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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.
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김소리,이용철,김희정,김동임,이양근,이흥범,박성주,최영훈,박승용 대한결핵 및 호흡기학회 2013 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.116 No.-
IL-17 has been increasingly known to be implicated in the pathogenesis of asthma as a pro-inflammatory regulator by inducing the expression of various inflammatory mediators. Recent studies have demonstrated that excess of endoplasmic reticulum (ER) stress interferes with protein synthesis and secretion, induces reactive oxygen species generation, increases inflammation via NF-κB activation, and mediates apoptotic cell death through the expression of CHOP, thereby being involved in various disorders. In addition, while various inflammatory stimuli can induce the excess of ER stress, there is little information dealing with the relationship between IL-17 and ER stress in airway inflammatory disorders. In this study, we have evaluated the interaction between IL-17 and ER stress using a murine model of asthma. The OVALPS-OVA mice showed that the expression of ER stress markers and the protein levels of unfolded-protein response (UPR)-related marker in lung tissues were significantly increased after OVA challenge. Our results also showed that IL-17 neutralizing antibody significantly reduced the increases in ER stress, inflammatory cytokines, airway inflammation, and bronchial hyperresponsiveness. Moreover, our data showed that 4-phenylbutyric acid (4-PBA), a chemical chaperone significantly reduced the increases in ER stress, inflammatory cytokines, airway inflammation, and bronchial hyperresponsiveness. These findings suggest that IL-17 plays an important role in the pathogenesis of bronchial asthma, at least in part, through the modulation of ER stress.IL-17 has been increasingly known to be implicated in the pathogenesis of asthma as a pro-inflammatory regulator by inducing the expression of various inflammatory mediators. Recent studies have demonstrated that excess of endoplasmic reticulum (ER) stress interferes with protein synthesis and secretion, induces reactive oxygen species generation, increases inflammation via NF-κB activation, and mediates apoptotic cell death through the expression of CHOP, thereby being involved in various disorders. In addition, while various inflammatory stimuli can induce the excess of ER stress, there is little information dealing with the relationship between IL-17 and ER stress in airway inflammatory disorders. In this study, we have evaluated the interaction between IL-17 and ER stress using a murine model of asthma. The OVALPS-OVA mice showed that the expression of ER stress markers and the protein levels of unfolded-protein response (UPR)-related marker in lung tissues were significantly increased after OVA challenge. Our results also showed that IL-17 neutralizing antibody significantly reduced the increases in ER stress, inflammatory cytokines, airway inflammation, and bronchial hyperresponsiveness. Moreover, our data showed that 4-phenylbutyric acid (4-PBA), a chemical chaperone significantly reduced the increases in ER stress, inflammatory cytokines, airway inflammation, and bronchial hyperresponsiveness. These findings suggest that IL-17 plays an important role in the pathogenesis of bronchial asthma, at least in part, through the modulation of ER stress.
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김소리,이용철,김동임,이양근,이흥범,박성주,최영훈,박승용,강미란 대한결핵 및 호흡기학회 2013 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.116 No.-
Oxidative stress is well known to be implicated in the development of asthma. The mitochondrial respiratory chain is a major site of intracellular reactive oxygen species (ROS) generation and, at the same time, an important target for the damaging effects of ROS. Mito-Tempo is a specific mitochondrial ROS inhibitor and it is known to be associated with opening of mitochondrial permeability transition pore and inhibition of cell necroptosis or apoptosis. However, there is little information on the protective effects of Mito-Tempo on the inflammatory airway disorders including bronchial asthma and its acute exacerbation. We investigate the effects of Mito-tempo on the allergic airway inflammation and hyperresponsiveness using the mice sensitized with OVA and LPS and then challenged with OVA (OVALPS-OVA mice). The OVALPS-OVA mice showed the typical features of neutrophilic asthma; increased airway inflammatory cells, the pathologic changes, the increased levels of Th2 cytokines in lungs of OVALPS-OVA mice, increased mitochondrial ROS generation, and increased bronchial hyperresponsiveness. Interestingly, we found that in OVALPS-OVA mice, Mito-Tempo, a novel mitochondrial targeting agent significantly reduced the increases in inflammatory cytokines, mitochondrial ROS generation, airway inflammation, and bronchial hyperresponsiveness. These findings indicate that mitochondrial dysfunction including oxidative damage may be implicated in the pathogenesis of bronchial asthma and provide the therapeutic potential of a mitochondrial targeting agent, Mito-Tempo, for bronchial asthma.Oxidative stress is well known to be implicated in the development of asthma. The mitochondrial respiratory chain is a major site of intracellular reactive oxygen species (ROS) generation and, at the same time, an important target for the damaging effects of ROS. Mito-Tempo is a specific mitochondrial ROS inhibitor and it is known to be associated with opening of mitochondrial permeability transition pore and inhibition of cell necroptosis or apoptosis. However, there is little information on the protective effects of Mito-Tempo on the inflammatory airway disorders including bronchial asthma and its acute exacerbation. We investigate the effects of Mito-tempo on the allergic airway inflammation and hyperresponsiveness using the mice sensitized with OVA and LPS and then challenged with OVA (OVALPS-OVA mice). The OVALPS-OVA mice showed the typical features of neutrophilic asthma; increased airway inflammatory cells, the pathologic changes, the increased levels of Th2 cytokines in lungs of OVALPS-OVA mice, increased mitochondrial ROS generation, and increased bronchial hyperresponsiveness. Interestingly, we found that in OVALPS-OVA mice, Mito-Tempo, a novel mitochondrial targeting agent significantly reduced the increases in inflammatory cytokines, mitochondrial ROS generation, airway inflammation, and bronchial hyperresponsiveness. These findings indicate that mitochondrial dysfunction including oxidative damage may be implicated in the pathogenesis of bronchial asthma and provide the therapeutic potential of a mitochondrial targeting agent, Mito-Tempo, for bronchial asthma.
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TP-7 : Thematic Poster ; Mitochondrial Dynamics Is Associated with ER Stress in Bronchial Asthma
김소리,이용철,김동임,강미란,이양근,이흥범,박성주,최영훈,박승용 대한결핵 및 호흡기학회 2013 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.116 No.-
Mitochondria are dynamic organelles that undergo fission and fusion events. In mammals, fission-related proteins are Drp1, while fusion-related proteins are named mitofusin (MFN)1, MFN2, and opa1. Recent studies have demonstrated that under persistent stressful condition, that is, pathologic condition, the balance between fission and fusion of mitochondria is out of control. In this study, we aimed to evaluate the morphologic changes of mitochondria in airway inflammatory cells from a murine model of bronchial asthma and focused on the effects of endoplasmic reticulum (ER) stress on the mitochondrial dynamics. The mice sensitized with OVA and LPS and then challenged with OVA (OVALPS-OVA mice) mice showed the typical features of bronchial asthma. Interestingly, electron-microscopic analysis revealed that in BAL cells from OVALPS-OVA mice, the mitochondria were dramatically elongated, fused, and moved to ER compared to the findings of cells from control mice. In addition, the fusion protein, MFN levels were significantly increased in lung tissues of OVALPS-OVA mice. Administration of 4-PBA, an ER stress regulator significantly reduced the increases in inflammatory cytokines, airway inflammation, and bronchial hyperresponsiveness. In addition, the inhibition of ER stress restored the mitochondrial dynamics into the similar state to physiologic condition. These findings indicate that the mitochondrial hyperfusion may be induced by allergen stimulation in airway inflammatory cells and it can be normalized by the suppression of ER stress. Mitochondria are dynamic organelles that undergo fission and fusion events. In mammals, fission-related proteins are Drp1, while fusion-related proteins are named mitofusin (MFN)1, MFN2, and opa1. Recent studies have demonstrated that under persistent stressful condition, that is, pathologic condition, the balance between fission and fusion of mitochondria is out of control. In this study, we aimed to evaluate the morphologic changes of mitochondria in airway inflammatory cells from a murine model of bronchial asthma and focused on the effects of endoplasmic reticulum (ER) stress on the mitochondrial dynamics. The mice sensitized with OVA and LPS and then challenged with OVA (OVALPS-OVA mice) mice showed the typical features of bronchial asthma. Interestingly, electron-microscopic analysis revealed that in BAL cells from OVALPS-OVA mice, the mitochondria were dramatically elongated, fused, and moved to ER compared to the findings of cells from control mice. In addition, the fusion protein, MFN levels were significantly increased in lung tissues of OVALPS-OVA mice. Administration of 4-PBA, an ER stress regulator significantly reduced the increases in inflammatory cytokines, airway inflammation, and bronchial hyperresponsiveness. In addition, the inhibition of ER stress restored the mitochondrial dynamics into the similar state to physiologic condition. These findings indicate that the mitochondrial hyperfusion may be induced by allergen stimulation in airway inflammatory cells and it can be normalized by the suppression of ER stress.
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내시경 조직 생검 후 발생한 급성 거대 출혈성 위궤양 1예
김소리,민경훈,남상우,김현철,조용근,김인희,이수택,안득수 대한소화기내시경학회 2005 Clinical Endoscopy Vol.31 No.2
Although most diagnostic upper gastrointestinal endoscopic procedures are performed on an outpatient basis with relatively low risk, complications related with these procedures can occur. The reported complications are cardiopulmonary complications, drug side effects, perforation, hemorrhage and infection. Hemorrhage may occur from the site of biopsy or polyp removal. It is usually minimal and heals spontaneously with or without endoscopic treatment and rarely requires transfusion or surgery. Acute hemorrhagic ulceration associated with endoscopic mucosal biopsy is very rare. We report a case of a 46-year-old woman with an acute hemorrhagic gastric ulcer after an endoscopic mucosal biopsy. She has been receiving upper gastrointestinal endoscopic examinations annually for the gastric polyp detected 4 years ago. Endoscopic mucosal biopsy was performed without complications. Twelve hours later, she admitted to the emergency room because of melena. Emergent upper gastrointestinal endoscopy showed an acute huge hemorrhagic ulceration along the antrum. She was treated conservatively and discharged 5 days later. 상부 위장관 내시경 검사는 안전한 검사로 알려져 있으며 최근 그 시행대상이나 범위가 보다 확장되고 있다. 상부 위장관 내시경의 합병증은 거의 없다고 알려져 있지만 보고되고 있는 대표적 합병증으로는 심혈관 및 호흡기계 합병증, 전 처치 약물에 의한 합병증, 출혈, 천공 및 감염 등이다. 이 중 출혈은 그 빈도 자체가 낮고, 발생시에도 경미하여 관찰만으로 자연치유되는 경우가 많고, 간단한 내시경적 지혈술로 해결되어 특별한 치료가 필요 없는 경우가 대부분이다. 내시경적 점막 생검은 진단 목적으로 흔히 이루어지는 검사로 생검 출혈성 위궤양이 발생하는 경우는 거의 드물며, 문헌에도 보고된 바가 드물다. 저자들은 46세 여자환자에서 내시경적 점막 생검 후 급성으로 발생한 거대 출혈성 위궤양 1예를 경험하였다. 환자는 4년 전 발견된 위용종에 대해 정기적 내시경 검사를 시행 받아 오던 환자로 정기 검사의 일환으로 용종에 대한 내시경 점막 생검 후 특별한 문제없이 귀가하였다. 12시간 후 환자는 흑색 변을 주소로 응급실에 내원하였으며 다시 시행한 내시경 검사에서 생검 당시 정상 점막으로 관찰된 부분에 새롭게 발생한 급성 출혈성 위궤양이 확인되었다. 환자는 5일간의 내과적 치료로 호전되어 퇴원하였다.
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