Yeong Hun Choe

Chonbuk National University Hospital, Sŏul, Seoul, South Korea

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Publications (20)59.55 Total impact

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    ABSTRACT: Bronchial asthma is a chronic inflammatory disorder of the airways characterized by increased expression of multiple inflammatory genes. Acetylation of histones by histone acetyltransferases is associated with increased gene transcription, whereas hypoacetylation induced by histone deacetylases is associated with suppression of gene expression. Sirtuin 1 (SIRT1) is a member of the silent information regulator 2 family that belongs to class III histone deacetylase. This study aimed to investigate the role of SIRT1 and the related molecular mechanisms in the pathogenesis of allergic airway disease. By using a murine model of ovalbumin (OVA)-induced allergic airway disease and murine tracheal epithelial cells, this study investigated the involvement of SIRT1 and its signaling networks in allergic airway inflammation and hyperresponsiveness. In this study with mice after inhalation of OVA, the increased levels of SIRT1, hypoxia-inducible factor 1alpha (HIF-1alpha), and vascular endothelial growth factor protein in the lungs after OVA inhalation were decreased substantially by the administration of a SIRT1 inhibitor, sirtinol. We also showed that the administration of sirtinol reduced significantly the increased numbers of inflammatory cells of the airways; airway hyperresponsiveness; increased levels of IL-4, IL-5, and IL-13; and increased vascular permeability in the lungs after OVA inhalation. In addition, we have found that inhibition of SIRT1 reduced OVA-induced upregulation of HIF-1alpha in airway epithelial cells. These results indicate that inhibition of SIRT1 might attenuate antigen-induced airway inflammation and hyperresponsiveness through the modulation of vascular endothelial growth factor expression mediated by HIF-1alpha in mice.
    The Journal of allergy and clinical immunology 10/2009; 125(2):449-460.e14. · 12.05 Impact Factor
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    ABSTRACT: Pulmonary crystal-storing histiocytoma is a very rare disorder and is characterized by infiltration of histiocytes with intracytoplasmic accumulation of crystallized immunoglobulins. It is usually associated with lymphoproliferative diseases or plasma cell dyscrasia. Here, we report a case of pulmonary crystal-storing histiocytoma in a 64-year-old man, presenting as a chronic pulmonary consolidation in the lung exposed to asbestos. Video-assisted thoracoscopic surgical biopsy displayed sheets of large, epithelioid histiocytes filled with a large number of needle-like crystals, showing the accumulation of crystallized polyclonal immunoglobulins. This lesion was consistent with crystal-storing histiocytosis or crystal-storing histiocytoma. With extensive clinical work-up, the current case was not associated with lymphoproliferative diseases. Herein, we present this extremely rare entity of pulmonary pathology, a pulmonary crystal-storing histiocytoma arising in the lung exposed to asbestos, and demonstrate the clinical, radiologic, and pathologic features of the tumor.
    The American Journal of the Medical Sciences 09/2009; 338(5):421-4. · 1.33 Impact Factor
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    ABSTRACT: Peroxisome proliferator-activated receptor gamma (PPARgamma) plays a critical role in the control of airway inflammation. Recently, IL-17 has been found to be implicated in many immune and inflammatory responses, including airway inflammation. However, no data are available concerning the effect of PPARgamma on IL-17 production in airway inflammatory diseases. In this study, we used a mouse model of asthma to evaluate the effect of two PPARgamma agonists, rosiglitazone or pioglitazone, on IL-17 expression in allergic airway disease. After OVA inhalation, mice developed the typical pathophysiological features of asthma, and the expression of IL-17 protein and mRNA in the lungs was increased. Administration of rosiglitazone or pioglitazone reduced the pathophysiological features of asthma and decreased the increased IL-17 protein and mRNA expression after OVA inhalation. In addition, the attenuating effect of PPARgamma agonist on allergic airway inflammation and bronchial hyperresponsiveness is abrogated by coadministration of rIL-17. This study also showed that the inhibition of IL-17 activity with anti-IL-17 Ab remarkably reduced the increased numbers of inflammatory cells of the airways, airway hyperresponsiveness, and the increased levels of IL-4, IL-5, and IL-13 in bronchoalveolar lavage fluid and OVA-specific IgE in serum. In addition, we found that administration of rosiglitazone or pioglitazone decreased the increased NF-kappaB activity and that a NF-kappaB inhibitor, BAY 11-7085, substantially reduced the increased IL-17 protein levels in the lung tissues after OVA inhalation. These findings suggest that the therapeutic effect of PPARgamma in asthma is partly mediated by regulation of IL-17 expression via NF-kappaB pathway.
    The Journal of Immunology 08/2009; 183(5):3259-67. · 5.52 Impact Factor
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    ABSTRACT: Pulmonary cryptococcosis tends to occur commonly in immunocompromized patients. However, as more individuals are undergoing regular medical examinations, the number of cases of pulmonary cryptococcosis detected incidentally in immunocompetent individuals is increasing. The aim of the present study was to evaluate the radiologic manifestations of pulmonary cryptococcosis in immunocompetent patients with no significant symptoms. The clinical records and radiographic findings of 7 immunocompetent subjects with isolated pulmonary cryptococcosis who were diagnosed by pathological examinations, were reviewed. The mean age of patients was 68.4 y (range 58-80 y), and 6 of them were female. The radiographic manifestations in all patients were 1 or more nodules. Computed tomography (CT) demonstrated 22 pulmonary nodules with diameter from 3 mm to 22 mm, and multiple nodules were more frequent than solitary nodules (5 cases versus 2 cases). Axial analysis of patients showed that an involvement of the upper lobe was observed in all patients. Most nodules were well defined and smoothly marginated (21 nodules) and cavitations were infrequent findings (2 nodules). Lymphadenopathies were found in 2 patients. The most common imaging finding of pulmonary cryptococcosis in asymptomatic immunocompetent hosts was the presence of multiple nodules marginated smoothly with upper lobe predominance.
    Scandinavian Journal of Infectious Diseases 07/2009; 41(8):602-7. · 1.71 Impact Factor
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    ABSTRACT: Pulmonary benign metastasizing leiomyoma (BML) is a rare disease occurring predominantly in women of reproductive age and usually develops several years after the resection of a uterine leiomyoma. A 52-year-old postmenopausal woman was admitted to our hospital because of a right-sided empyema. Contrast-enhanced computed tomography showed a multiloculated pleural effusion on the right side and multiple small nodules in the left lung. A wedge biopsy revealed the pulmonary nodule consisting of branching glandular structures surrounded by abundant smooth muscle cells with no atypia. We performed a gynecologic examination to identify the primary origin of the pulmonary smooth muscle tumors. A uterine leiomyoma was found, and the patient underwent a total hysterectomy. Both pulmonary nodules and uterine leiomyoma were positive for estrogen and progesterone receptors. Therefore, we diagnosed the pulmonary lesions as BMLs. This is an interesting case of pulmonary BML identified simultaneously with uterine myoma in a postmenopausal woman. BML should be considered in women with multiple pulmonary nodules, even though it is rare.
    The American Journal of the Medical Sciences 07/2009; 338(1):72-4. · 1.33 Impact Factor
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    ABSTRACT: Minimally invasive percutaneous ablative therapies for treating lung cancers are currently being studied as treatment alternatives. This present study investigated the efficacies of percutaneous thoracic cryotherapy (PTC) and radiofrequency ablation (RFA) on clinical courses of pulmonary malignant tumours, especially in the setting of non-surgical candidates. Sixty-five patients with lung malignancy underwent sixty-seven sessions of RFA and nine sessions of PTC. We evaluated the results of RFA and PTC including efficacies, local progression rate, survival rate, and complications. Twenty-nine patients (43.3%) treated with RFA and six patients (66.7%) with PTC attained complete ablation. In small-sized lung mass (3 cm), complete ablation rate of RFA and PTC was increased to 76.2% and 85.7%, respectively. Additionally, we have found that the complete ablation group had significantly higher survival duration and progression free survival duration compared with the partial ablation group. Moreover, the complication profile was acceptable and the pain associated with the procedures disappeared within 1 day; 42 patients (62.7%) after RFA and all patients after PTC. This study provides evidence for the use of PTC and RFA as treatment alternatives with low procedural morbidity in the management of inoperable pulmonary malignant tumours, although the current study is limited by the small sample size and the short follow-up period.
    European journal of cancer (Oxford, England: 1990) 04/2009; 45(10):1773-9. · 4.12 Impact Factor
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    ABSTRACT: Clear cell tumor of the lung is a rare and very unusual benign pulmonary tumor. As clear cell tumor of the lung contains abundant cytoplasmic glycogen, this tumor is called "sugar tumor". We report a case of sugar tumor in a 64-yr-old man presenting as a round pulmonary nodule. On dynamic computed tomography (CT) scans, the solitary pulmonary nodule showed early wash-in enhancement with an early washout pattern like a lung malignancy. The patient underwent wedge resection for the tumor. Pathologic examination, including immunohistochemical studies, revealed that the nodule was a benign clear cell tumor, so-called "sugar tumor". Because only a small number of cases have been reported previously, clinical aspects, radiological characteristics on dynamic contrast-enhanced CT, and differential diagnosis of the tumor are not well established. Herein we present a clear cell tumor of the lung and discuss the clinical, radiological, and pathological features of the tumor.
    Journal of Korean Medical Science 01/2009; 23(6):1121-4. · 1.25 Impact Factor
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    ABSTRACT: Vascular endothelial growth factor (VEGF) is a mediator of airway inflammation and remodeling in asthma. We investigated whether VEGF levels are elevated in plasma and serum obtained from patients with asthma and evaluated whether levels of plasma VEGF correlated with those of serum VEGF. We measured levels of plasma and serum VEGF in patients with stable asthma or with acute asthma and examined the correlation between plasma and serum VEGF concentration with initial forced expiratory volume in 1 second (FEV(1)). We found that levels of VEGF in plasma or in serum were significantly increased in stable asthmatic patients and even higher in acute asthmatic patients compared with the levels in healthy control subjects. The levels of serum VEGF correlated significantly with those of plasma VEGF. Additionally, the circulating VEGF levels were significantly inversely correlated with the percent predicted FEV(1). These results suggest that the overproduction of VEGF is implicated in asthma exacerbation and that measurement of either plasma or serum VEGF level can be a valid index in asthmatic patients. Therefore, the changes in the VEGF levels in peripheral blood of asthmatic patients can be used as a measure for progression of asthma during treatment.
    Journal of Asthma 12/2008; 45(9):735-9. · 1.85 Impact Factor
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    ABSTRACT: Asthma is a chronic inflammatory disorder of the airways characterized by airflow limitation and airway hyperresponsiveness. Lung density indices on quantitative computed tomography (QCT) are assumed to reflect the degree of air trapping originated from airflow limitation in airway diseases. The present study investigated the availability of lung density indices on QCT in clinical evaluation of asthma. Eleven asthmatic patients and 48 healthy control subjects were prospectively evaluated by QCT, pulmonary function testing, and a methacholine challenge test. High-resolution computed tomography scans were performed at full-inspiratory and full-expiratory phases, and percentage of lung field occupied by low attenuation area (LAA%) and mean lung density (MLD) at both inspiratory and expiratory phases were measured. MLD values at inspiratory phase were significantly increased in asthmatic patients compared with those in healthy control subjects. Inspiratory LAA% values were significantly decreased in asthmatics compared with the values in control subjects. On expiratory scans, MLD values of asthmatics were significantly lower than the values of control subjects. Expiratory LAA% values of asthmatics were significantly higher than the values of control subjects. The LAA% in the expiratory phase showed significant negative correlation with forced expiratory volume in 1 second (FEV(1)), FEV(1)/forced vital capacity, and the provocative dose of methacholine causing a 20% decrease in FEV(1) in asthmatic patients. These results suggest that lung density indices on QCT may be useful for clinical evaluation of asthmatic patients and increased LAA% in the expiratory phase is associated with airflow limitation and airway hyperresponsiveness in asthma.
    Journal of Asthma 12/2008; 45(9):774-9. · 1.85 Impact Factor
  • The American Journal of the Medical Sciences 10/2008; 336(3):278. · 1.33 Impact Factor
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    ABSTRACT: Bronchial inflammation is usually accompanied by increased vascular permeability. Mast cells release a number of mediators that act directly on the vasculature, resulting in vasodilatation, increased permeability, and subsequent plasma protein extravasation. Vascular endothelial growth factor (VEGF) has been implicated to contribute to asthmatic tissue edema through its effect on vascular permeability. However, the effects of mast cells on VEGF-mediated signaling in allergic airway disease are not clearly understood. Objectives: An aim of the present study was to investigate the role of mast cells on VEGF-mediated signal transduction in allergic airway disease. We used genetically mast cell-deficient WBB6F(1)-Kit(W)/Kit(W-v) (W/W(v)) mice and the congenic normal WBB6F(1)(+/+) mouse model for allergic airway disease to investigate the role of mast cells on VEGF-mediated signal transduction in allergic airway disease, more specifically in vascular permeability. Our present study, with ovalbumin (OVA)-sensitized without adjuvant and OVA-challenged mice, revealed the following typical pathophysiologic features of allergic airway diseases: increased inflammatory cells of the airways, airway hyperresponsiveness, increased vascular permeability, and increased levels of VEGF. However, levels of VEGF and plasma exudation in W/W(v) mice after OVA inhalation were significantly lower than levels in WBB6F(1)(+/+) mice. Moreover, mast cell-reconstituted W/W(v) mice restored vascular permeability and VEGF levels similar to those of the WBB6F(1)(+/+) mice. Our data also showed that VEGF expression was regulated by hypoxia-inducible factor-1alpha (HIF-1alpha) activation through the phosphatidylinositol 3-kinase (PI3K)-HIF-1alpha pathway in allergic airway disease. These results suggest that mast cells modulate vascular permeability by the regulation of the PI3K-HIF-1alpha-VEGF axis.
    American Journal of Respiratory and Critical Care Medicine 08/2008; 178(8):787-97. · 11.04 Impact Factor
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    ABSTRACT: Reactive oxygen species (ROS) play a crucial role in acute lung injury. Tissue inflammation, the increased vascular permeability, and plasma exudation are cardinal features of acute lung injury. Angiopoietin-1 (Ang1) has potential therapeutic applications in preventing vascular leakage and also has beneficial effects in several inflammatory disorders. Recently developed COMP-Ang1 is more potent than native Ang1 in phosphorylating tyrosine kinase with immunoglobulin and EGF homology domain 2 receptor in endothelial cells. However, there are no data on effects and related molecular mechanisms of COMP- Ang1 on ROS-induced acute lung injury. We used hydrogen peroxide (H2O2)-inhaled mice to evaluate the effect of COMP-Ang1 on pulmonary inflammation, bronchial hyper-responsiveness, and vascular leakage in acute lung injury. The results have revealed that VEGF expression, the levels of IL-4, TNF-alpha, IL-1beta, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1 in lungs, the levels of hypoxia-inducible factor-1alpha (HIF-1alpha) and NF-kappaB in nuclear protein extracts, phosphorylation of Akt, and vascular permeability were increased after inhalation of H2O2 and that the administration of COMP-Ang1 markedly reduced airway hyper-responsiveness, pulmonary inflammation, plasma extravasation, and the increases of cytokines, adhesion molecules, and VEGF in lungs treated with H2O2. We have also found that the activation of HIF-1a and NF-kB and the increase of phosphoinositide 3-kinase activity in lung tissues after H2O2 inhalation were decreased by the administration of COMP-Ang1. These results suggest that COMP-Ang1 ameliorates ROS-induced acute lung injury through attenuating vascular leakage and modulating inflammatory mediators.
    Experimental and Molecular Medicine 07/2008; 40(3):320-31. · 2.57 Impact Factor
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    ABSTRACT: Chordomas are slow-growing, malignant tumors of bone that are thought to be derived from the primitive notochord and occur almost exclusively in the axial skeleton. The so-called extra-axial chordoma has been shown to demonstrate identical features to the classic chordoma, except that it is found outside the axial skeleton. Only six cases of extra-axial chordoma have been reported in the literature to date. In this report, we present another case of extra-axial chordoma for the first time originating from the lung parenchyma. A 79-year-old man presented a 7.3-cm-sized cavitary lung mass. Pathologic examination, including immunohistochemical studies, revealed that the mass was a chordoma. We report an extra-axial chordoma for the first time presenting as a lung mass.
    Respiration 06/2008; 77(2):219-23. · 2.92 Impact Factor
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    Yeong Hun Choe, Yong Chul Lee
    Tuberculosis and Respiratory Diseases 01/2008; 64(1).
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    Tuberculosis and Respiratory Diseases 01/2008; 64(2).
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    ABSTRACT: Reactive oxygen species (ROS) play an important role in the pathogenesis of airway inflammation and hyperresponsiveness. Recent studies have demonstrated that antioxidants are able to reduce airway inflammation and hyperreactivity in animal models of allergic airway disease. A newly developed antioxidant, small molecular weight thiol compound, N-acetylcysteine amide (AD4) has been shown to increase cellular levels of glutathione and to attenuate oxidative stress related disorders such as Alzheimer's disease, Parkinson's disease, and multiple sclerosis. However, the effects of AD4 on allergic airway disease such as asthma are unknown. We used ovalbumin (OVA)-inhaled mice to evaluate the role of AD4 in allergic airway disease. In this study with OVA-inhaled mice, the increased ROS generation, the increased levels of Th2 cytokines and VEGF, the increased vascular permeability, the increased mucus production, and the increased airway resistance in the lungs were significantly reduced by the administration of AD4. We also found that the administration of AD4 decreased the increases of the NF-kappaB and hypoxia-inducible factor-1alpha (HIF-1alpha) levels in nuclear protein extracts of lung tissues after OVA inhalation. These results suggest that AD4 attenuates airway inflammation and hyperresponsiveness by regulating activation of NF-kappaB and HIF-1alpha as well as reducing ROS generation in allergic airway disease.
    Experimental and Molecular Medicine 01/2008; 39(6):756-68. · 2.57 Impact Factor
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    ABSTRACT: Toluene diisocyanate (TDI)-induced airway disease is a disorder characterized by chronic airway inflammation and airway remodeling. A recently discovered group of cytokines is the IL-17 family, which has been introduced as an important regulator of immune and inflammatory responses, including airway inflammation. Recently, we have reported that phosphatase and tensin homologue deleted on chromosome 10 (PTEN) plays a pivotal role in the pathogenesis of bronchial asthma. However, there are no available data for the effects of PTEN or IL-17 on TDI-induced airway disease and the relationship between PTEN and IL-17. We used a murine model to determine the role of PTEN in the pathogenesis of TDI-induced airway disease and the regulation of IL-17 production. These mice developed the typical pathophysiological features of TDI-induced airway disease and increased IL-17 expression in the lungs. Administration of phosphoinositide 3-kinase inhibitors or adenoviruses carrying PTEN cDNA (AdPTEN) reduced the pathophysiological features of TDI-induced airway disease and decreased the increased levels of IL-17 expression. Our results also showed that PI3K inhibitors or AdPTEN down-regulated a transcription factor, NF-kappaB activity, and BAY 11-7085 substantially reduced the increased levels of IL-17 after TDI inhalation. We also found that inhibition of IL-17 activity with an anti-IL-17 Ab reduced airway inflammation and airway hyperresponsiveness. These results suggest that PTEN plays a protective role in the pathogenesis of TDI-induced airway disease, at least in part through the regulation of IL-17 expression. Thus, PTEN may be a useful target for treating TDI-induced airway disease by modulating IL-17 expression.
    The Journal of Immunology 12/2007; 179(10):6820-9. · 5.52 Impact Factor
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    ABSTRACT: Gap junction channels formed with connexins directly link to the cytoplasm of adjacent cells and have been implicated in intercellular signaling. Connexin 37 (Cx37) is expressed in the gas-exchange region of the lung. Recently, Cx37 has been reported to be involved in the pathogenesis of inflammatory disease. However, no data are available on the role of Cx37 in allergic airway inflammatory disease. In the present study, we used a murine model of ovalbumin (OVA)- induced allergic airway disease and primary murine epithelial cells to examine the change of Cx37 in allergic airway disease. These mice develop the following typical pathophysiological features of asthma: airway hyperresponsiveness, airway inflammation, and increased IL-4, IL-5, IL-13, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, eotaxin, and RANTES levels in lungs. Cx37 protein and mRNA expression were decreased in OVA-induced allergic airway disease. Immunoreactive Cx37 localized in epithelial layers around the bronchioles in control mice, which dramatically disappeared in allergen-induced asthmatic lungs. Moreover, the levels of Cx37 protein in lung tissues showed significantly negative correlations with airway inflammation, airway responsiveness, and levels of Th2 cytokines in lungs. These findings indicate that change of Cx37 may be associated with the asthma phenotype.
    Experimental and Molecular Medicine 11/2007; 39(5):629-40. · 2.57 Impact Factor
  • World Allergy Organization Journal. 01/2007;
  • World Allergy Organization Journal. 01/2007;