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Effect of nitrogen dioxide on respiratory viral infection in airway epithelial cells

ENVIRONMENTAL RESEARCH 1999年第2期81卷 159-166页

作者： Becker, S Soukup, JM US EPA Natl Hlth & Environm Effects Res Lab Res Triangle Pk NC 27711 USA

Nitrogen dioxide (NO2) is a common air pollutant outdoors and indoors in homes with unvented combustion sources. It is also a constituent of tobacco smoke. Epidemiological studies suggest that children exposed to NO2, or living with smoking parents, have an increased incidence of respiratory viral infections. The most common virus causing severe respiratory symptoms in infants and young children is respiratory syncytial virus (RSV), In the present study we investigated whether NO2 exposure affects RSV infection in airway epithelial cells, the host cells for viral replication and virus-induced cytokine production. Cultures of the bronchial epithelial cell line BEAS-2B exposed to 0.5, 1.0, and 1.5 ppm NO2 for 60 min were infected with RSV Viral replication, as well as RSV-induced interleukin (IL)-6 and IL-8, was assessed at various times postinfection, The NO2 doses used were not toxic to the BEAS-2B cells as measured by release of lactic dehydrogenase (LDH). The internalization of RSV was increased by exposure to 0.5 ppm NO2 and decreased by exposure to 1.5 ppm NO2, On the other hand, the release of infectious virus 48 h postexposure was not affected by the two lower doses of NO2, but was significantly reduced in cells exposed to 1.5 ppm NO2, Virus-induced cytokine production was also significantly reduced in cells exposed to 1.5 ppm NO2, and not affected by 0.5 and 1.0 ppm. It is likely that the decrease in cytokine production is related to the decrease in viral burden. These data suggest that possible increases in viral clinical symptoms associated with NO2 may not be caused by increased susceptibility of the epithelial cells to infection but may result from effects of NO2 on host defenses that prevent the spread of virus. (C) 1999 Academic Press.

关键词：空气污染物/毒性支气管/药物作用支气管/免疫学支气管/病毒学细胞系细胞因子类/生物合成剂量效应关系药物上皮细胞/药物作用上皮细胞/免疫学上皮细胞/病毒学二氧化氮/毒性呼吸道合胞病毒/药物作用病毒复制/药物作用人类

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CD40 expression by human bronchial epithelial cells

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SCANDINAVIAN JOURNAL OF IMMUNOLOGY 1999年第4期49卷 355-361页

作者： Gormand, F Briere, F Peyrol, S Raccurt, M Durand, I Aït-Yahia, S Lebecque, S Banchereau, J Pacheco, Y Ctr Hosp Lyon Sud Lab Immunoallergol Resp F-69310 Pierre Benite France Schering Plough Lab Rech Dardilly France Inst Pasteur Lyon France Baylor Inst Dallas TX USA

CD40 is a 50-kDa protein expressed on B cells, dendritic cells, monocytes and epithelial cells, but the distribution of CD40 expression in humans is not completely known. It binds to a ligand (CD40 L) which is expressed essentially on activated T cells. The interaction between CD40 and CD40 L plays important roles in immune responses. CD40 expression was investigated on bronchial tissues and human bronchial cell lines using immunohistochemistry, immunofluorescence staining and analysis with a cytometer, respectively. Constitutive CD40 expression, but not that of CD40 L, was slightly detectable on normal human bronchial epithelial cells (HBEC) in situ and on an adult lung adenocarcinoma (SKLU1) cell line, while another cell line, a bronchial transformed SV40 cell line (WI26VA4), was negative for CD40. Among the various cytokines tested, only interferon (IFN)-gamma was found to induce CD40 expression on WI26VA4. Tumour necrosis factor (TNF)-alpha was the best cytokine able to up-regulate CD40 in SKLU1 cells. A combination of IFN-gamma and TNF-alpha was slightly more effective than the cytokine alone at up-regulating CD40 expression on both cell lines. We further investigated the functional consequences of CD40 ligation on both cell lines. These bronchial cells expressed CD40, HLADR and CD54 under basal conditions or when stimulated by cytokines. Stimulation through CD40 did not affect cell-surface-antigen expression on either cell line. The production of cytokines such as interleukin (IL)-6 and granulocyte macrophage-colony stimulating factor (GM-CSF) by HBEC has been described. SKLU1 and WI26VA4 cells released IL-6 and GM-CSF spontaneously. Whatever the case, CD40 engagement did not modulate spontaneous or TNF-alpha-induced production of these two cytokines. These data indicate fur the first time that normal HBEC express CD40 in situ. Further investigations are required in order to determine the role of CD40 on normal HBEC.

关键词：支气管/细胞学支气管/免疫学支气管/代谢细胞系细胞因子类/药理学上皮细胞/药物作用上皮细胞/免疫学上皮细胞/代谢肿瘤细胞培养的女(雌)性人类男(雄)性中年人

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Pathogenesis of mucous cell metaplasia in a murine asthma model

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AMERICAN JOURNAL OF PATHOLOGY 2003年第6期162卷 2069-2078页

作者： Reader, JR Tepper, JS Schelegle, ES Aldrich, MC Putney, LF Pfeiffer, JW Hyde, DM Univ Calif Davis Sch Vet Med Calif Reg Primate Res Ctr Dept Anat Physiol & Cell Biol Davis CA 95616 USA Genentech Inc San Francisco CA 94080 USA

Increased mucus production in asthma is an important cause of airflow obstruction during severe exacerbations. To better understand the changes in airway epithelium that lead to increased mucus production, ovalbumin-sensitized and -challenged mice were used. The phenotype of the epithelium was dramatically altered, resulting in increased numbers of mucous cells, predominantly in the proximal airways. However, the total numbers of epithelial cells per unit area of basement membrane did not change. A 75% decrease in Clara cells and a 25% decrease in ciliated cells were completely compensated for by an increase in mucous cells. Consequently, by day 22, 70% of the total epithelial cell population in the proximal airways was mucous cells. Electron microscopy illustrated that Clara cells were undergoing metaplasia to mucous cells. Conversely, epithelial proliferation, detected with 5-chloro-2-deoxyuridine immunohistochemistry, was most marked in the distal airways. Using ethidium. homodimer cell labeling to evaluate necrosis and terminal dUTP nick-end labeling immunohistochemistry to evaluate apoptosis, this proliferation was accompanied by negligible cell death. In conclusion, epithelial cell death did not appear to be the stimulus driving epithelial proliferation and the increase in mucous cell numbers was primarily a result of Clara cell metaplasia. (Am J Pathol 2003, 162:2069-2078)

关键词：哮喘/免疫学哮喘/病理学支气管/免疫学支气管/病理学细胞分裂疾病模型动物上皮细胞/病理学上皮细胞/超微结构化生/病因学小鼠近交BALBC 显微镜检查电子卵白蛋白/免疫学呼吸道黏膜/病理学呼吸道黏膜/超微结构动物男(雄)性小鼠

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Rapid activation of nuclear factor-κB in airway epithelium in a murine model of allergic airway inflammation

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AMERICAN JOURNAL OF PATHOLOGY 2002年第4期160卷 1325-1334页

作者： Poynter, ME Irvin, CG Janssen-Heininger, YMW Univ Vermont Dept Pathol Burlington VT 05405 USA Univ Vermont Dept Med Burlington VT 05405 USA Univ Vermont Vermont Lung Ctr Burlington VT 05405 USA

Bronchiolar epithelium is postulated to play a critical role in the orchestration of responses to inhaled allergens, and may contribute to the pathogenesis of asthma. Using a murine model of allergic airway inflammation and hyperresponsiveness, we demonstrate in mice sensitized with ovalbumin (OVA) that following a single challenge with nebulized OVA, a rapid and protracted activation of inhibitor of kappa B kinase (IKK) occurred in lung tissue. IKK activation was followed by nuclear localization of nuclear factor (NF)-kappaB within the bronchiolar epithelium and increased luciferase activity in lungs of mice containing a NF-kappaB-dependent reporter gene. Challenge of sensitized mice with OVA also induced mRNA expression of the chemokines, macrophage inflammatory protein-2 (MIP-2) and eotaxin in lung tissue, which corresponded temporally with the observed influx of neutrophils and eosinophils, respectively, into the airspaces. Using laser capture microdissection and quantitative polymerase chain reaction, we demonstrated that MIP-2 and eotaxin were predominantly expressed in bronchiolar epithelium, in contrast to distal regions of the lungs, which expressed lower or undetectable levels of these mRNAs. These studies strengthen the potential importance of the bronchiolar epithelial cell as a source of production of NF-kappaB-dependent mediators that play a role in asthma.

关键词：变应原/免疫学支气管/免疫学支气管/代谢支气管高反应性/代谢支气管炎/代谢炎症趋化因子类/代谢上皮/免疫学上皮/代谢基因表达基因报告/遗传学超敏反应/代谢免疫法小鼠近交BALBC NF-κB/遗传学 NF-κB/生理学时间因素动物女(雌)性小鼠

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Basement membrane pores in human bronchial epithelium -: A conduit for infiltrating cells?

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AMERICAN JOURNAL OF PATHOLOGY 2001年第2期158卷 673-680页

作者： Howat, WJ Holmes, JA Holgate, ST Lackie, PM Univ Southampton Sch Med Div Resp Cell & Mol Biol Southampton Hants England

This study reports the presence of oval-shaped pores in the basement membrane of the human bronchial airway that may be used as conduits for immune cells to traffic between the epithelial and mesenchymal compartments. Human bronchial mucosa collected after surgery was stripped of epithelial cells without damaging the basement membrane. Both scanning and transmission electron microscopy showed oval-shaped pores 0.75 to 3.85 mum in diameter in the bronchial basement membrane at a density of 863 pores/ mm(2). Transmission electron microscopy showed that the pores spanned the full depth of the basement membrane, with a concentration of collagen-like fibers at the lateral edges of the pore. Infiltrating cells apparently moved through the pores, both in the presence and absence of the epithelium. Taken together, these results suggest that immune cells use basement membrane pores as predefined routes to move between the epithelial and mesenchymal compartments without disruption of the basement membrane. As a persistent feature of the basement membrane, pores could facilitate inflammatory cell access to the epithelium and greatly increase the frequency of intercellular contact between trafficking cells.

关键词：基膜/生理学基膜/超微结构支气管/免疫学支气管/超微结构上皮/超微结构免疫细胞/生理学显微镜检查电子显微镜检查电子扫描人类

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