 (95% CI, 1.37-13.08), respectively. Only 21 out of 74 patients (28.4%) with increased FeNO prescribed ICS-containing inhaler and 18 of 86 patients (20.9%) with normal FeNO were given ICS-containing inhaler. Previous exacerbation, asthma, and wheezing were the major factors to maintain ICS at normal FeNO level and not to initiate ICS at increased FeNO level. Conclusion: Increased FeNO was associated with the history of asthma irrespective of wheezing. However, FeNO seemed to play a subsidiary role in the use of ICS-containing inhalers in real-world clinics, which was determined with prior exacerbation and clinical features suggesting Th2 inflammation.

• IMMUNE NETWORK
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• 제24권3호
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• pp.20.1-20.21
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• 2024

The brain and lungs, vital organs in the body, play essential roles in maintaining overall well-being and survival. These organs interact through complex and sophisticated bi-directional pathways known as the 'lung-brain axis', facilitated by their close proximity and neural connections. Numerous studies have underscored the mediation of the lung-brain axis by inflammatory responses and hypoxia-induced damage, which are pivotal to the progression of both pulmonary and neurological diseases. This review aims to delve into how pulmonary diseases, including acute/chronic airway diseases and pulmonary conditions, can instigate neurological disorders such as stroke, Alzheimer's disease, and Parkinson's disease. Additionally, we highlight the emerging research on the lung microbiome which, drawing parallels between the gut and lungs in terms of microbiome contents, may play a significant role in modulating brain health. Ultimately, this review paves the way for exciting avenues of future research and therapeutics in addressing respiratory and neurological diseases.

• IMMUNE NETWORK
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• 제10권4호
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• pp.109-114
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• 2010

The molecular mechanisms involved in the pathogenesis of chronic obstructive pulmonary disease (COPD) are poorly defined. Accumulating evidences indicate that chronic inflammatory responses and adaptive immunity play important roles in the development and progression of the disease. Recently, it has been shown that IL-17 producing CD4 T cells, named Th17 cells, which have been implicated in the pathogenesis of several inflammatory and autoimmune diseases, are involved in airway inflammation and COPD. In addition, we and others suggest that autoimmunity may play a critical role in the pathogenesis of COPD. Here, we will review the current understanding of roles of Th17 cells and autoimmune responses in COPD.

• Tuberculosis and Respiratory Diseases
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• 제86권3호
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• pp.151-157
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• 2023

The introduction of inhaled corticosteroids (ICS) for the management of asthma has led to a decrease in acute exacerbation of asthma. However, there are concerns regarding the safety of long-term ICS use, particularly pneumonia. Growing evidence indicates that ICS use is associated with an increased risk of pneumonia in patients with chronic obstructive pulmonary disease, whereas the risk in patients with asthma remains unclear. This review discusses the effect of ICS on pneumonia among patients with asthma to update the existing literature. Asthma is associated with an increased risk of pneumonia. Several hypotheses have been proposed to explain this association, including that asthma impairs the clearance of bacteria owing to chronic inflammation. Therefore, controlling airway inflammation with ICS may prevent the occurrence of pneumonia in asthma. In addition, two meta-analyses investigating randomized control trials showed that ICS use was associated with a protective effect against pneumonia in asthma.

• 한국독성학회:학술대회논문집
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• 한국독성학회 2005년도 춘계 국제심포지엄 및 학술대회
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• pp.51-82
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• 2005

To compare the pulmonary toxicity between ultrafine colloidal silica particles (UFCSs) and fine colloidal silica particles (FCSs), mice were intratracheally instilled with 3 mg of 14-nm UFCSs and 230-nm FCSs and pathologically examined from 30 mill to 24 hr post-exposure. Histopathologically, lungs exposed to both sizes of particles showed bronchiolar degeneration and necrosis, neutrophilic inflammation in alveoli with alveolar type II cell proliferation and particle-laden alveolar macrophage accumulation. UFCSs, however, induced extensive alveolar hemorrhage compared to FCSs from 30 min onwards. UFCSs also caused more severe bronchiolar epithelial cell necrosis and neutrophil influx in alveoli than FCSs at 12 and 24 hr post-exposure. Laminin positive immunolabellings in basement membranes of bronchioles and alveoli of UFCSs treated animals was weaker than those of FCSs treated animals in all observation times. Electron microscopy demonstrated UFCSs and FCSs on bronchiolar and alveolar wall surface as well as in the cytoplasm of alveolar epithelial cells, alveolar macrophages and neutrophils. Type I alveolar epithelial cell erosion with basement membrane damage in UFCSs treated animals was more severe than those in FCSs treated animals. At 12 and 24 hr post-exposure, bronchiolar epithelia cells in UFCSs treated animals showed more intense vacuolation and necrosis compared to FCSs treated animals. These findings suggest that UFCSs has greater ability to induce lung inflammation and tissue damages than FCSs.

• Journal of Microbiology and Biotechnology
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• 제33권9호
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• pp.1111-1118
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• 2023

As a long-term condition that affects the airways and lungs, chronic obstructive pulmonary disease (COPD) is characterized by inflammation, emphysema, breathlessness, chronic cough, and sputum production. Currently, the bronchodilators and anti-inflammatory drugs prescribed for COPD are mostly off-target, warranting new disease management strategies. Accumulating research has revealed the gut-lung axis to be a bidirectional communication system. Cigarette smoke, a major exacerbating factor in COPD and lung inflammation, affects gut microbiota composition and diversity, causing gut microbiota dysbiosis, a condition that has recently been described in COPD patients and animal models. For this review, we focused on the gut-lung axis, which is influenced by gut microbial metabolites, bacterial translocation, and immune cell modulation. Further, we have summarized the findings of preclinical and clinical studies on the association between gut microbiota and COPD to provide a basis for using gut microbiota in therapeutic strategies against COPD. Our review also proposes that further research on probiotics, prebiotics, short-chain fatty acids, and fecal microbiota transplantation could assist therapeutic approaches targeting the gut microbiota to alleviate COPD.

• 동의생리병리학회지
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• 제21권6호
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• pp.1525-1533
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• 2007

The discovery of drugs on the treatment of rhinitis and allergic disease is a very important subject in human heath. The Shinbijen has been used for centruries as a traditional medicine in Korea and is known to have an anti-inflammatory effect. However, its specific mechanism of action is still unknown. In this report, we investigated the effect of hot water extract from Shinbijen on OVA-mediated allergic reaction and studied its possible mechanism of action using fluorescenc microscopy and RT-PCR analysis. Shinbijen inhibited OVA-induced rhinitis, total cells in BFA and lymphocyte related to inflammation in mice. Shinbijen decreased immuno response, which activated by IL-4, COX-2 and iNOS expression. in tissue. Shinbijen reduced inflammatory molecule release from mice lung tissue and CD4/CD8 cells activated by cardiac blood. Shinbijen decreased OVA-induced IL-4 and iNOS levels in pulmonary alveoli. Our findings provide evidence that Shinbijen inhibits OVA-induced allergic reactions, and also demonstrate the involvement of inflammation and allergic disease in these effects.