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Interleukin-10 inhibits elevated chemokine interleukin-8 and regulated on activation normal T cell expressed and secreted production in cystic fibrosis bronchial epithelial cells by targeting the l_kB kinase α/β complex

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AMERICAN JOURNAL OF PATHOLOGY 2003年第1期162卷 293-302页

作者： Tabary, O Muselet, C Escotte, S Antonicelli, F Hubert, D Dusser, D Jacquot, J Hop Trousseau Unite Biol Mol INSERM E213 F-75571 Paris France INSERM U514 Reims France CNRS Biochim Lab Reims France Hop Cochin Serv Pneumol F-75674 Paris France

Accumulating evidence suggests that in cystic fibrosis (CF) patients, airway fluids are characterized by decreased antibacterial activity, elevated NaCl concentration, and high levels of chemokines, resulting in exaggerated activation of the transcriptional nuclear factor (NF)-kappaB in airway epithelial cells. The present study was undertaken to evaluate the effects of anti-inflammatory cytokine interleukin-10 (IL-10) on NaCl-induced chemokine IL-8 and regulated on activation normal T cell expressed and secreted (RANTES) expression through the NF-kappaB signaling in primary DeltaF508 CF and non-CF (control) human bronchial epithelial cells. Exposure of CF and non-CF bronchial epithelial cells to hypertonic (170 mmol/L NaCl) milieu compared to isotonic (115 mmol/L NaCl) and hypotonic (85 mmol/L NaCl) milieu caused a significant, NaCl-dependent increase in IL-8 and RANTES gene expression and protein production. Compared to non-CF cells, CF bronchial epithelial cells were characterized by a higher susceptibility to produce elevated IL-8 and RANTES production in an hypertonic NaCl milieu in response to IL-1beta activation. Treatment with IL-10 suppressed IL-8 and RANTES gene expression in both non-CF and CF bronchial epithelial cells was associated with a reduced expression of IkB (IKK) alpha/beta kinases, particularly for IKKalpha which is greater expressed in CF bronchial epithelial cells, and resulting in reduced NF-kappaB activation. These findings suggest that IL-10 might have anti-inflammatory benefits in airways of CF patients.

关键词：支气管/病理学细胞培养的趋化因子CCL5/拮抗剂和抑制剂趋化因子CCL5/生物合成趋化因子CCL5/遗传学炎症趋化因子类/拮抗剂和抑制剂炎症趋化因子类/生物合成炎症趋化因子类/遗传学囊性纤维化/代谢囊性纤维化/病理学上皮细胞/药物作用上皮细胞/代谢上皮细胞/病理学基因表达/药物作用 I-κB激酶 I-κB蛋白质类/代谢白细胞介素1/药理学白细胞介素10/药理学白细胞介素8/拮抗剂和抑制剂白细胞介素8/生物合成白细胞介素8/遗传学大分子物质 NF-κB/代谢蛋白质丝氨酸苏氨酸激酶/代谢呼吸道黏膜/药物作用呼吸道黏膜/代谢呼吸道黏膜/病理学氯化钠/药理学肿瘤坏死因子α/药理学人类

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The role of hepatic stellate cells and transforming growth factor-β₁ in cystic fibrosis liver disease

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AMERICAN JOURNAL OF PATHOLOGY 2002年第5期160卷 1705-1715页

作者： Lewindon, PJ Pereira, TN Hoskins, AC Bridle, KR Williamson, RM Shepherd, RW Ramm, GA Royal Childrens Hosp Dept Gastroenterol Brisbane Qld Australia Royal Brisbane Hosp Dept Histopathol Brisbane Qld 4029 Australia Washington Univ Sch Med Dept Pediat St Louis MO 63110 USA Queensland Inst Med Res Hepat Fibrosis Grp Herston Qld 4029 Australia

Liver disease causes significant morbidity and mortality from multilobular cirrhosis in patients with cystic fibrosis. Abnormal bile transport and biliary fibrosis implicate abnormal biliary physiology in the pathogenesis of cystic fibrosis-associated liver disease (CFLD), yet the mediators linking biliary events to fibrosis remain unknown. Activated hepatic stellate cells (HSCs) are the pre-eminent mediators of fibrosis in a range of hepatic disorders. The dominant stimulus for matrix production by HSCs is the cytokine transforming growth factor (TGF)-beta(1). In CFLD, the role of HSCs and the source of TGF-beta(1) have not been evaluated. Liver biopsy tissue obtained from 38 children with CFLD was analyzed. Activated HSCs, identified by co-localization of procollagen alpha(1)(I) mRNA and a-smooth muscle actin, were demonstrated as the cellular source of excess collagen production in the fibrosis surrounding the bile ducts and the advancing edge of scar tissue. TGF-beta protein and TGF-beta(1) mRNA expression were shown to be predominantly expressed by bile duct epithelial cells. TGF-beta(1) expression was significantly correlated with both hepatic fibrosis and the percentage of portal tracts showing histological abnormalities associated with CFLD. This study demonstrates a definitive role for HSCs in fibrogenesis associated with CFLD and establishes a potential mechanism for the induction of HSC collagen gene expression through the production of TGF-beta(1) by bile duct epithelial cells.

关键词：肌动蛋白类/遗传学肌动蛋白类/代谢胶原/代谢囊性纤维化/遗传学囊性纤维化/代谢囊性纤维化/病理学基因表达免疫组织化学原位杂交角蛋白质类/分析肝/代谢肝/病理学肝疾病/遗传学肝疾病/代谢肝疾病/病理学肌平滑/化学前胶原/遗传学前胶原/代谢 RNA 信使/遗传学 RNA 信使/代谢转化生长因子β/遗传学转化生长因子β/代谢转化生长因子β1 青少年儿童儿童学龄前女(雌)性人类婴儿男(雄)性

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Extent of pathological changes in the paranasal sinuses of patients with cystic fibrosis: CT analysis

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AMERICAN JOURNAL OF RHINOLOGY 2001年第3期15卷 207-210页

作者： Krzeski, A Kapiszewska-Dzedzej, D Jakubczyk, I Jedrusik, A Held-Ziolkowska, M Med Univ Warsaw Dept Otorhinolaryngol PL-02097 Warsaw Poland

The aim of the study was to define the characteristic changes revealed by computed tomography (CT) examination of the paranasal sinuses in patients with cystic fibrosis (CF). The group of 30 CF patients was evaluated in the outpatient clinic of the Department of Otorhinolaryngology, Medical University of Warsaw, from 1996 to 1998. The control group consisted of 30 patients with chronic rhinosinusitis (CRS). CT scans were obtained from both groups of patients, and findings revealed more advanced pathological changes in the CF than CRS group. The extensive inflammatory process observed in CT scans of CF patients resulted in the impairment of frontal and maxillary sinus development, destruction of bony structures, and medial projection of the lateral nasal wall.

关键词：病例对照研究囊性纤维化/病理学囊性纤维化/放射摄影术鼻窦/病理学鼻窦/放射摄影术鼻窦炎/病理学鼻窦炎/放射摄影术体层摄影术 X线计算机/方法青少年成年人儿童女(雌)性人类男(雄)性

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myo-inositol 3,4,5,6-tetrakisphosphate inhibits an apical calcium-activated chloride conductance in polarized monolayers of a cystic fibrosis cell line

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第35期275卷 26906-26913页

作者： Carew, MA Yang, XN Schultz, C Shears, SB NIEHS Inositide Signaling Sect Lab Signal Transduct NIH Res Triangle Pk NC 27709 USA Univ Bremen Inst Organ Chem UFT D-28359 Bremen Germany

Does inositol 3,4,5,6 tetrakisphosphate (Ins(3,4,5,6)P-4) inhibit apical Ca2+-activated Cl- conductance (CaCC)? We studied this question using human CFPAC-1 pancreatoma cells grown in polarized monolayers. Cellular Ins(3,4,5,6)P-4 levels were acutely sensitive to purinergic receptor activation, rising 3-fold within 1 min of agonist addition. Intracellular Ins(3,4,5,6)P-4, levels were therefore specifically elevated, independently of receptor activation, by incubating cells with a cell-permeant bioactivable analogue, 1,2-di-O-butyl-myo-inositol 3,4,5,6-tetrakisphosphate octakis(acetoxymethyl)ester (Bt(2)Ins (3,4,5,6)P-4/AM). The latter inhibited Ca2+-activated Cl- secretion by 60%. We next used nystatin to selectively permeabilize the basolateral membrane to monovalent anions and cations, thereby preventing this membrane from electrochemically dominating ion movements through the apical membrane. Thus, we studied autonomous regulation of apical Cl- channels in situ. The properties of Cl- flux across the apical membrane were those expected of CaCC: niflumic acid sensitivity, outward rectification, and 2-fold greater permeability of I- over Cl-. Following nystatin-treatment, we elevated intracellular levels of Ins(3,4,5,6)P-4, with either purinergic agonists or with Bt(2)Ins(3,4,5,6)P-4/AM. Both protocols inhibited Ca2+-activated Cl- secretion (up to 70%). These studies provide the first demonstration that, in a physiologically relevant context of a polarized monolayer, there is an apical, Ins(3,4,5,6)P-4-inhibited CaCC.

关键词：钙/代谢细胞系细胞膜/药物作用氯化物通道/药物作用囊性纤维化/代谢囊性纤维化/病理学肌醇磷酸类/代谢肌醇磷酸类/药理学膜电位制霉菌素/药理学人类

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Cystic fibrosis revisited

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MOLECULAR GENETICS AND METABOLISM 2000年第3期71卷 470-477页

作者： Larson, JE Cohen, JC Alton Ochsner Med Fdn & Ochsner Clin Lab Mol Therapeut New Orleans LA 70121 USA Louisiana State Univ Hlth Sci Ctr Sch Med Dept Med New Orleans LA 70112 USA

Cystic fibrosis is a pleiotropic disease whose primary defect is thought to be abnormal chloride conductance. Despite intensive study, the role of the protein in the airway and the mechanism for its direct participation in the disease pathology remain unclear. This paper reviews CFTR's cell regulatory functions and data supporting the role of CFTR in secretory epithelial cell development. A hypothesis for CF pathophysiology based on secretory cell differentiation is proposed. (C) 2000 Academic Press.

关键词：囊性纤维化/遗传学囊性纤维化/病理学囊性纤维化跨膜传导调节因子/遗传学基因表达调控发育期动物人类

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Cystic fibrosis transmembrane conductance regulator does not affect neutrophil migration across cystic fibrosis airway epithelial monolayers

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AMERICAN JOURNAL OF PATHOLOGY 2000年第4期156卷 1407-1416页

作者： Pizurki, L Morris, MA Chanson, M Solomon, M Pavirani, A Bouchardy, I Suter, S Univ Geneva Hop Cantonal Lab Clin Invest 3 Dept Pediat CH-1211 Geneva 14 Switzerland Univ Geneva Sch Med Div Med Genet CH-1211 Geneva Switzerland Transgene SA Strasbourg France

Recent studies have shown that airway inflammation dominated by neutrophils, ie, polymorphonuclear;tr cells (PMN) was observed in infants and children with cystic fibrosis (CF) even in the absence of detectable infection. To assess whether there is a CF-related anomaly of PMN migration across airway epithelial cells, we developed an. in vitro model of chemotactic migration across tight and polarized CF15 cells, a CF human nasal epithelial cell line, seeded on porous filters. To compare PMN migration across a pair of CF and control monolayers in the physiological direction, inverted CF15 cells were infected with increasing concentrations of recombinant adenoviruses containing either the normal cystic fibrosis transmembrane conductance regulator (CFTR) cDNA, the Delta F508 CFTR cDNA, or the beta-galactosidase gene. The number of PMN migrating in response to N-formyl-Met-Leu-Phe across inverted CF15 monolayers expressing beta-galactosidase was similar to that seen across CF15 monolayers rescued with CFTR, whatever the proportion of cells expressing the transgene, Moreover, PMN migration across monolayers expressing various amounts of mutated CFTR was not different from that observed across matched counterparts expressing normal CFTR, Finally, PMN migration in response to adherent or Pseudomonas aeruginosa was equivalent across CF and corrected monolayers, The possibility that mutated CFTR may exert indirect effects on PMN recruitment, via an abnormal production of the chemotactic cytokine interleukin-8, was also explored. Apical and basolateral production of interleukin-8 by polarized CF cells expressing mutated CFTR was not different from that observed with rescued cells, either in baseline or stimulated conditions. CF15 cells displayed a CF phenotype that could be corrected by CFTR-containing adenoviruses, because two known CF defects, Cl- secretion and increased P. aeruginosa adherence, were normalized after infection with those viruses. Thus, we conclude that the p

关键词：腺病毒科/遗传学细菌黏附/生理学细胞运动/药物作用细胞极性细胞培养的囊性纤维化/病理学囊性纤维化/病理生理学囊性纤维化跨膜传导调节因子/遗传学囊性纤维化跨膜传导调节因子/药理学基因表达白细胞介素8/代谢突变/生理学鼻黏膜/病理学鼻黏膜/病理生理学中性白细胞/药物作用中性白细胞/微生物学中性白细胞/生理学假单胞菌铜绿/生理学参考值转基因/遗传学人类

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Evidence of chronic inflammation in morphologically normal small intestine of cystic fibrosis patients

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PEDIATRIC RESEARCH 2000年第3期47卷 344-350页

作者： Raia, V Maiuri, L De Ritis, G De Vizia, B Vacca, L Conte, R Auricchio, S Londei, M Univ Naples Federico II Dept Pediat Cyst Fibrosis Unit I-80131 Naples Italy Childrens Hosp Santobono I-80127 Naples Italy Univ Cagliari Cattedra Neonatol I-09100 Cagliari Italy Kennedy Inst Rheumatol Div Immunol London W6 8LH England

Cystic fibrosis (CF) is caused by mutations in the CF transmembrane conductance regulator gene and characteristically leads to prominent lung and pancreatic malfunctions. Although an inflammatory reaction is normally observed in the CF airways, no studies have been performed to establish whether a chronic inflammatory response is also present in the CF intestine. We have investigated whether immunologic alterations and signs of inflammation are observed in CF small intestine. Fourteen CF, 20 negative, and four disease controls underwent duodenal endoscopy for diagnostic purposes. Two CF patients were rebiopsied, one after 3 mo of an elemental diet and the other after 2 wk of pancreatic enzyme withdrawal. In three CF and 10 controls, in vitro small intestine organ cultures were also performed. Expression of ICAM-1, IL-2 receptor, IL-2, IFN-gamma, CD80, and transferrin receptor was studied by immunohistochemistry before and after in vitro organ culture. In CF small intestine, an increased number of lamina propria mononuclear cells express ICAM-1 [mean 114 (SD 82.8), p < 0.001 versus controls], CD25 [20.2 (18.7), p < 0.01], IL-2 [23.6 (13.7), p < 0.05], and IFN-gamma [19 (15.9), p < 0.05], whereas villus enterocytes highly express transferrin receptor. Reduced expression of immunologic markers wets observed after 24 h of in vitro culture in all three CF patients as well as in the patient kept on elemental diet for 3 mo. These results indicate that chronic inflammation is observed in CF duodenum and suggest that the perturbation of local mucosal immune response may contribute to the overall clinical picture in CF patients.

关键词：慢性病囊性纤维化/免疫学囊性纤维化/代谢囊性纤维化/病理学免疫组织化学小肠/免疫学小肠/代谢小肠/病理学青少年成年人儿童儿童学龄前女(雌)性人类男(雄)性

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Increased sweat chloride concentrations in adult patients with pancreatic insufficiency: Cystic fibrosis phenotype or lack of specificity of sweat test?

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SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY 1999年第12期34卷 1260-1260页

作者： Durieu, I Durupt, S Josserand, RN Durand, DV Bey-Omar, F Ctr Hosp Lyon Sud Dept Internal Med F-69495 Pierre Benite France Hop Debrousse INSERM U 329 Lab Biochim Endocrinienne & Mol F-69005 Lyon France

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关键词：氯化物/分析囊性纤维化/遗传学囊性纤维化/病理学囊性纤维化跨膜传导调节因子/遗传学胰腺外分泌功能不全/遗传学胰腺外分泌功能不全/病理学突变汗/化学成年人人类男(雄)性

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CONJUNCTIVAL GOBLET CELLS IN PATIENTS WITH CYSTIC-FIBROSIS

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ACTA OPHTHALMOLOGICA 1975年第2期53卷 167-172页

作者： HOLM, K KESSING, SV UNIV COPENHAGEN RIGS HOSPDEPT OPHTHALMOL EDK-2100 COPENHAGENDENMARK UNIV COPENHAGEN RIGS HOSPDEPT PEDIAT TGDK-2100 COPENHAGENDENMARK

In five patients with cystic fibrosis of the pancreas the mucous glandular system of the conjunctiva was studied, as changes, if any, in the conjunctival goblet cells might be applicable as a diagnostic test in questionable cases. A whole-mount technique was used, specially developed for studying conjunctival goblet cells. In all five cases the qualitative as well as quantitative goblet-cell findings were in accordance with a previously reported normal material. In particular, there were no signs of stagnated secretion.

关键词：结膜/病理学囊性纤维化/病理学上皮细胞儿童儿童学龄前人类

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