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Bronchial Epithelial (bronchial + epithelial)
Kinds of Bronchial Epithelial Terms modified by Bronchial Epithelial Selected AbstractsPosttransplant Bronchiolitis Obliterans Syndrome Is Associated with Bronchial Epithelial to Mesenchymal TransitionAMERICAN JOURNAL OF TRANSPLANTATION, Issue 4 2009S. Hodge Bronchiolitis obliterans syndrome (BOS) compromises lung transplant outcomes and is characterised by airway epithelial damage and fibrosis. The process whereby the normal epithelial configuration is replaced by fibroblastic scar tissue is poorly understood, but recent studies have implicated epithelial mesenchymal transition (EMT). The primary aim of this study was to assess the utility of flow cytometry in detecting and quantifying EMT in bronchial epithelial cells. Large airway brushings were obtained at 33 bronchoscopies in 16 BOS-free and 6 BOS grade 1,3 patients at 2,120 months posttransplant. Flow cytometry was used to assess expression of the mesenchymal markers ,SMA, S100A4 and ED-A FN and HLA-DR. TGF ,1 and HGF were measured in Bronchoalveolar lavage (BAL). Expression of all three mesenchymal markers was increased in BOS, as was HLA-DR. BAL HGF, but not TGF ,1 was increased in BOS. Longitudinal investigation of one patient revealed a 100% increase in EMT markers concurrent with a 6-fold increase in BAL TGF ,1 and the diagnosis of BOS at 17 months posttransplant. Flow cytometric evaluation of bronchial epithelium may provide a novel and rapid means to assess lung allografts at risk of BOS. [source] Chromium (VI) inhibits heme oxygenase-1 expression in vivo and in arsenic-exposed human airway epithelial cellsJOURNAL OF CELLULAR PHYSIOLOGY, Issue 1 2006Kimberley A. O'Hara Inhaled hexavalent chromium (Cr(VI)) promotes lung injury and pulmonary diseases through poorly defined mechanisms. One hypothesis for this lung pathogenesis is that Cr(VI) silences induction of cytoprotective genes, such as heme oxygenase-1 (HO-1), whose total lung mRNA levels were reduced 21 days after nasal instillation of potassium dichromate in C57BL/6 mice. To investigate the mechanisms for this inhibition, Cr(VI) effects on basal and arsenic (As(III))-induced HO-1 expression were examined in cultured human bronchial epithelial (BEAS-2B) cells. An effect of Cr(VI) on the low basal HO-1 mRNA and protein levels in BEAS-2B cells was not detectible. In contrast, Cr(VI) added to the cells before As(III), but not simultaneously with As(III), attenuated As(III)-induced HO-1 expression. Transient transfection with luciferase reporter gene constructs controlled by the full length ho-1 promoter or deletion mutants demonstrated that this inhibition occurred in the E1 enhancer region containing critical antioxidant response elements (ARE). Cr(VI) pretreatment inhibited As(III)-induced activity of a transiently expressed reporter construct regulated by three ARE tandem repeats. The mechanism for this Cr(VI)-attenuated transactivation appeared to be Cr(VI) reduction of the nuclear levels of the transcription factor Nrf2 and As(III)-stimulated Nrf2 transcriptional complex binding to the ARE cis element. Finally, exposing cells to Cr(VI) prior to co-exposure with As(III) synergized for apoptosis and loss of membrane integrity. These data suggest that Cr(VI) silences induction of ARE-driven genes required for protection from secondary insults. The data also have important implications for understanding the toxic mechanisms of low level, mixed metal exposures in the lung. J. Cell. Physiol. 209: 113,121, 2006. © 2006 Wiley-Liss, Inc. [source] Matrix metalloproteinase-9 and tissue inhibitor of matrix metalloproteinase-1 in the respiratory tracts of human infants following paramyxovirus infectionJOURNAL OF MEDICAL VIROLOGY, Issue 4 2007Matthew B. Elliott Abstract Respiratory syncytial (RSV) and parainfluenza (PIV) viruses are primary causes of acute bronchiolitis and wheezing illnesses in infants and young children. To further understand inflammation in the airways following infection, we tested for the presence of matrix metalloproteinases (MMP) and natural tissue inhibitors of MMP (TIMP) in primary and established human cell lines, and in the nasopharyngeal secretions (NPS) of human infants infected with RSV or PIV. Using ELISA and multiplex-based assays, MMP-9 and TIMP-1 proteins were, respectively, detected in 66/67 and 67/67 NPS. During PIV or RSV infection TIMP-1 concentrations were associated with hypoxic bronchiolitis. TIMP-1 amounts were also negatively correlated with O2 saturation, and positively correlated with IL-6, MIP-1,, and G-CSF amounts following RSV infection. IL-6, MIP-1,, and G-CSF were negatively correlated with O2 saturation during RSV infection. Acute respiratory tract disease was not associated with MMP-9 protein/protease activity. Additional studies using real-time quantitative PCR suggested that MMP-9 mRNA copy numbers were elevated in normal human bronchial epithelial (NHBE) cells infected with RSV, while TIMP-1 and TIMP-2 were not increased. However, ELISA did not reveal MMP-9 protein in the NHBE cell culture supernatants. Hence, the data implied that airway epithelial cells were not the primary source of MMP or TIMP following paramyxovirus infection. Taken together, the data suggested that paramyxovirus infection perturbs MMP-9/TIMP-1 homeostasis that in turn may contribute to the severity of respiratory tract disease. J. Med. Virol. 79:447,456, 2007. © 2007 Wiley-Liss, Inc. [source] Air-liquid interface (ALI) culture of human bronchial epithelial cell monolayers as an in vitro model for airway drug transport studiesJOURNAL OF PHARMACEUTICAL SCIENCES, Issue 2 2007Hongxia Lin Abstract Serially passaged normal human bronchial epithelial (NHBE) cell monolayers were established on Transwell® inserts via an air-liquid interface (ALI) culture method. NHBE cells were seeded on polyester Transwell® inserts, followed by an ALI culture from day 3, which resulted in peak TEER value of 766,±,154 ,,×,cm2 on the 8th day. Morphological characteristics were observed by light microscopy and SEM, while the formation of tight junctions was visualized by actin staining, and confirmed successful formation of a tight monolayer. The transepithelial permeability (Papp) of model drugs significantly increased with the increase of lipophilicity and showed a good linear relationship, which indicated that lipophilicity is an important factor in determining the Papp value. The expression of P-gp transporter in NHBE cell monolayers was confirmed by the significantly higher basolateral to apical permeability of rhodamine123 than that of reverse direction and RT-PCR of MDR1 mRNA. However, the symmetric transport of fexofenadine,·,HCl in this NHBE cell monolayers study seems to be due to the low expression of P-gp transporter and/or to its saturation with high concentration of fexofenadine,·,HCl. Thus, the development of tight junction and the expression of P-gp in the NHBE cell monolayers in this study imply that they could be a suitable in vitro model for evaluation of systemic drug absorption via airway delivery, and that they reflect in vivo condition better than P-gp over-expressed cell line models. ©2006 Wiley-Liss, Inc. and the American Pharmacists Association J Pharm Sci 96:341,350, 2007 [source] Airway inflammation in employees involved in cultivating Japanese mushrooms (bunashimeji)RESPIROLOGY, Issue 4 2008Kenji TSUSHIMA Background and objective: Chronic inhalation of spores may cause respiratory symptoms such as productive cough and sputum. The purpose of this study was to determine the clinical pathophysiology of airway inflammation caused by bunashimeji spores and to investigate whether the spores have direct toxic inflammatory effects. Methods: Sensitized employees with respiratory symptoms and a stimulation index (SI) > 200%, and non-sensitized employees with a SI < 200% were enrolled. They underwent sputum induction and chest high-resolution computed tomography (HRCT). The in vitro effect of bunashimeji spore solutions on normal human bronchial epithelial (NHBE) cell cultures was investigated using the air,liquid interface method. Bunashimeji spore solution was added at 104 or 106 spores per 20 ,L/well. The interleukin (IL)-8 and epithelial neutrophil-activating peptide-78 (ENA-78) concentrations in the medium and IL-8 mRNA expression of NHBE cells were assessed after each stimulation. Results: Sensitized employees were divided into 14 with normal HRCT and 9 with abnormal HRCT. Fifteen of the sensitized group and five of the non-sensitized group had a productive cough and sputum. The neutrophil counts in induced sputum were significantly higher in subjects with abnormal HRCT than in those with normal HRCT. IL-8 and ENA-78 concentrations following stimulation with 104 and 106 spores were significantly increased compared with PBS only on day 9. IL-8 mRNA expression due to spore stimulation was significantly increased compared with control. IL-8 mRNA expression with 106 spore stimulation was significantly increased on days 6 and 12 compared with 104 spores. Conclusion: The inhalation of spores directly produces toxic inflammatory effects in the airways, independent of the degree of sensitization. [source] Modulation of the epithelial inflammatory response to rhinovirus in an atopic environmentCLINICAL & EXPERIMENTAL ALLERGY, Issue 3 2008M. Xatzipsalti Summary Background Immune responses to rhinovirus (RV) as well as direct effects of RV on respiratory epithelium may contribute to the induction of asthma exacerbations. Objective To evaluate the effect of the environment resulting from an atopic immune response on RV-induced epithelial inflammation, replication and cytotoxicity. Methods Peripheral blood mononuclear cells (PBMC) from atopic asthmatic subjects and matched controls (12 pairs) were isolated and stimulated by RVs. Human bronchial epithelial (BEAS-2B) cells were infected with RV in the presence of conditioned media from RV-stimulated PBMC cultures. IL-6, IL-8, RANTES and TGF-,1 levels were measured by ELISA, RV-induced cytotoxicity by a colorimetric method and RV titres on Ohio-HeLa cells. Results RV-induced epithelial production of IL-6, IL-8 and RANTES was significantly lower, while TGF-,1 was higher when cells were exposed to conditioned media from atopic asthmatic subjects compared with those from normal controls. Exposure to the ,atopic' environment also resulted in elevated RV titres and increased RV-induced cytotoxicity. Conclusions Under the influence of an atopic environment, the epithelial inflammatory response to RV is down-regulated, associated with increased viral proliferation and augmented cell damage, while TGF is up-regulated. These changes may help explain the propensity of atopic asthmatic individuals to develop lower airway symptoms after respiratory infections and indicate a mechanism through which viral infections may promote airway remodelling. [source] | |||||||||||||