A. Villa, A. Kostihova, S. Cattaneo, A. Croce, M. Luperto
We report a case of exogenous lipoid pneumonia caused by inhalation of liquid paraffin in a fire eater young man. The patient was admitted to the Emergency Department because of acute retrosternal pain, dry cough and dyspnea. Chest radiograph showed multiple bilateral basal alveolar opacities associated to left pleural effusion; CT chest scan showed multiple bilateral areas of consolidation with cavity areas. BAL cytologic examination revealed abundant lipid-laden macrophages. Clinical symptoms resolved after corticosteroid treatment. Lipoid pneumonia is a rare and often underdiagnosed entity. The presence of lipid-laden macrophages in sputum or BAL fluid helps to confirm the diagnosis.
{"title":"Do Not Play with Fire","authors":"A. Villa, A. Kostihova, S. Cattaneo, A. Croce, M. Luperto","doi":"10.4236/OJRD.2013.33018","DOIUrl":"https://doi.org/10.4236/OJRD.2013.33018","url":null,"abstract":"We report a case of exogenous lipoid pneumonia caused by inhalation of liquid paraffin in a fire eater young man. The patient was admitted to the Emergency Department because of acute retrosternal pain, dry cough and dyspnea. Chest radiograph showed multiple bilateral basal alveolar opacities associated to left pleural effusion; CT chest scan showed multiple bilateral areas of consolidation with cavity areas. BAL cytologic examination revealed abundant lipid-laden macrophages. Clinical symptoms resolved after corticosteroid treatment. Lipoid pneumonia is a rare and often underdiagnosed entity. The presence of lipid-laden macrophages in sputum or BAL fluid helps to confirm the diagnosis.","PeriodicalId":83134,"journal":{"name":"The Journal of respiratory diseases","volume":"3 1","pages":"116-118"},"PeriodicalIF":0.0,"publicationDate":"2013-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70582795","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
F. Abdallah, H. Gharsalli, H. Kwas, S. Taktak, A. Chtourou, A. B. Kheder
Hemothorax caused by rupture of aortic aneurysm or aortic dissection is an uncommon manifestation and carries a high mortality rate. We report two cases of 75- and 80-year-old men, who were referred to our department for exploration of a left pleural opacity. Thoracentesis produced a hemorrhagic fluid. The computed tomography scan revealed an aortic dissection type B of Stanford in the first case and an aneurysm of the descending thoracic aorta in the second patient. Emergency operation was performed in the first case but the patient died of multiple organ failure 48 hours after surgery. Aortic dissection or aneurysm can result in a hemothorax especially in patient with favourable conditions such as elderly patient and systemic hypertension. Diagnosis relies on computed tomography (CT) scan and echocardiography.
{"title":"Hemothorax Revealing Aortic Aneurism and Aortic Dissection","authors":"F. Abdallah, H. Gharsalli, H. Kwas, S. Taktak, A. Chtourou, A. B. Kheder","doi":"10.4236/OJRD.2013.33017","DOIUrl":"https://doi.org/10.4236/OJRD.2013.33017","url":null,"abstract":"Hemothorax \u0000caused by rupture of aortic aneurysm or aortic dissection is an uncommon \u0000manifestation and carries a high mortality rate. We report two cases of 75- and 80-year-old men, who were referred to our department for exploration of a \u0000left pleural opacity. Thoracentesis produced a hemorrhagic fluid. The computed \u0000tomography scan revealed an aortic dissection type B of Stanford in the first \u0000case and an aneurysm of the descending thoracic aorta in the second patient. \u0000Emergency operation was performed in the first \u0000case but the patient died of multiple organ failure 48 hours after surgery. \u0000Aortic dissection or aneurysm can result in a hemothorax especially in patient \u0000with favourable conditions such as elderly patient and systemic hypertension. \u0000Diagnosis relies on computed tomography (CT) scan and echocardiography.","PeriodicalId":83134,"journal":{"name":"The Journal of respiratory diseases","volume":"3 1","pages":"113-115"},"PeriodicalIF":0.0,"publicationDate":"2013-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70583082","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
K. Miyamoto, S. Tasaka, Yasushi Nakano, Hiromi Shinoda, H. Kamata, W. Yamasawa, M. Ishii, N. Hasegawa, T. Betsuyaku
Background and Objectives: Peroxisome proliferator-activated receptor-g (PPAR-g) is a nuclear receptor whose activation regulates inflammation and fibrosis in various organs. We aimed to investigate the effect of two PPAR-g ligands, telmisartan and rosiglitazone, on lung injury and fibrosis induced by intratracheal bleomycin (BLM). Methods: Lung injury and fibrosis was induced in female C57Bl/6 mice by intratracheal instillation of 1.0 mg/kg of BLM. Some of the animals received rosiglitazone intraperitoneally or telmisartan in drinking water. Bronchoalveolar lavage (BAL) was performed 2, 7, 14 or 21 days after BLM instillation for cell counting and measurement of mediators in the lung. In a separate series, the lungs were sampled for collagen assay and histopathological evaluation. Results: Treatment with rosiglitazone or telmisartan significantly attenuated the BLM-induced increases in lung collagen content, pathological score, and inflammatory cells in BAL fluid. Rosiglitazone significantly suppressed BLM-induced elevation of TGF-b1, MCP-1, and IL-6 levels in the lung. In contrast, telmisartan made no changes in these cytokines, whereas it mitigated the BLM-induced increase in prostaglandin F2a in the lung. Higher concentrations of rosiglitazone and telmisartan attenuated proliferation of lung fibroblasts in vitro. Conclusions: Two PPAR-g ligands, rosiglitazone and telmisartan, exert protective effects on BLM-induced lung fibrosis through the suppression of different profibrotic mediators.
{"title":"Differential Mechanisms of the Effect of Peroxisome Proliferator-Activated Receptor Gamma Agonists on Bleomycin-Induced Lung Fibrosis","authors":"K. Miyamoto, S. Tasaka, Yasushi Nakano, Hiromi Shinoda, H. Kamata, W. Yamasawa, M. Ishii, N. Hasegawa, T. Betsuyaku","doi":"10.4236/OJRD.2013.32006","DOIUrl":"https://doi.org/10.4236/OJRD.2013.32006","url":null,"abstract":"Background and Objectives: Peroxisome proliferator-activated receptor-g (PPAR-g) is a nuclear receptor whose activation regulates inflammation and fibrosis in various organs. We aimed to investigate the effect of two PPAR-g ligands, telmisartan and rosiglitazone, on lung injury and fibrosis induced by intratracheal bleomycin (BLM). Methods: Lung injury and fibrosis was induced in female C57Bl/6 mice by intratracheal instillation of 1.0 mg/kg of BLM. Some of the animals received rosiglitazone intraperitoneally or telmisartan in drinking water. Bronchoalveolar lavage (BAL) was performed 2, 7, 14 or 21 days after BLM instillation for cell counting and measurement of mediators in the lung. In a separate series, the lungs were sampled for collagen assay and histopathological evaluation. Results: Treatment with rosiglitazone or telmisartan significantly attenuated the BLM-induced increases in lung collagen content, pathological score, and inflammatory cells in BAL fluid. Rosiglitazone significantly suppressed BLM-induced elevation of TGF-b1, MCP-1, and IL-6 levels in the lung. In contrast, telmisartan made no changes in these cytokines, whereas it mitigated the BLM-induced increase in prostaglandin F2a in the lung. Higher concentrations of rosiglitazone and telmisartan attenuated proliferation of lung fibroblasts in vitro. Conclusions: Two PPAR-g ligands, rosiglitazone and telmisartan, exert protective effects on BLM-induced lung fibrosis through the suppression of different profibrotic mediators.","PeriodicalId":83134,"journal":{"name":"The Journal of respiratory diseases","volume":"03 1","pages":"31-38"},"PeriodicalIF":0.0,"publicationDate":"2013-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70582430","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Churg-Strauss syndrome (CSS) is a very rare small-vessel vasculitis. Clinical features include asthma, rhinitis and/or sinusitis, and peripheral eosinophilia. Although cardiac findings are observed in 50% of cases, coronary artery disease is rarely reported and even more rarely suggestive. The value of cardiac MRI for these patients is discussed here. A 52-year-old non-smoker male without family antecedents of cardiovascular disease presented with worsening of atypical asthma that developed 10 months earlier. A month before, he had been admitted to the ICU because of respiratory distress and cardiogenic shock with chest pain. The angiogram revealed stenosis of the three main coronary arteries requiring the placement of several stents. Follow-up cardiac assessments showed good results. General impairment, unstable asthma associated with rhinitis, and eosinophilia suggested a systemic disease. The diagnosis of CSS was established considering that five criteria of the American College of Rheumatology were found. Prednisolone was prescribed at 1 mg/kg/day, which completely suppressed all symptoms and eosinophilia. Cardiac MRI was performed two months later and revealed a good control of myocardial lesions characterized by fibrosis beneath the anterior endocardium and the median septum. Immunosuppressive treatment was then administered together with corticosteroid therapy. These results suggest that acute coronary artery disease can reveal CSS in some cases. Here, the patient’s cardiac assessment was normal apart from the acute episode, and cardiac MRI helped detect signs of myocarditis and establish a prognosis of CSS.
{"title":"Churg-Strauss Syndrome Revealed by Acute Coronary Artery Disease: A Case Report *","authors":"M. Estivals, Marc Périé, D. Colombier, B. Farah","doi":"10.4236/OJRD.2013.32007","DOIUrl":"https://doi.org/10.4236/OJRD.2013.32007","url":null,"abstract":"Churg-Strauss syndrome (CSS) is a very rare small-vessel vasculitis. Clinical features include asthma, rhinitis and/or sinusitis, and peripheral eosinophilia. Although cardiac findings are observed in 50% of cases, coronary artery disease is rarely reported and even more rarely suggestive. The value of cardiac MRI for these patients is discussed here. A 52-year-old non-smoker male without family antecedents of cardiovascular disease presented with worsening of atypical asthma that developed 10 months earlier. A month before, he had been admitted to the ICU because of respiratory distress and cardiogenic shock with chest pain. The angiogram revealed stenosis of the three main coronary arteries requiring the placement of several stents. Follow-up cardiac assessments showed good results. General impairment, unstable asthma associated with rhinitis, and eosinophilia suggested a systemic disease. The diagnosis of CSS was established considering that five criteria of the American College of Rheumatology were found. Prednisolone was prescribed at 1 mg/kg/day, which completely suppressed all symptoms and eosinophilia. Cardiac MRI was performed two months later and revealed a good control of myocardial lesions characterized by fibrosis beneath the anterior endocardium and the median septum. Immunosuppressive treatment was then administered together with corticosteroid therapy. These results suggest that acute coronary artery disease can reveal CSS in some cases. Here, the patient’s cardiac assessment was normal apart from the acute episode, and cardiac MRI helped detect signs of myocarditis and establish a prognosis of CSS.","PeriodicalId":83134,"journal":{"name":"The Journal of respiratory diseases","volume":"03 1","pages":"39-43"},"PeriodicalIF":0.0,"publicationDate":"2013-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70582482","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Diffuse Idiopathic Neuroendocrine Cell Hyperplasia (DIPNECH) is a rare pulmonary disease. It was first described by Aguayo et al. in 1992, and recognised by the World Health Organisation in 2004 as a precursor lesion to the development of pulmonary carcinoid tumour. DIPNECH has been described in several isolated case reports and series. This article describes a case of DIPNECH and summaries the recent literature in an attempt to raise awareness of this disease and management options.
{"title":"A Case of DIPNECH and Review of the Current Literature","authors":"P. Mitchell, M. Kennedy, M. Henry","doi":"10.4236/OJRD.2013.32011","DOIUrl":"https://doi.org/10.4236/OJRD.2013.32011","url":null,"abstract":"Diffuse Idiopathic Neuroendocrine Cell Hyperplasia (DIPNECH) is a rare pulmonary disease. It was first described by Aguayo et al. in 1992, and recognised by the World Health Organisation in 2004 as a precursor lesion to the development of pulmonary carcinoid tumour. DIPNECH has been described in several isolated case reports and series. This article describes a case of DIPNECH and summaries the recent literature in an attempt to raise awareness of this disease and management options.","PeriodicalId":83134,"journal":{"name":"The Journal of respiratory diseases","volume":"03 1","pages":"68-72"},"PeriodicalIF":0.0,"publicationDate":"2013-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70582129","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Chronic Obstructive Pulmonary Disease (COPD) is a multifactorial disease in the pathogenesis of which contributes a variety of causative factors including genetic and environmental ones. They may also be interactions of genetic susceptibilities and environmental influences. Towards to that in the pathogenesis of the disease except smoking, it seems to have a great impact the genetic predisposition of the individuals suffering from that serious progressive disease. Regarding to these observations and findings very interesting studies have been conducted in order to elucidate the implications of different genes, and their polymorphisms in disease aetiology. This is a review which elucidates the impact of genetic susceptibility in COPD.
{"title":"Genetic Implications in COPD. The Current Knowledge","authors":"I. Sotiriou, D. Makris","doi":"10.4236/OJRD.2013.32009","DOIUrl":"https://doi.org/10.4236/OJRD.2013.32009","url":null,"abstract":"Chronic Obstructive Pulmonary Disease (COPD) is a multifactorial disease in the pathogenesis of which contributes a variety of causative factors including genetic and environmental ones. They may also be interactions of genetic susceptibilities and environmental influences. Towards to that in the pathogenesis of the disease except smoking, it seems to have a great impact the genetic predisposition of the individuals suffering from that serious progressive disease. Regarding to these observations and findings very interesting studies have been conducted in order to elucidate the implications of different genes, and their polymorphisms in disease aetiology. This is a review which elucidates the impact of genetic susceptibility in COPD.","PeriodicalId":83134,"journal":{"name":"The Journal of respiratory diseases","volume":"3 1","pages":"52-62"},"PeriodicalIF":0.0,"publicationDate":"2013-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70582499","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
M. Schäffer, S. Roy, Shyamali Mukherjee, Salil K. Das
Vitamin A (VA) and its active metabolites play an essential role in lung airway function. Patients with moderate to severe chronic obstructive pulmonary disease (COPD) have a lower serum retinol concentration, and improvement of their 1-second Forced Expiratory Volume (FEV1) is achieved with VA supplementation. In order to test our hypothesis that the VA signaling pathway is compromised in COPD, we obtained 20 lung samples from COPD patients differing in the degree of emphysema as judged by their FEV% values. All were smokers or were exposed to secondhand smoke. Levels of VA (retinol/retinyl ester), tocopherols and carotenoids (lutein, beta-carotene) in these samples were determined using HPLC. Additional analytes beside VA were included for their known roles as antioxidants and modulators of VA-action. VA levels (retinol/retinyl ester) decreased significantly with the increase in severity of emphysema. Among other analytes, α-tocopherol levels fell by 25.8% in the severe emphysema group in comparison to the mild emphysema group, and lutein levels similarly decreased in severe compared to moderate emphysema groups. However, beta-carotene levels remained unchanged. Thus there is a significant linear correlation between lung VA-levels and the severity of emphysema. There was also a significant reduction in the levels of α-, δ-tocopherol and lutein in the severe emphysema group of COPD patients who either smoked or were exposed to smoke.
{"title":"Vitamin A, Vitamin E, Lutein and β-Carotene in Lung Tissues from Subjects with Chronic Obstructive Pulmonary Disease and Emphysema","authors":"M. Schäffer, S. Roy, Shyamali Mukherjee, Salil K. Das","doi":"10.4236/OJRD.2013.32008","DOIUrl":"https://doi.org/10.4236/OJRD.2013.32008","url":null,"abstract":"Vitamin A (VA) and its active metabolites play an essential role in lung airway function. Patients with moderate to severe chronic obstructive pulmonary disease (COPD) have a lower serum retinol concentration, and improvement of their 1-second Forced Expiratory Volume (FEV1) is achieved with VA supplementation. In order to test our hypothesis that the VA signaling pathway is compromised in COPD, we obtained 20 lung samples from COPD patients differing in the degree of emphysema as judged by their FEV% values. All were smokers or were exposed to secondhand smoke. Levels of VA (retinol/retinyl ester), tocopherols and carotenoids (lutein, beta-carotene) in these samples were determined using HPLC. Additional analytes beside VA were included for their known roles as antioxidants and modulators of VA-action. VA levels (retinol/retinyl ester) decreased significantly with the increase in severity of emphysema. Among other analytes, α-tocopherol levels fell by 25.8% in the severe emphysema group in comparison to the mild emphysema group, and lutein levels similarly decreased in severe compared to moderate emphysema groups. However, beta-carotene levels remained unchanged. Thus there is a significant linear correlation between lung VA-levels and the severity of emphysema. There was also a significant reduction in the levels of α-, δ-tocopherol and lutein in the severe emphysema group of COPD patients who either smoked or were exposed to smoke.","PeriodicalId":83134,"journal":{"name":"The Journal of respiratory diseases","volume":"03 1","pages":"44-51"},"PeriodicalIF":0.0,"publicationDate":"2013-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70582489","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
M. Lagranderie, J. Vanoirbeek, B. Vargaftig, P. Guyonvarc’h, G. Marchal, X. Roux
Background: We previously showed that treatment with Mycobacterium bovis BCG killed by extended freeze-drying (EFD BCG) modulates inflammation through regulatory T cells (Tregs) in an acute asthma model. In this study, we investigated the kinetics of Treg induction as well as their long-term homing in spleen and lungs correlating with reduced airway hyperresponsiveness (AHR) in a murine model of acute allergic asthma. We then evaluated the therapeutic implication of EFD BCG in a chronic asthma model. Methods: Tregs expressing Foxp3 were analyzed in various organs shortly and long-term after EFD BCG, live- and Heat Killed-(HK-) BCG treatments in an acute model of asthma. We further studied EFD BCG treatment on airway inflammation using a chronic model of asthma in mice. Results: Foxp3 expression peaked in the inguinal draining lymph-nodes (iDLNs) 2-4 days after EFD BCG treatment whereas it was long-term observed in spleen (days 7 to 90). This increase in Foxp3 expression was also found in lungs upon intranasal ovalbumin (OVA) challenge in OVA-sensitized mice. The loss of protection 4 months after EFD BCG treatment was correlated with the end of this phenomenon. Moreover, major lung inflammation hallmarks of severe asthma after multiple allergen challenges promoting chronic airway inflammation in OVA sensitized mice were reduced by EFD BCG treatment: AHR, eosinophils and neutrophils in bronchoalveolar lavage (BAL), mucus metaplasia, Th2 as well as Th17 cytokine levels in BAL and sera. EFD BCG treatment also enhances PPAR-γ expression and regulates NF-κBp65 translocation in lung extracts in this model of chronic asthma. Conclusions: EFD BCG treatment induced long-term protective effect associated to Foxp3 Tregs in the spleen and lungs in an acute model of asthma and inhibits AHR in a chronic model of asthma. EFD BCG could be a new and promising immuno-modulatory alternative treatment to corticoids in severe human asthma.
{"title":"Therapeutic Administration of Mycobacterium bovis BCG Killed by Extended Freeze-Drying Modulates Airway Inflammation in a Chronic Murine Model of Asthma","authors":"M. Lagranderie, J. Vanoirbeek, B. Vargaftig, P. Guyonvarc’h, G. Marchal, X. Roux","doi":"10.4236/OJRD.2013.32013","DOIUrl":"https://doi.org/10.4236/OJRD.2013.32013","url":null,"abstract":"Background: We previously showed that treatment with Mycobacterium bovis BCG killed by extended freeze-drying (EFD BCG) modulates inflammation through regulatory T cells (Tregs) in an acute asthma model. In this study, we investigated the kinetics of Treg induction as well as their long-term homing in spleen and lungs correlating with reduced airway hyperresponsiveness (AHR) in a murine model of acute allergic asthma. We then evaluated the therapeutic implication of EFD BCG in a chronic asthma model. Methods: Tregs expressing Foxp3 were analyzed in various organs shortly and long-term after EFD BCG, live- and Heat Killed-(HK-) BCG treatments in an acute model of asthma. We further studied EFD BCG treatment on airway inflammation using a chronic model of asthma in mice. Results: Foxp3 expression peaked in the inguinal draining lymph-nodes (iDLNs) 2-4 days after EFD BCG treatment whereas it was long-term observed in spleen (days 7 to 90). This increase in Foxp3 expression was also found in lungs upon intranasal ovalbumin (OVA) challenge in OVA-sensitized mice. The loss of protection 4 months after EFD BCG treatment was correlated with the end of this phenomenon. Moreover, major lung inflammation hallmarks of severe asthma after multiple allergen challenges promoting chronic airway inflammation in OVA sensitized mice were reduced by EFD BCG treatment: AHR, eosinophils and neutrophils in bronchoalveolar lavage (BAL), mucus metaplasia, Th2 as well as Th17 cytokine levels in BAL and sera. EFD BCG treatment also enhances PPAR-γ expression and regulates NF-κBp65 translocation in lung extracts in this model of chronic asthma. Conclusions: EFD BCG treatment induced long-term protective effect associated to Foxp3 Tregs in the spleen and lungs in an acute model of asthma and inhibits AHR in a chronic model of asthma. EFD BCG could be a new and promising immuno-modulatory alternative treatment to corticoids in severe human asthma.","PeriodicalId":83134,"journal":{"name":"The Journal of respiratory diseases","volume":"03 1","pages":"79-88"},"PeriodicalIF":0.0,"publicationDate":"2013-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70582368","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
W. R. Lampe, S. Fang, Q. Yin, A. Crews, Joungjoa Park, K. Adler
Hypersecretion of mucus characterizes many inflammatory airway diseases, including asthma, chronic bronchitis, and cystic fibrosis. Excess mucus causes airway obstruction, reduces pulmonary function, and can lead to increased morbidity and mortality. MicroRNAs are small non-coding pieces of RNA which regulate other genes by binding to a complementary sequence in the target mRNA. The microRNA miR-21 is upregulated in many inflammatory conditions and, interestingly, miR-21 has been shown to target the mRNA of Myristoylated Alanine-Rich C Kinase Substrate (MARCKS), a protein that is an important regulator of airway mucin (the solid component of mucus) secretion. In these studies, we determined that exposure of primary, well-differentiated, normal human bronchial epithelial (NHBE) cells to the pro-inflammatory stimulus lipopolysaccharide (LPS) increased expression of both miR-21 and MARCKS in a time-dependent manner. To investigate whether miR-21 regulation of MARCKS played a role in mucin secretion, two separate airway epithelial cell lines, HBE1 (papilloma virus transformed) and NCI-H292 (mucodepidermoid derived) were utilized, since manipulation of miR-21 is performed via transfection of commercially-available miR-21 inhibitors and mimics/activators. Treatment of HBE1 cells with LPS caused concentration-dependent increases in expression of both miR-21 and MARCKS mRNA and protein. The miR-21 inhibitor effectively reduced levels of miR-21 in the cells, coincident with an increase in MARCKS mRNA expression over time as well as enhanced mucin secretion, while the miR-21 mimic/activator increased levels of miR-21, which coincided with a decrease in expression of MARCKS and a decrease in mucin secretion. These results suggest that miR-21 is increased in airway epithelial cells following exposure to LPS, and that miR-21 downregulates expression of MARCKS, which may decrease mucin secretion by the cells. Thus, miR-21 may act as a negative feedback regulator of mucin secretion in airway epithelial cells, and may do so, at least in part, by downregulating expression of MARCKS.
{"title":"Mir-21 Regulation of MARCKS Protein and Mucin Secretion in Airway Epithelial Cells","authors":"W. R. Lampe, S. Fang, Q. Yin, A. Crews, Joungjoa Park, K. Adler","doi":"10.4236/OJRD.2013.32014","DOIUrl":"https://doi.org/10.4236/OJRD.2013.32014","url":null,"abstract":"Hypersecretion of mucus characterizes many inflammatory airway diseases, including asthma, chronic bronchitis, and cystic fibrosis. Excess mucus causes airway obstruction, reduces pulmonary function, and can lead to increased morbidity and mortality. MicroRNAs are small non-coding pieces of RNA which regulate other genes by binding to a complementary sequence in the target mRNA. The microRNA miR-21 is upregulated in many inflammatory conditions and, interestingly, miR-21 has been shown to target the mRNA of Myristoylated Alanine-Rich C Kinase Substrate (MARCKS), a protein that is an important regulator of airway mucin (the solid component of mucus) secretion. In these studies, we determined that exposure of primary, well-differentiated, normal human bronchial epithelial (NHBE) cells to the pro-inflammatory stimulus lipopolysaccharide (LPS) increased expression of both miR-21 and MARCKS in a time-dependent manner. To investigate whether miR-21 regulation of MARCKS played a role in mucin secretion, two separate airway epithelial cell lines, HBE1 (papilloma virus transformed) and NCI-H292 (mucodepidermoid derived) were utilized, since manipulation of miR-21 is performed via transfection of commercially-available miR-21 inhibitors and mimics/activators. Treatment of HBE1 cells with LPS caused concentration-dependent increases in expression of both miR-21 and MARCKS mRNA and protein. The miR-21 inhibitor effectively reduced levels of miR-21 in the cells, coincident with an increase in MARCKS mRNA expression over time as well as enhanced mucin secretion, while the miR-21 mimic/activator increased levels of miR-21, which coincided with a decrease in expression of MARCKS and a decrease in mucin secretion. These results suggest that miR-21 is increased in airway epithelial cells following exposure to LPS, and that miR-21 downregulates expression of MARCKS, which may decrease mucin secretion by the cells. Thus, miR-21 may act as a negative feedback regulator of mucin secretion in airway epithelial cells, and may do so, at least in part, by downregulating expression of MARCKS.","PeriodicalId":83134,"journal":{"name":"The Journal of respiratory diseases","volume":"233 1","pages":"89-96"},"PeriodicalIF":0.0,"publicationDate":"2013-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70582448","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Xavier Soler, C. Díaz-Piedra, W. Bardwell, S. Ancoli-Israel, L. Palinkas, J. Dimsdale, J. Loredo
Objectives: To investigate differences in sleep quality between Hispanics of Mexican descent (HMD) and Non-Hispanic Whites (NHW) and evaluate the effect of acculturation to the US lifestyle in sleep health. We hypothesize that the detrimental effect of acculturation on health outcomes will impact sleep quality among HMD. Design: We performed a population-based random digit dialing telephone survey to determine sleep quality in HMD and NHW. We collected from 3667 subjects, demographics, previous diagnosis of depression or anxiety, past treatment for sleep disorders, the Pittsburgh Sleep Quality Index (PSQI) and the Short Acculturation Scale for Hispanics. Results: The prevalence of poor sleep quality (PSQI > 5) was 64.4% for HMD and 64.3% for NHW (p = 0.93). A prior diagnosis of depression or anxiety was an independent predictor of poor sleep quality in both groups (OR 3.4 and 2.7 for HMD and NHW. Ethnicity was not a predictor of poor sleep quality in HMD or NHW. Acculturation was not a predictor of poor sleep quality in HMD. However, highly acculturated young HMD males had significantly more prevalence of poor sleep quality compared to NHW (64.8% vs. 49.8%, p < 0.001). Conclusion: The absence of sleep quality differences in a large sample of HMD and NHW living in San Diego County is contrary to current data of having poorer sleep quality among Latinos. We found that neither ethnicity nor acculturation were predictors of poor sleep quality in HMD. However, we demonstrated a highly prevalent poor sleep quality among the two ethnic groups. The finding of significantly lower sleep quality in young highly acculturated HMD men may represent the heterogeneity of ethnicity related to sleep. Programs to improve sleep quality in subjects with depression and/or anxiety, and in young highly-acculturated HMD seems warranted.
{"title":"Sleep Quality among Hispanics of Mexican Descent and Non-Hispanic Whites: Results from the Sleep Health and Knowledge in US Hispanics Study","authors":"Xavier Soler, C. Díaz-Piedra, W. Bardwell, S. Ancoli-Israel, L. Palinkas, J. Dimsdale, J. Loredo","doi":"10.4236/OJRD.2013.32015","DOIUrl":"https://doi.org/10.4236/OJRD.2013.32015","url":null,"abstract":"Objectives: To investigate differences in sleep quality between Hispanics of Mexican descent (HMD) and Non-Hispanic Whites (NHW) and evaluate the effect of acculturation to the US lifestyle in sleep health. We hypothesize that the detrimental effect of acculturation on health outcomes will impact sleep quality among HMD. Design: We performed a population-based random digit dialing telephone survey to determine sleep quality in HMD and NHW. We collected from 3667 subjects, demographics, previous diagnosis of depression or anxiety, past treatment for sleep disorders, the Pittsburgh Sleep Quality Index (PSQI) and the Short Acculturation Scale for Hispanics. Results: The prevalence of poor sleep quality (PSQI > 5) was 64.4% for HMD and 64.3% for NHW (p = 0.93). A prior diagnosis of depression or anxiety was an independent predictor of poor sleep quality in both groups (OR 3.4 and 2.7 for HMD and NHW. Ethnicity was not a predictor of poor sleep quality in HMD or NHW. Acculturation was not a predictor of poor sleep quality in HMD. However, highly acculturated young HMD males had significantly more prevalence of poor sleep quality compared to NHW (64.8% vs. 49.8%, p < 0.001). Conclusion: The absence of sleep quality differences in a large sample of HMD and NHW living in San Diego County is contrary to current data of having poorer sleep quality among Latinos. We found that neither ethnicity nor acculturation were predictors of poor sleep quality in HMD. However, we demonstrated a highly prevalent poor sleep quality among the two ethnic groups. The finding of significantly lower sleep quality in young highly acculturated HMD men may represent the heterogeneity of ethnicity related to sleep. Programs to improve sleep quality in subjects with depression and/or anxiety, and in young highly-acculturated HMD seems warranted.","PeriodicalId":83134,"journal":{"name":"The Journal of respiratory diseases","volume":"03 1","pages":"97-106"},"PeriodicalIF":0.0,"publicationDate":"2013-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70582844","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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