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Rhinovirus infection induces expression of its own receptor intercellular adhesion molecule 1 (ICAM-1) via increased NF-κB-mediated transcription

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JOURNAL OF BIOLOGICAL CHEMISTRY 1999年第14期274卷 9707-9720页

作者： Papi, A Johnston, SL Univ Southampton Southampton Gen Hosp Southampton SO16 6YD Hants England

Virus infections, the majority of which are rhinovirus infections, are the major cause of asthma exacerbations. Treatment is unsatisfactory, and the pathogenesis unclear. Lower airway lymphocyte and eosinophil recruitment and activation are strongly implicated, but the mechanisms regulating these processes are unknown. Intercellular adhesion molecule-1 (ICAM-1) has a central role in inflammatory cell recruitment to the airways in asthma and is the cellular receptor for 90% of rhinoviruses. We hypothesized that rhinovirus infection of lower airway epithelium might induce ICARI-1 expression, promoting both inflammatory cell infiltration and rhinovirus infection. We therefore investigated the effect of rhinovirus infection on respiratory epithelial cell ICAM-1 expression and regulation to identify new targets for treatment of virus-induced asthma exacerbations. We observed that rhinovirus infection of primary bronchial epithelial cells and the A549 respiratory epithelial cell line increased ICAM-1 cell surface expression over 12- and 3-fold, respectively. We then investigated the mechanisms of this induction in A549 cells and observed rhinovirus-induction of ICAM-1 promoter activity and ICAM-1 mRNA transcription. Rhinovirus induction of ICAM-1 promoter activity was critically dependent upon up-regulation of NP-kappa B proteins binding to the -187/-178 NF-kappa B binding site on the ICAM-1 promoter. The principal components of the rhinovirus-induced binding proteins were NF-kappa B p65 homo- or heterodimers. These studies identify ICAM-1 and NF-kappa B as new targets for the development of therapeutic interventions for virus-induced asthma exacerbations.

关键词：哮喘/并发症哮喘/病毒学结合部位支气管/代谢支气管/病毒学细胞系上皮细胞/代谢上皮细胞/病毒学胞间黏附分子1/生物合成 NF-κB/代谢细小RNA病毒科感染/并发症细小RNA病毒科感染/代谢细小RNA病毒科感染/病毒学 RNA 信使/代谢鼻病毒属/代谢鼻病毒属/致病力鼻病毒属/生理学转录因子AP-1/代谢转录遗传病毒复制人类

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Stimulation of Cl^- secretion by chlorzoxazone

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 2000年第2期292卷 778-787页

作者： Singh, AK Devor, DC Gerlach, AC Gondor, M Pilewski, JM Bridges, RJ Univ Pittsburgh Sch Med Dept Cell Biol & Physiol Pittsburgh PA 15261 USA Univ Pittsburgh Dept Med Pittsburgh PA 15261 USA Univ Pittsburgh Dept Pediat Pittsburgh PA 15261 USA

We previously demonstrated that 1-ethyl-2-benzimidazolone (1-EBIO) directly activates basolateral membrane calcium-activated K+ channels (K-Ca), thereby stimulating Cl- secretion across several epithelia. In our pursuit to identify potent modulators of Cl- secretion that may be useful to overcome the Cl- secretory defect in cystic fibrosis (CF), we have identified chlorzoxazone [5-chloro-2(3H)-benzoxazolone], a clinically used centrally acting muscle relaxant, as a stimulator of Cl- secretion in several epithelial cell types, including T84, Calu-3, and human bronchial epithelium. The Cl- secretory response induced by chlorzoxazone was blocked by charybdotoxin (CTX), a known blocker of K-Ca. In nystatin-permeabilized monolayers, chlorzoxazone stimulated a basolateral membrane I-K, which was inhibited by CTX and also stimulated an apical I-Cl that was inhibited by glibenclamide, indicating that the G(Cl) responsible for this I-Cl may be cystic fibrosis transmembrane conductance regulator (CFTR). In membrane vesicles prepared from T84 cells, chlorzoxazone stimulated Rb-86(+) uptake in a CTX-sensitive manner. In excised, inside-out patches, chlorzoxazone activated an inwardly-rectifying K+ channel, which was inhibited by CTX. 6-Hydroxychlorzoxazone, the major metabolite of chlorzoxazone, did not activate K-Ca, whereas zoxazolamine (2-amino-5-chlorzoxazole) showed a similar response profile as chlorzoxazone. In normal human nasal epithelium, chlorzoxazone elicited hyperpolarization of the potential difference that was similar in magnitude to isoproterenol. However, in the nasal epithelium of CF patients with the Delta F508 mutation of CFTR, there was no detectable Cl- secretory response to chlorzoxazone. These studies demonstrate that chlorzoxazone stimulates transepithelial Cl- secretion in normal airway epithelium in vitro and in vivo, and suggest that stimulation requires functional CFTR in the epithelia.

关键词：阿米洛利/药理学阴离子/代谢支气管/代谢布美他尼/药理学细胞膜/药物作用细胞培养的蝎毒素/药理学氯/代谢氯唑沙宗/类似物和衍生物氯唑沙宗/药理学囊性纤维化/代谢囊性纤维化跨膜传导调节因子/遗传学药物相互作用上皮/代谢福司柯林/药理学格列本脲/药理学异丙肾上腺素/药理学鼻黏膜/药物作用制霉菌素/药理学钾通道阻滞剂铷/药代动力学氯苯恶唑胺/药理学人类

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POSTOPERATIVE PULMONARY-FUNCTION

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BRITISH JOURNAL OF ANAESTHESIA 1975年第2期47卷 102-107页

作者： HEWLETT, AM BRANTHWAITE, MA BROMPTON HOSP FULHAM RD LONDON SW3 6HP ENGLAND

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Immunocytochemical analyses and targeted gene disruption of GTPBP1

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MOLECULAR AND CELLULAR BIOLOGY 2000年第17期20卷 6195-6200页

作者： Senju, S Iyama, K Kudo, H Aizawa, S Nishimura, Y Kumamoto Univ Grad Sch Med Sci Dept Neurosci & Immunol Div Immunogenet Kumamoto 8600811 Japan Kumamoto Univ Sch Med Dept Surg Pathol Kumamoto 860 Japan Kumamoto Univ Sch Med Dept Morphogenesis Ins Mol Embryol & Genet Kumamoto 860 Japan

We previously identified a gene encoding a putative GTPase, GTPBP1, which is structurally related to elongation factor lot, a key component of protein biosynthesis machinery. The primary structure of GTPBP1 is highly conserved between human and mouse (97% identical at the amino acid level). Expression of this gene is enhanced by gamma interferon in a monocytic cell line, THP-1, Although counterparts of this molecule in Caenorhabditis elegans and Ascaris suum have also been identified, the function of this molecule remains to be clarified. In the present study, our immunohistochemical analyses on mouse tissues revealed that GTPBP1 is expressed in some neurons and smooth muscle cells of various organs as well as macrophages, Immunofluorescence analyses revealed that GTPBP1 is localized exclusively in cytoplasm and shows a diffuse granular network forming a gradient from the nucleus to the periphery of the cells in smooth muscle cell lines and macrophages, To investigate the physiological role of GTPBP1, we used targeted gene disruption in embryonic stem cells to generate GTPBP1-deficient mice. The mutant mice were born at the expected Mendelian frequency, developed normally, and were fertile. No manifest anatomical or behavioral abnormality was observed in the mutant mice. Functions of macrophages, including chemotaxis, phagocytosis, and nitric oxide production, in mutant mice were equivalent to those seen in wild-type mice. No significant difference was observed in the immune response to protein antigen between mutant mice and wild-type mice, suggesting normal function of antigen-presenting cells of the mutant mice. The absence of an eminent phenotype in GTPBP1 deficient mice may he due to functional compensation by GTPBP2, a molecule we recently identified which is similar to GTPBP1 in structure and tissue distribution.

关键词：脑/代谢支气管/代谢 COS细胞细胞黏附细胞培养的大脑皮质/代谢细胞质/代谢 DNA 互补/代谢上皮细胞/代谢荧光抗体技术基因文库免疫印迹法免疫组织化学巨噬细胞腹膜/代谢小鼠转基因模型遗传学单体GTP结合蛋白质类/生物合成单体GTP结合蛋白质类/遗传学单体GTP结合蛋白质类/生理学肌平滑血管/代谢诱变定点吞噬作用表型胸腺/代谢组织分布转染动物女(雌)性男(雄)性小鼠

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Cyclin D1 proteolysis: A retinoid chemoprevention signal in normal, immortalized, and transformed human bronchial epithelial cells

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JOURNAL OF THE NATIONAL CANCER INSTITUTE 1999年第4期91卷 373-379页

作者： Boyle, JO Langenfeld, J Lonardo, F Sekula, D Reczek, P Rusch, V Dawson, MI Dmitrovsky, E Mem Sloan Kettering Canc Ctr Sloan Kettering Inst Head & Neck Serv New York NY 10021 USA Mem Sloan Kettering Canc Ctr Sloan Kettering Inst Mol Med Lab New York NY 10021 USA Mem Sloan Kettering Canc Ctr Sloan Ketting Inst Thorac Surg Serv New York NY 10021 USA Mem Sloan Kettering Canc Ctr Sloan Kettering Inst Mol Pharmacol & Therapeut Program New York NY 10021 USA Mem Sloan Kettering Canc Ctr Sloan Kettering Inst Dept Pathol New York NY 10021 USA Bristol Myers Squibb Pharmaceut Res Inst Buffalo NY USA SRI Int Retinoid Program Menlo Park CA 94025 USA

Background: Retinoids (derivatives of vitamin A) are reported to reduce the occurrence of some second primary cancers, including aerodigestive tract tumors. In contrast, beta-carotene does not reduce the occurrence of primary aerodigestive tract cancers. Mechanisms explaining these effective retinoid and ineffective carotenoid chemoprevention results are poorly defined. Recently, the all-trans-retinoic acid (RA)-induced proteolysis of cyclin D1 that leads to the arrest of cells in G(1), phase of the cell cycle was described in human bronchial epithelial cells and is a promising candidate for such a mechanism. In this study, we have investigated this proteolysis as a common signal used by carotenoids or receptor-selective and receptor-nonselective retinoids, Methods: We treated cultured normal human bronchial epithelial cells, immortalized human bronchial epithelial cells (BEAS-2B), and transformed human bronchial epithelial cells (BEAS-2B(NNK)) with receptor-selective or receptor-nonselective retinoids or with carotenoids and studied the effects on cell proliferation by means of tritiated thymidine incorporation and on cyclin D1 expression by means of immunoblot analysis. We also examined whether calpain inhibitor I, an inhibitor of the 26S proteasome degradation pathway, affected the decline (i,e., proteolysis) of cyclin D1, Results: Receptor-nonselective retinoids were superior to the carotenoids studied in mediating the decline in cyclin D1 expression and in suppressing the growth of bronchial epithelial cells. Retinoids that activated retinoic acid receptor beta or retinoid X receptor pathways preferentially led to a decrease in the amount of cyclin D1 protein and a corresponding decline in growth. The retinoid-mediated degradation of cyclin D1 was blocked by cotreatment with calpain inhibitor I. Conclusions: Retinoid-dependent cyclin D1 proteolysis is a common chemoprevention signal in normal and neoplastic human bronchial epithelial cells. In contrast, caroten

关键词：抗致癌药/药理学支气管/药物作用支气管/代谢支气管肿瘤/代谢支气管肿瘤/预防和控制卡配因/拮抗剂和抑制剂类胡萝卜素类/药理学细胞培养的细胞周期蛋白D1/代谢上皮细胞/药物作用上皮细胞/代谢维生素A酸类/药理学人类

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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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Integrin αvβ8-mediated activation of transforming growth factor-β inhibits human airway epithelial proliferation in intact bronchial tissue

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AMERICAN JOURNAL OF PATHOLOGY 2003年第2期163卷 533-542页

作者： Fjellbirkeland, L Cambier, S Broaddus, VC Hill, A Brunetta, P Dolganov, G Jablons, D Nishimura, SL Univ Calif San Francisco San Francisco Gen Hosp Dept Anat Pathol San Francisco CA USA Univ Calif San Francisco San Francisco Gen Hosp Lung Biol Ctr San Francisco CA USA Univ Calif San Francisco Mt Zion Canc Ctr San Francisco CA 94143 USA Univ Calif San Francisco Dept Med San Francisco CA 94143 USA Univ Calif San Francisco Div Pulm San Francisco CA 94143 USA Univ Calif San Francisco Dept Surg San Francisco CA 94143 USA

Transforming growth factor (TGF)-beta is a potent multifunctional cytokine that is an essential regulator of epithelial proliferation. Because TGF-beta is expressed almost entirely in a latent state in vivo, a major source of regulation of TGF-beta function is its activation. A subset of integrins, alphavbeta8 and alphavbeta6, which are expressed in the human airway, has recently been shown to activate latent TGF-beta in vitro, suggesting a regulatory role for integrins in TGF-beta function in vivo. Here we have developed a novel, biologically relevant experimental model of human airway epithelium using intact human bronchial tissue. We have used this model to determine the function of integrin-mediated activation of TGF-beta in the airway. In human bronchial fragments cultured in vitro, authentic epithelial-stromal interactions were maintained and integrin and TGF-beta expression profiles correlated with profiles found in normal lung. In addition, in this model, we found that either the integrin alphavbeta8 or TGF-beta could inhibit airway epithelial cell proliferation. Furthermore, we found that one mechanism of integrin-alphavbeta8-dependent inhibition of cell proliferation was through activation of TGF-beta because anti-beta38 antibody blocked the majority (76%) of active TGF-beta released from bronchial fragments. These data provide compelling evidence for a functional role for integrinmediated activation of TGF-beta in control of human airway epithelial proliferation in vivo.

关键词：支气管/细胞学支气管/代谢细胞分裂/生理学培养技术基因表达谱内环境稳定整合素类/代谢角蛋白质类/代谢 Ki-67抗原/代谢呼吸道黏膜/细胞学呼吸道黏膜/代谢转化生长因子β/代谢老年人老年人 80以上女(雌)性人类男(雄)性中年人

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IL-4 and IL-13 stimulate human bronchial epithelial cells to release IL-8

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INFLAMMATION 1999年第6期23卷 545-555页

作者： Stríz, I Mio, T Adachi, Y Robbins, RA Romberger, DJ Rennard, SI Inst Clin & Expt Med Dept Immunol Prague Czech Republic Univ Nebraska Med Ctr Dept Internal Med Pulm & Crit Care Med Sect Omaha NE USA Vet Adm Hosp Omaha NE USA

Cytokine networks are important in regulating the traffic of inflammatory cells in the airways. Interleukin-8 (IL-8) released by human bronchial epithelial cells (HBECs) is thought to be of particular importance in attracting neutrophils and monocytes to sites of inflammation. Increased release of IL-8 by HBECs in response to Th-1 cytokines such as TNF alpha and IL-1 beta may be an important pathophysiologic pathway. The present study was designed to explore the role of the Th2 cytokine IL-4 and the functionally related interleukins IL-10, and IL-13 on the regulation of IL-8 release by HBECs. HBECs (passage 4-6) were cultured in LHC9/RPMI and when confluent cells were stimulated in unsupplemented medium LHCD/RPMI by IL-4, IL-10, and IL-13 at 10 ng/ml concentration for all cytokines. TNF alpha stimulation was used as a positive control. After 24 hours supernatants were collected and tested for IL-8 by a sandwich ELISA. Unstimulated HBECs spontaneously released limited amounts of IL-8 (11 +/- 1 pM) and significantly increased cytokine production in response to IL-4 (42 +/- 1 pM), IL-13 (30 +/- 1 pM) and TNF(128 +/- 11 pM). Stimulation with IL-10 (11 +/- 1 pM) did not change basal production of IL-8. When HBECs were co-stimulated with IL-4 plus TNF, the production of IL-8 was further increased (204 +/- 5 pM). In contrast, IL-10 attenuated the effect of TNF during co-stimulation (82 +/- 5 pM). IL-13 did not affect the release of IL-8 induced by TNF(111 +/- 9 pM). Northern blot analysis of IL-8 mRNA levels showed the highest induction of IL-8 mRNA in HBECs co-stimulated with TNF and IL-4. We conclude from our study that IL-4 directly induces IL-8 release from HBECs and amplifies the release of IL-8 in response to TNF alpha. IL-13 is less active and IL-10 has an inhibitory effect. Airway epithelial cells are able to interact, therefore, with products of both Th1 and Th2 cells with respect to modulating release of IL-8.

关键词：支气管/代谢支气管/病理学细胞培养的上皮细胞/代谢上皮细胞/病理学白细胞介素13/药理学白细胞介素4/药理学白细胞介素8/分泌人类

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A lung model describing uptake of organic solvents and roles of mucosal blood flow and metabolism in the bronchioles

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INHALATION TOXICOLOGY 2000年第6期12卷 491-510页

作者： Kumagai, S Matsunaga, I Osaka Prefectural Inst Publ Hlth Dept Occupat Hlth Higashinari Ku Osaka 537 Japan

A simple lung model (mucosal blood flow and metabolism model, MBM model) was developed to describe the uptake of organic solvents and investigate the role of mucosal blood flow and metabolism. The model separates the lung into four compartments, the peripheral bronchial tract (gas phase), the mucus layer lining the wail surface of the tract, the alveolar space (gas phase), and the alveolar blood. Solvent molecules are absorbed in the mucus layer during inhalation and released during exhalation. The deposited solvent diffuses radially into the mucosal tissue of the respiratory tract and transfers to the mucosal blood flow. To describe this behavior, a hypothetical mucosal blood flow throughout the mucus layer was used. The solvent in the mucosal tissue may be also metabolized, and a hypothetical metabolism in the mucus layer was used. The rate of the hypothetical mucosal blood flow was determined to be 5.2 ml/min based on the best fitting of previously obtained data for seven polar organic solvents. The MBM model predicts that as the blood-air partition coefficient (lambda(B)) increases from 0.1 to 20, the relative end-exhalation (E-end) will decrease from 0.89 to 0.07, and as lambda(B) increases to 500, E-end will increase to 0.33. After lambda(B) = 500, E-end is predicted to decrease again, and at lambda(B) = 10000, E-end is 0.09. The model also predicts that as lambda(B) increases from 0.1 to 10, the relative uptake (U) increases from 0.08 to 0.61, and as lambda(B) increases to 150, U decreases to 0.50. After lambda(B) = 150, U increases again, and at lambda(B) = 10,000, U is 0.8. The predictions show good agreement with values observed in human experimental studies. The MBM model predicts that uptake by the mucosal blood (U-Al) would be equal to uptake by the alveolar blood (U-Mu) at lambda(B) of 1000 and U-Al is more than 90% of total uptake at lambda(B) > 10,000. The model also shows that U is significantly increased by the mucosal metabolism at lambda(B) betwe

关键词：投药吸入血气屏障/生理学支气管/血液供给支气管/代谢肺/代谢模型生物学有机化学品/药代动力学可重复性结果呼吸道黏膜/血液供给呼吸道黏膜/代谢溶解度溶剂/药代动力学时间因素动物人类

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Genistein inhibits constitutive and inducible NFκB activation and decreases IL-8 production by human cystic fibrosis bronchial gland cells

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AMERICAN JOURNAL OF PATHOLOGY 1999年第2期155卷 473-481页

作者： Tabary, O Escotte, S Couetil, JP Hubert, D Dusser, D Puchelle, E Jacquot, J INSERM U514 F-51092 Reims France Hop Broussais Dept Chirurg Cardiovasc F-75674 Paris France Hop Cochin Serv Pneumol F-75674 Paris France

The inflammatory pathogenesis in airways of patients with cystic fibrosis (CF) is still unresolved. We demonstrate here that in in situ human Delta F508 homozygous CF bronchial tissues, submucosal gland cells exhibit an absence of inhibitor factor kappa B alpha (I kappa B alpha) and high levels of chemokine interleukin-8 (IL-8) expression. These results were confirmed by cultured human CF bronchial gland cells in which a lack of cytosolic I kappa B alpha and high levels of constitutively activated nuclear factor kappa B (NF kappa B) associated with an up-regulation of IL-8 production (13-fold increase) were found when compared to non-CF (control) disease bronchial gland cells. We also demonstrated that the isoflavone genistein, a well known CFTR mutant Cl- channel stimulator, significantly reduces the endogenous and Pseudomonas aeruginosa lipopolysaccharide-induced IL-8 production in cultured CF bronchial gland cells by increasing cytosolic I kappa B alpha protein levels. Overall, results show that genistein is a potent inhibitor of the activated NF kappa B identified in CF gland cells. This strong inhibition of constitutively activated NF kappa B and the resulting down-regulation of IL-8 production by genistein in the CF gland cells highlights the key role played by cytosolic I kappa B alpha in the regulation of inflammatory processes in CF human airway cells.

关键词：支气管/药物作用支气管/代谢细胞核/代谢细胞培养的囊性纤维化/代谢剂量效应关系药物酶抑制剂/药理学酶联免疫吸附测定染料木黄酮/药理学免疫组织化学白细胞介素8/生物合成脂多糖类/药理学肺移植 NF-κB/分析 NF-κB/拮抗剂和抑制剂 NF-κB/代谢铜绿假单胞菌/代谢时间因素青少年成年人老年人儿童女(雌)性人类男(雄)性中年人

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