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김소리,이용철,김희정,김순하,이양근,이흥범,박성주,최영훈,박승용 대한결핵 및 호흡기학회 2016 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.121 No.-
There is little information on which molecular mechanisms contribute to the assembly of NLRP3 inflammasome induced by mitochondrial ROS, especially in lung. In this study, we used LPS-instilled mice to define the molecular mechanisms implicated in mitochondrial ROS-induced NLRP3 inflammasome activation in lung inflammation, specifically in the relationship with PI3K-HIF-VEGF axis activation. The administration of mitochondrial ROS inhibitors, Nerox-5 or -7 decreased the features of LPS-induced lung inflammation including mitochondrial ROS generation and the levels of NLRP3 expression. In addition, the increases in phosphorylation of Akt, activation of HIF-1α and HIF-2α, and expression of VEGF in lung tissues from LPS-instilled mice were significantly inhibited with the administration of NecroX compounds. Our results also revealed that LPS-induced increases of nuclear translocation of NF-κB, infiltration of DCs, and TLR4 expression in the lung were significantly reduced by inhibition of NecroX compounds. TLR4 inhibition using TAK-242 decreased mitochondrial ROS and the phosphorylation of Akt and p85 expression in lung tissues and attenuates the LPS-inflammation. Interestingly, blockade of VEGF resulted in the substantial suppression of the activation of NLRP3 inflammasome. These findings suggest that mitochondrial ROS activates NLRP3 inflammasome, a crucial player in the pathogenesis of LPS-induced lung inflammation, at least in part through PI3K-HIF-VEGF axis.
김소리,이용철,최영훈,이양근,이흥범,박성주,박승용 대한결핵 및 호흡기학회 2016 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.121 No.-
Hamartoma is a clinically frequent benign lung tumor, accounting for 77% of all benign lung tumors. This abnormality is thought to be the result of variations in the quality, arrangement, or degree of differentiation of the tissues. The majority of pulmonary hamartomas are asymptomatic and show slow annual growth. Depending on the location of the tumor, surgical resection can be recommended, however, hamartoma is considered to be a benign tumor with a good prognosis and often followed up by observation without surgery due to slow annual growth. The mean transverse diameter of hamartomas at discovery was reported to be 21.7 ± 16.2 mm, and the average increase in transverse diameter was 3.2 ± 2.6 mm per year. In addition, the recurrence of hamartoma after surgical resection or excision is extreamly rare. Here, we report a case with an endobronchial hamartoma that was excised totally under rigid bronchoscopy and then recurred within one month after the excision. The rapid growing recurrent harmatoma was completely resected by bronchoscopic cryotherapy and there was no evidence of recurrence up to ten-month follow-up after the cryotherapy.
F-157 Effects of anti-IL-5 antibody on severe asthma with fungal sensitization
김소리,이용철,박해진,이양근,이흥범,박성주,최영훈,박승용 대한결핵 및 호흡기학회 2016 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.121 No.-
Recently, a subphenotype of severe asthma with fungal sensitization (SAFS) has been described in adults and is associated with reduced lung function and increased morbidity. Anti-IL-5 antibody has been approved as a therapeutic agent for patients with severe eosinophilic asthma. In this study, we evaluated the molecular mechanisms associated with severe asthma with fungal sensitization focusing on the role of IL-5. The mice sensitized and challenged with Aspergillus fumigatus (Af-inhaled mice) showed the typical features of bronchial asthma; increased airway inflammatory cells, the pathologic changes, the increased levels of Th2 cytokines in lungs of Af-inhaled mice, and increased bronchial hyper-responsiveness. These asthmatic features were refractory to the treatment with oral dexamethasone. Interestingly, airway inflammatory cells including eosinophils, peribronchial and perivascular inflammation, the expression of IL-5 in lung tissues and airway hyperresponsiveness were reduced markedly by the administration of anti-IL-5 antibody intraperitoneally. However, the expression of other Th2 cytokines, IL-4 and IL-13 did not affected significantly by the treatment with anti-IL-5 antibody. These findings suggest that IL-5 plays more ciritcal roles in SAFS than other Th2 cytokines and that anti-IL-5 antibody can control its own expression of IL-5 in lung tissues maybe partly due to the reduction of source cells of IL-5.
Angiopoietin-1 variant, COMP-Ang1 attenuates hydrogenperoxide-induced acute lung injury
김소리,Kyung Sun Lee,박성주,Kyung Hoon Min,Ka Young Lee,Yeong Hun Choe,Sang Hyun Hong,고규영,이용철 생화학분자생물학회 2008 Experimental and molecular medicine Vol.40 No.3
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-α, IL-1β, intercellular adhesion molecule-1, and vascular cell adhesion molecule- 1 in lungs, the levels of hypoxia-inducible factor- 1α (HIF-1α) and NF-κB 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-1α and NF-κB 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. 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-α, IL-1β, intercellular adhesion molecule-1, and vascular cell adhesion molecule- 1 in lungs, the levels of hypoxia-inducible factor- 1α (HIF-1α) and NF-κB 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-1α and NF-κB 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.
김소리,이용철,이경배,이양근,이흥범,박성주,최영훈,박승용,김동임 대한결핵 및 호흡기학회 2013 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.116 No.-
House dust mites (HDM) are one of the commonest aeroallergens worldwide. Specifically, NLRP3 is one of PRR systems activated by HDM extract in airway epithelial cells. In this study, we have investigated the effects of IC87114, a representative inhibitor of PI3K-δ isoform, on the HDM-induced airway inflammation and hyperresponsiveness, focusing on NLRP3 inflammasome activation and its related molecular mechanisms. HDM-sensitized and -challenged mice showed the typical allergic airway inflammation and hyperresponsivenss, the increased levels of Th2 cytokines, IL-17, IL-1β, and TNF-α in lungs, and increased levels of GSSG and decreased levels of GSH in lung tissues. Moreover, we found the increases of mitochondrial ROS and the NLRP3 inflammasome activation in HDM-exposed lung. Very interestingly, the administration of IC87114 restored the levels of GSH, decreased the numbers of airway inflammatory cells in BAL fluids, the peribronchial and perivascular inflammation in lung tissues, the increase in the levels of inflammatory cytokines, the levels of mitochondrial ROS, NLRP3 activation, and bronchial hyperresponsiveness in HDM-sensitized and -challenged mice. Primary cultured tracheal epithelial cells from HDM-inhaled mice showed the increased expression of NLRP3, IL-1β, and caspase-1 compared to the levels in cells from control mice. These findings suggest PI3K-δ plays an important role in HDM-induced bronchial asthma through the regulation of NLRP3 activation mediated by mitochondrial ROS.House dust mites (HDM) are one of the commonest aeroallergens worldwide. Specifically, NLRP3 is one of PRR systems activated by HDM extract in airway epithelial cells. In this study, we have investigated the effects of IC87114, a representative inhibitor of PI3K-δ isoform, on the HDM-induced airway inflammation and hyperresponsiveness, focusing on NLRP3 inflammasome activation and its related molecular mechanisms. HDM-sensitized and -challenged mice showed the typical allergic airway inflammation and hyperresponsivenss, the increased levels of Th2 cytokines, IL-17, IL-1β, and TNF-α in lungs, and increased levels of GSSG and decreased levels of GSH in lung tissues. Moreover, we found the increases of mitochondrial ROS and the NLRP3 inflammasome activation in HDM-exposed lung. Very interestingly, the administration of IC87114 restored the levels of GSH, decreased the numbers of airway inflammatory cells in BAL fluids, the peribronchial and perivascular inflammation in lung tissues, the increase in the levels of inflammatory cytokines, the levels of mitochondrial ROS, NLRP3 activation, and bronchial hyperresponsiveness in HDM-sensitized and -challenged mice. Primary cultured tracheal epithelial cells from HDM-inhaled mice showed the increased expression of NLRP3, IL-1β, and caspase-1 compared to the levels in cells from control mice. These findings suggest PI3K-δ plays an important role in HDM-induced bronchial asthma through the regulation of NLRP3 activation mediated by mitochondrial ROS.
김소리,이용철,성명주,배혜원 대한결핵및호흡기학회 2017 Tuberculosis and Respiratory Diseases Vol.80 No.3
Since 2015, the Health Insurance Review and Assessment Service (HIRA) has performed annual qualitative assessments of asthma management provided by all medical institutions that care for asthma patients in Korea. According to the third report of qualitative assessment of asthma management in 2017, the assessment appears to have contributed to improving the quality of asthma care provided by medical institutions, especially primary clinics. However, there is still a gap between the ideal goals of asthma management and actual health care policies/regulations in real clinical settings, which leads to the state of standstill with respect to the quality of asthma management despite considerable efforts such as the qualitative assessment of asthma management by national agencies such as the HIRA. At this point, a harmonized approach is needed to raise the level of asthma management among several components including medical policies, efforts of academic associations such as education and distribution of the guideline for management, and reliable financial support by the government.