15 results on '"Kuo-Hsiung Huang"'
Search Results
2. Heat shock protein70 is implicated in modulating NF-κB activation in alveolar macrophages of patients with active pulmonary tuberculosis
- Author
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Chun-Hua Wang, Pai-Chien Chou, Fu-Tsai Chung, Horng-Chyuan Lin, Kuo-Hsiung Huang, and Han-Pin Kuo
- Subjects
Medicine ,Science - Abstract
Abstract Heat shock proteins (HSPs) have been shown to modulate NF-κB activation. It is unknown whether HSP70 plays a role in modulating NF-κB-mediated pro-inflammatory cytokines released from alveolar macrophage (AM) of patients with active pulmonary tuberculosis (TB). Peripheral blood monocytes (PBMs) and AM were sampled from nineteen active TB patients and 14 healthy individuals. HSP70 expression was 3-fold higher in AMs of active TB patients than normal subjects, and declined after receiving 3-month anti-TB treatment. Overexpression of HSP70 by transfection with HSP70 plasmid decreased p-IκBα and p65 NF-κB activities. Inhibition of NF-κB activation using NF-κB or MAPK inhibitors increased HSP70 expression in AM of TB patients. Blocking p38- or ERK-MAPK decreased NF-κB and IκB activities, leading to up-regulated HSP70 expression. Overexpression of HSP70 alone or with p38 or ERK inhibitors decreased TNF-α (57%, 83% and 74%, respectively) and IL-6 (53%, 70%, and 67%, respectively) release from macrophages of TB patients. In conclusion, HSP70 modulates NF-κB activation in AM of TB patients, through inhibiting IκB-α phosphorylation or acting as a chaperon molecule to prevent NF-κB binding to the target genes by facilitating degradation. The upregulated HSP70 may suppress the release of pro-inflammatory cytokines during active PTB infection, and prevent overwhelming tissue damage.
- Published
- 2017
- Full Text
- View/download PDF
3. NF-κB repressing factor inhibits chemokine synthesis by peripheral blood mononuclear cells and alveolar macrophages in active pulmonary tuberculosis.
- Author
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Kuo-Hsiung Huang, Chun-Hua Wang, Kang-Yun Lee, Shu-Min Lin, Chien-Huang Lin, and Han-Pin Kuo
- Subjects
Medicine ,Science - Abstract
NF-κB repressing factor (NRF) is a transcriptional silencer implicated in the basal silencing of specific NF-κB targeting genes, including iNOS, IFN-β and IL-8/CXCL8. IP-10/CXCL10 and IL-8/CXCL8 are involved in neutrophil and lymphocyte recruitment against M. tuberculosis (MTb) and disease progression of pulmonary tuberculosis (TB). Alveolar macrophages (AM) and peripheral blood mononuclear cells (PBMC) were used to study the regulatory role of NRF in pulmonary TB. AM and PBMC were purified from 19 TB patients and 15 normal subjects. To study the underlying mechanism, PBMC were exposed to heated TB bacilli. The regulation role of NRF in IP-10/CXCL10 and IL-8/CXCL8 was determined by NRF knock-down or over-expression. NRF binding capabilities in promoter sites were measured by chromatin immunoprecipitation (ChIP) assay. The levels of IP-10/CXCL10, IL-8/CXCL8 and NRF were significantly higher in AM and PBMC in patients with active TB. NRF played an inhibitory role in IP-10/CXCL10 and IL-8/CXCL8 inductions. We delineate the role of NRF in pulmonary TB, which inhibits the expressions of IP-10/CXCL10 and IL-8/CXCL8 in AM and PBMC of patients with high bacterial load. NRF may serve as an endogenous repressor to prevent robust increase in IP-10/CXCL10 and IL-8/CXCL8 when TB bacterial load is high.
- Published
- 2013
- Full Text
- View/download PDF
4. Heat shock protein70 is implicated in modulating NF-κB activation in alveolar macrophages of patients with active pulmonary tuberculosis
- Author
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Pai Chien Chou, Fu Tsai Chung, Han Pin Kuo, Kuo Hsiung Huang, Chun Hua Wang, and Horng Chyuan Lin
- Subjects
0301 basic medicine ,MAPK/ERK pathway ,Male ,p38 mitogen-activated protein kinases ,Science ,Article ,03 medical and health sciences ,Downregulation and upregulation ,Heat shock protein ,Macrophages, Alveolar ,Medicine ,Humans ,HSP70 Heat-Shock Proteins ,Tuberculosis, Pulmonary ,Multidisciplinary ,business.industry ,NF-kappa B ,Transfection ,Macrophage Activation ,Middle Aged ,Hsp70 ,030104 developmental biology ,Immunology ,Alveolar macrophage ,Cancer research ,Tumor necrosis factor alpha ,Female ,business - Abstract
Heat shock proteins (HSPs) have been shown to modulate NF-κB activation. It is unknown whether HSP70 plays a role in modulating NF-κB-mediated pro-inflammatory cytokines released from alveolar macrophage (AM) of patients with active pulmonary tuberculosis (TB). Peripheral blood monocytes (PBMs) and AM were sampled from nineteen active TB patients and 14 healthy individuals. HSP70 expression was 3-fold higher in AMs of active TB patients than normal subjects, and declined after receiving 3-month anti-TB treatment. Overexpression of HSP70 by transfection with HSP70 plasmid decreased p-IκBα and p65 NF-κB activities. Inhibition of NF-κB activation using NF-κB or MAPK inhibitors increased HSP70 expression in AM of TB patients. Blocking p38- or ERK-MAPK decreased NF-κB and IκB activities, leading to up-regulated HSP70 expression. Overexpression of HSP70 alone or with p38 or ERK inhibitors decreased TNF-α (57%, 83% and 74%, respectively) and IL-6 (53%, 70%, and 67%, respectively) release from macrophages of TB patients. In conclusion, HSP70 modulates NF-κB activation in AM of TB patients, through inhibiting IκB-α phosphorylation or acting as a chaperon molecule to prevent NF-κB binding to the target genes by facilitating degradation. The upregulated HSP70 may suppress the release of pro-inflammatory cytokines during active PTB infection, and prevent overwhelming tissue damage.
- Published
- 2016
5. Increased Circulating Fibrocytes in Asthma with Chronic Airflow Obstruction
- Author
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Chien-Da Huang, Kang-Yun Lee, Shu-Min Lin, Han Pin Kuo, Kuo-Hsiung Huang, Yu-Shien Ko, Horng-Chyuan Lin, Chien-Ying Liu, Kian Fan Chung, and Chun Hua Wang
- Subjects
Male ,Pulmonary and Respiratory Medicine ,Receptors, CCR7 ,Receptors, CXCR4 ,CD34 ,Antigens, CD34 ,Critical Care and Intensive Care Medicine ,Statistics, Nonparametric ,Transforming Growth Factor beta1 ,Forced Expiratory Volume ,Intensive care ,Fibrocyte ,medicine ,Humans ,Progenitor cell ,Cell Proliferation ,Asthma ,Interleukin-13 ,business.industry ,Stem Cells ,Respiratory disease ,Cell Differentiation ,Middle Aged ,Airway obstruction ,Flow Cytometry ,medicine.disease ,Actins ,respiratory tract diseases ,Airway Obstruction ,Immunology ,Interleukin 13 ,Leukocytes, Mononuclear ,Leukocyte Common Antigens ,Female ,business - Abstract
A proportion of patients with asthma present with chronic airflow obstruction (CAO). We hypothesized that this effect may result from increased activity of circulating fibroblast-like progenitor cells (fibrocytes) that could home to the airway mucosal wall.To compare the proportion, proliferation, and differentiation of circulating fibrocytes from patients with asthma with CAO or no airflow obstruction (NOA) and control subjects.We investigated circulating fibrocytes in 11 patients with asthma with CAO and a rapid decline in FEV(1), 9 patients with asthma with NOA, and 10 nonasthmatic control subjects. Blood nonadherent non-T (NANT) cells were incubated with fetal calf serum or each patient's own serum and fibrocytes expressing CD34, CD45, and collagen I with alpha-smooth muscle actin were identified by flow cytometry.A higher percentage of circulating fibrocytes in NANT cells was found in patients with CAO when compared with patients with NOA and control subjects. In CAO, the slope of the yearly decline in FEV(1) correlated with circulating fibrocytes (r = -0.756, n = 11, P0.01). When NANT cells from patients with CAO were cultured in the patients' own sera, more fibrocytes were detected than when cultured in sera from patients with NOA or from normal subjects. An anti-transforming growth factor (TGF)-beta(1)-neutralizing antibody inhibited alpha-smooth muscle actin-positive fibrocyte transformation from NANT cells of patients with CAO. Serum TGF-beta(1) levels were higher in patients with CAO than in patients with NOA or in normal subjects.Circulating fibrocytes are increased in patients with asthma with CAO and can be transformed by TGF-beta(1) to myofibroblasts. Fibrocytes may contribute to airway obstruction in asthma.
- Published
- 2008
6. Matrix metalloproteinase-1 polymorphism in Taiwanese patients with endobronchial tuberculosis
- Author
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Chun Hua Wang, Chih Chen He, Han Pin Kuo, Chien Da Huang, Yu Min Wang, Horng Chyuan Lin, Ling-Ling Hsieh, Chien Ying Liu, Shu Min Lin, and Kuo Hsiung Huang
- Subjects
Adult ,Male ,Microbiology (medical) ,Pathology ,medicine.medical_specialty ,Tuberculosis ,Genotype ,Interleukin-1beta ,Molecular Sequence Data ,Immunology ,Bronchi ,Matrix metalloproteinase ,Microbiology ,Endobronchial tuberculosis ,medicine ,Humans ,Allele ,Tuberculosis, Pulmonary ,Aged ,Polymorphism, Genetic ,Base Sequence ,business.industry ,Bronchial Diseases ,Middle Aged ,medicine.disease ,Up-Regulation ,Stenosis ,Infectious Diseases ,Tissue remodeling ,Granuloma ,Female ,Matrix Metalloproteinase 1 ,Tracheal Stenosis ,business - Abstract
Summary Endobronchial tuberculosis (TB) often leads to some degree of tracheobronchial stenosis. Because matrix metalloproteinases (MMPs) play an essential role in tissue remodeling in the airways, we investigated the role of MMP-1 polymorphism in patients with endobronchial TB. One hundred and one cases of pulmonary TB in Taiwanese patients were genotyped for the 1G/2G polymorphism of MMP-1 promoter (−1607bp). Bronchoscopic examination was performed to determine the presence of endobronchial involvement. Levels of MMP-1 in peripheral blood monocytes and in bronchial biopsies were also determined. 1G genotypes of MMP-1 polymorphism, containing at least one 1G allele, were associated with the presence of endobronchial TB. Using multivariate analysis, 1G genotypes and female gender were independent predictors of the development of endobronchial TB. Endobronchial TB patients with 1G genotypes had a 9.86-fold greater risk of developing tracheobronchial stenosis. IL-1 β increased levels of MMP-1 in peripheral blood monocytes of TB patients with 1G genotypes. MMP-1 activity was also present in the endobronchial TB granuloma from patients with 1G/1G genotype. 1G genotypes of MMP-1 polymorphism were associated with a greater risk of developing tracheobronchial stenosis through up-regulation of MMP-1 activity.
- Published
- 2008
7. Effect of theophylline and specific phosphodiesterase IV inhibition on proliferation and apoptosis of progenitor cells in bronchial asthma
- Author
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Han Pin Kuo, Horng Chyuan Lin, Chien-Huang Lin, Kuo Hsiung Huang, Kian Fan Chung, Chun Hua Wang, Su Ling Liu, and Chih Teng Yu
- Subjects
Pharmacology ,medicine.medical_specialty ,medicine.diagnostic_test ,Stem cell factor ,Eosinophil ,Biology ,Flow cytometry ,medicine.anatomical_structure ,Endocrinology ,Apoptosis ,Internal medicine ,medicine ,Theophylline ,Progenitor cell ,Stem cell ,Rolipram ,medicine.drug - Abstract
1. Theophylline possesses anti-inflammatory activities in asthma. We examined whether theophylline and agents that modulate cyclic AMP can determine the survival and proliferation of progenitor cells. 2. Progenitor cells from the blood of normal and asthmatic subjects were cultured for 14 days in methylcellulose with GM-CSF, stem cell factor, IL-3 and IL-5. Apoptosis was measured by flow cytometry of propidium-iodide-stained cells. 3. A greater number of colonies with a higher proportion of cells of eosinophil lineage from asthmatics compared to normal subjects were grown. Theophylline (at 5 and 20 micro g ml(-1)) significantly inhibited colony formation and increased apoptotic cells in asthmatics compared to control. Salbutamol (0.1, 1, 10 micro M), dibutyryl-cAMP (0.1, 1 mM) and rolipram (0.1, 1 mM), a phosphodiesterase IV inhibitor, also dose-dependently decreased colony numbers and increased apoptosis of progenitor cells from asthmatics. 4. There was no significant effect of theophylline, db-cAMP, salbutamol or rolipram on colony formation or the survival of progenitor cells from normal subjects. AMP did not affect the colony formation and apoptosis. Expression of Bcl-2 protein on progenitor cells of asthma was downregulated by theophylline, salbutamol, db-cAMP and rolipram. 5. Theophylline and rolipram decreased colony formation committed to the eosinophil lineage, together with an increase in apoptosis through an inhibition of Bcl-2 expression effects that may occur through cAMP. The anti-inflammatory properties of theophylline include an inhibition of circulating progenitor cells.
- Published
- 2003
8. NF-κB repressing factor downregulates basal expression and mycobacterium tuberculosis induced IP-10 and IL-8 synthesis via interference with NF-κB in monocytes
- Author
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Han Pin Kuo, Chun Hua Wang, Chien-Huang Lin, and Kuo Hsiung Huang
- Subjects
Endocrinology, Diabetes and Metabolism ,Clinical Biochemistry ,Down-Regulation ,Repressor ,RNA polymerase II ,IP-10 ,Peripheral blood mononuclear cell ,Monocytes ,Cell Line ,Mycobacterium tuberculosis ,chemistry.chemical_compound ,NF-κB repressing factor ,Downregulation and upregulation ,Humans ,Tuberculosis ,Pharmacology (medical) ,Interleukin 8 ,Promoter Regions, Genetic ,Tuberculosis, Pulmonary ,Molecular Biology ,Biochemistry, medical ,IL-8 ,biology ,Research ,Interleukin-8 ,Biochemistry (medical) ,Transcription Factor RelA ,NF-κB ,Cell Biology ,General Medicine ,biology.organism_classification ,Molecular biology ,Chemokine CXCL10 ,Repressor Proteins ,chemistry ,Cell culture ,biology.protein ,RNA Polymerase II - Abstract
Background Our previous study showed NF-κB repressing factor (NKRF) downregulates IP-10 and IL-8 synthesis in the peripheral blood mononuclear cells and alveolar macrophages of TB patients with high bacterial loads. However, the mechanism underlying the repressive effect of NKRF is not fully understood. Results The levels of IP-10, IL-8 and NKRF were significantly up-regulated in THP-1 cells treated with heated mycobacterium tuberculosis (H. TB). NKRF inhibited NF-κB-mediated IP-10 and IL-8 synthesis and release induced by H. TB. The repressive effect of NKRF is mediated via interference with NF-κB (p65) binding and RNA polymerase II recruitment to promoter sites of IP-10 and IL-8. Conclusions We have elucidated that direct contact with MTb induces IP-10, IL-8 and a concomitant increase in NKRF in THP-1 cells. The up-regulated NKRF serves as an endogenous repressor for IP-10 and IL-8 synthesis to hinder host from robust response to MTb infection.
- Published
- 2014
9. Thermal and Mechanical Properties of Poly (4-methyl-m-phenyleneterephthalamide) Fiber
- Author
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Kozo Arai, Motomu Arisawa, Kuo Hsiung Huang, and Masaru Yoneyama
- Subjects
Stress (mechanics) ,Materials science ,Relaxation (NMR) ,Stress–strain curve ,Dispersion (optics) ,General Medicine ,Fiber ,Nomex ,Composite material ,Amorphous solid ,Stress concentration - Abstract
Thermal and mechanical properties of poly-(4-methyl-m-phenyleneterephthalamide) (PMMTA) fibers were investigated. PMMTA fibers showed excellent thermal properties comparable to Nomex fibers, but exhibited lower initial modulus and breaking stress than those of Nomex fibers. Intermoleculer cross-links were formed in PMMTA fibers when they were heat-treated at temperatures above 280°C. The striking decreases in breaking stress and strain of the fibers treated at 260°C were considered to be due to the stress concentration near the cross-linking points. Mechanical properties of PMMTA fibers were greatly improved by the treatment with water at 140°C. Dynamic viscoelasticity measurements showed four dispersion peaks located around - 32, 5, 225, and 365°C, which were attributed to the γ, β, β∗ and α relaxation, respectively. By heat-treatment at 300°C, the α dispersion peak shifted to higher temperature at ca. 400°C and the γ dispersion peak shifted to lower temperature at ca. -50°C These were likely to be related to the formation of cross-links followed by the disordering of molecular chains in the amorphous region.
- Published
- 1994
10. Dynamic Viscoelasticity of Poly(4-methyl-m-phenyleneterephthalamide) Film
- Author
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Masaru Yoneyama, Kazuhiko Koiwai, Kozo Arai, and Kuo Hsiung Huang
- Subjects
Materials science ,Hydrogen bond ,Intermolecular force ,Relaxation (NMR) ,Analytical chemistry ,General Medicine ,Nomex ,Activation energy ,Composite material ,Dispersion (chemistry) ,Glass transition ,Dynamic viscoelasticity - Abstract
Thermal and dynamic viscoelasticity of poly (4-methyl-m-phenyleneterephthalamide) (PMMTA) films were investigated and compared with those of Nomex films. In DTA curves, PMMTA and Nomex films showed glass transition around 293°C and 273°C, respectively. By heat-treatment at 280 to 300°C, intermolecular crosslinks were formed in PMMTA films but not in Nomex films. From dynamic viscoelasticity measurements, three dispersion peaks for PMMTA were observed at ca. -45, 210 and 350°C, which were attributed to γ, β∗ and α relaxation, respectively. For heat-treated PMMTA film at 300°C, the α dispersion peak shifted to higher temperature at ca. 378°C, and the apparent activation energy for α dispersion, 174 kcal/mol, was considerably greater than that obtained for the untreated film, 110 kcal/mol. On the contrary, for heat-treated Nomex films no perceptible change was observed for the α relaxation. It was suggested, therefore, that in PMMTA the molecular motion of chains was restricted by the cross-links formed. By the heat-treatment at 300°C, the γ dispersion peak of PMMTA film shifted to lower temperature at ca. -60°C. This was considered to be due to the breakdown of hydrogen bonds caused by the formation of cross-links.
- Published
- 1994
11. Persistence of lung inflammation and lung cytokines with high-resolution CT abnormalities during recovery from SARS
- Author
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Kian Fan Chung, Chun Liang Chou, Han Pin Kuo, Horng Chyuan Lin, Yung Liang Wan, Chun Huan Wang, Shu Min Lin, Tzou Yien Lin, Kuo Hsiung Huang, and Chien Ying Liu
- Subjects
Pulmonary and Respiratory Medicine ,Adult ,Male ,Pathology ,medicine.medical_specialty ,Time Factors ,Adolescent ,medicine.medical_treatment ,coronavirus ,medicine.disease_cause ,Severe Acute Respiratory Syndrome ,Alveolar cells ,medicine ,T lymphocyte ,Humans ,bronchoalveolar lavage ,Respiratory system ,Lung ,Hyaline ,Coronavirus ,Pneumonitis ,Retrospective Studies ,lcsh:RC705-779 ,SARS ,medicine.diagnostic_test ,business.industry ,Research ,lcsh:Diseases of the respiratory system ,Pneumonia ,Recovery of Function ,alveolar macrophages ,respiratory system ,Middle Aged ,medicine.disease ,cytokines ,respiratory tract diseases ,medicine.anatomical_structure ,Bronchoalveolar lavage ,Cytokine ,Severe acute respiratory syndrome-related coronavirus ,Female ,business ,Tomography, X-Ray Computed ,Bronchoalveolar Lavage Fluid - Abstract
BackgroundDuring the acute phase of severe acute respiratory syndrome (SARS), mononuclear cells infiltration, alveolar cell desquamation and hyaline membrane formation have been described, together with dysregulation of plasma cytokine levels. Persistent high-resolution computed tomography (HRCT) abnormalities occur in SARS patients up to 40 days after recovery.MethodsTo determine further the time course of recovery of lung inflammation, we investigated the HRCT and inflammatory profiles, and coronavirus persistence in bronchoalveolar lavage fluid (BALF) of 12 patients at recovery at 60 and 90 days.ResultsAt 60 days, compared to normal controls, SARS patients had increased cellularity of BALF with increased alveolar macrophages (AM) and CD8 cells. HRCT scores were increased and correlated with T-cell numbers and their subpopulations, and inversely with CD4/CD8 ratio. TNF-α, IL-6, IL-8, RANTES and MCP-1 levels were increased. Viral particles in AM were detected by electron microscopy in 7 of 12 SARS patients with high HRCT score. On day 90, HRCT scores improved significantly in 10 of 12 patients, with normalization of BALF cell counts in 6 of 12 patients with repeat bronchoscopy. Pulse steroid therapy and prolonged fever were two independent factors associated with delayed resolution of pneumonitis, in this non-randomized, retrospective analysis.ConclusionResolution of pneumonitis is delayed in some patients during SARS recovery and may be associated with delayed clearance of coronavirus, Complete resolution may occur by 90 days or later.
- Published
- 2005
12. Endogenous nitric oxide downregulates the Bcl-2 expression of eosinophils through mitogen-activated protein kinase in bronchial asthma
- Author
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Suh Hwa Maa, Horng Chyuan Lin, Chun Hua Wang, Han Pin Kuo, Chien Ying Liu, and Kuo Hsiung Huang
- Subjects
MAPK/ERK pathway ,Adult ,p38 mitogen-activated protein kinases ,Immunology ,Down-Regulation ,Nitric Oxide Synthase Type II ,Apoptosis ,Pharmacology ,Nitric Oxide ,Nitric oxide ,chemistry.chemical_compound ,medicine ,Immunology and Allergy ,Humans ,Protein kinase A ,Nitrites ,biology ,Eosinophil ,Asthma ,Eosinophils ,medicine.anatomical_structure ,chemistry ,Proto-Oncogene Proteins c-bcl-2 ,Mitogen-activated protein kinase ,Case-Control Studies ,biology.protein ,Signal transduction ,Mitogen-Activated Protein Kinases ,Nitric Oxide Synthase - Abstract
Background Eosinophil apoptosis might play a crucial role in the maintenance of persistent airway inflammation in asthma. Nitric oxide (NO) synthase activity is upregulated in eosinophils of asthmatic patients. Mitogen-activated protein kinase (MAPK) is implicated in regulating eosinophil apoptosis by modulating Bcl-2 expression. NO-induced cell apoptosis is associated with an inhibition of Bcl-2 expression. Objective We sought to study whether NO might induce eosinophil apoptosis through extracellular signal–regulated protein kinase (ERK) or p38 MAPK pathways and Bcl-2 expression. Methods Eosinophils were freshly isolated from peripheral blood of 16 asthmatic patients and 12 healthy subjects and then cultured with or without the NO synthase inhibitor N-nitro-l-arginine methyl ester (L-NAME) at 1 and 10 mmol/L for 16 hours. The expression of Bcl-2 and induced NO synthase on eosinophils was analyzed by means of flow cytometry. Apoptosis was assessed by means of propidium iodide and DNA ladder. The activity of ERK and p38 MAPK was determined by means of Western blotting. Results The induced NO synthase immunoreactivities and the spontaneous release of nitrite from the eosinophils of asthmatic patients were higher compared with those of healthy subjects. Eosinophils of asthmatic patients were found to express more highly constitutive Bcl-2 than those of healthy subjects. After incubation for 16 hours, the expression of Bcl-2 on eosinophils from patients with asthma was significantly enhanced by L-NAME. The percentage of apoptosis was decreased by the addition of 1 mmol/L L-NAME in patients with asthma. The activity of p38 MAPK and ERK in eosinophils from patients with asthma was enhanced in the presence of L-NAME. An inhibition of MAPK reduced the Bcl-2 expression and increased eosinophil apoptosis in patients with asthma. Conclusion We concluded that inhibition of endogenous NO might increase the expression of Bcl-2 in eosinophils from patients with asthma through the signaling pathway of ERK or p38 MAPK, which in turn decrease the apoptosis.
- Published
- 2003
13. Effect of theophylline and specific phosphodiesterase IV inhibition on proliferation and apoptosis of progenitor cells in bronchial asthma
- Author
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Chun-Hua, Wang, Horng-Chyuan, Lin, Chien-Huang, Lin, Chih-Teng, Yu, Su-Ling, Liu, Kuo-Hsiung, Huang, Kian Fan, Chung, and Han-Pin, Kuo
- Subjects
Male ,Time Factors ,Phosphodiesterase Inhibitors ,Stem Cells ,Antigens, CD34 ,Apoptosis ,Asthma ,Theophylline ,Papers ,Animals ,Humans ,Albuterol ,Female ,Rolipram ,Cell Division ,Methacholine Chloride - Abstract
1. Theophylline possesses anti-inflammatory activities in asthma. We examined whether theophylline and agents that modulate cyclic AMP can determine the survival and proliferation of progenitor cells. 2. Progenitor cells from the blood of normal and asthmatic subjects were cultured for 14 days in methylcellulose with GM-CSF, stem cell factor, IL-3 and IL-5. Apoptosis was measured by flow cytometry of propidium-iodide-stained cells. 3. A greater number of colonies with a higher proportion of cells of eosinophil lineage from asthmatics compared to normal subjects were grown. Theophylline (at 5 and 20 micro g ml(-1)) significantly inhibited colony formation and increased apoptotic cells in asthmatics compared to control. Salbutamol (0.1, 1, 10 micro M), dibutyryl-cAMP (0.1, 1 mM) and rolipram (0.1, 1 mM), a phosphodiesterase IV inhibitor, also dose-dependently decreased colony numbers and increased apoptosis of progenitor cells from asthmatics. 4. There was no significant effect of theophylline, db-cAMP, salbutamol or rolipram on colony formation or the survival of progenitor cells from normal subjects. AMP did not affect the colony formation and apoptosis. Expression of Bcl-2 protein on progenitor cells of asthma was downregulated by theophylline, salbutamol, db-cAMP and rolipram. 5. Theophylline and rolipram decreased colony formation committed to the eosinophil lineage, together with an increase in apoptosis through an inhibition of Bcl-2 expression effects that may occur through cAMP. The anti-inflammatory properties of theophylline include an inhibition of circulating progenitor cells.
- Published
- 2003
14. NF-κB repressing factor downregulates basal expression and mycobacteria tuberculosis induced IP-10 and IL-8 synthesis via interference with NF-κB in monocytes.
- Author
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Kuo-Hsiung Huang, Chun-Hua Wang, Chien-Huang Lin, and Han-Pin Kuo
- Subjects
- *
ELOCUTION , *TUBERCULOSIS , *ACTINOMYCETALES , *MYCOBACTERIUM tuberculosis , *LUNG diseases - Abstract
Background Our previous study showed NF-κB repressing factor (NKRF) downregulates IP-10 and IL-8 synthesis in the peripheral blood mononuclear cells and alveolar macrophages of TB patients with high bacterial loads. However, the mechanism underlying the repressive effect of NKRF is not fully understood. Results The levels of IP-10, IL-8 and NKRF were significantly up-regulated in THP-1 cells treated with heated mycobacterium tuberculosis (H. TB). NKRF inhibited NF-κB-mediated IP-10 and IL-8 synthesis and release induced by H. TB. The repressive effect of NKRF is mediated via interference with NF-κB (p65) binding and RNA polymerase II recruitment to promoter sites of IP-10 and IL-8. Conclusions We have elucidated that direct contact with MTb induces IP-10, IL-8 and a concomitant increase in NKRF in THP-1 cells. The up-regulated NKRF serves as an endogenous repressor for IP-10 and IL-8 synthesis to hinder host from robust response to MTb infection. [ABSTRACT FROM AUTHOR]
- Published
- 2014
- Full Text
- View/download PDF
15. Persistence of lung inflammation and lung cytokines with high-resolution CT abnormalities during recovery from SARS.
- Author
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Chun-Hua Wang, Chien-Ying Liu, Yung-Liang Wan, Chun-Liang Chou, Kuo-Hsiung Huang, Horng-Chyuan Lin, Shu-Min Lin, Tzou-Yien Lin, Kian Fan Chung, and Han-Pin Kuo
- Subjects
SARS disease ,BRONCHOALVEOLAR lavage ,LUNG diseases ,CYTOKINES ,INFLAMMATION ,IMMUNOREGULATION ,MEDICAL research - Abstract
Background: During the acute phase of severe acute respiratory syndrome (SARS), mononuclear cells infiltration, alveolar cell desquamation and hyaline membrane formation have been described, together with dysregulation of plasma cytokine levels. Persistent high-resolution computed tomography (HRCT) abnormalities occur in SARS patients up to 40 days after recovery. Methods: To determine further the time course of recovery of lung inflammation, we investigated the HRCT and inflammatory profiles, and coronavirus persistence in bronchoalveolar lavage fluid (BALF) of 12 patients at recovery at 60 and 90 days. Results: At 60 days, compared to normal controls, SARS patients had increased cellularity of BALF with increased alveolar macrophages (AM) and CD8 cells. HRCT scores were increased and correlated with T-cell numbers and their subpopulations, and inversely with CD4/CD8 ratio. TNF-α, IL-6, IL-8, RANTES and MCP-1 levels were increased. Viral particles in AM were detected by electron microscopy in 7 of 12 SARS patients with high HRCT score. On day 90, HRCT scores improved significantly in 10 of 12 patients, with normalization of BALF cell counts in 6 of 12 patients with repeat bronchoscopy. Pulse steroid therapy and prolonged fever were two independent factors associated with delayed resolution of pneumonitis, in this non-randomized, retrospective analysis. Conclusion: Resolution of pneumonitis is delayed in some patients during SARS recovery and may be associated with delayed clearance of coronavirus, Complete resolution may occur by 90 days or later. [ABSTRACT FROM AUTHOR]
- Published
- 2005
- Full Text
- View/download PDF
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