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Specialty: Respiratory Medicine
Condition: Cystic Fibrosis

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Total 8 results found since Jan 2013.

NF-kB activation in cystic fibrosis: The dream of A20
In conclusion, high expression of the repressor DREAM inhibits A20 transcription in CF epithelial cells. Our work suggests an important role of the A20-DREAM axis in (innate) inflammation, providing a new molecular target for the development of innovative anti-inflammatory therapies.
Source: European Respiratory Journal - November 20, 2019 Category: Respiratory Medicine Authors: Momtazi, G., Elbanna, A., Finnegan, S., Heritier, M., Lavery, L., Mccollum, K., Naranjo, J., Schock, B. Tags: Airway cell biology and immunopathology Source Type: research

S-Nitrosylation of CHIP Enhances F508Del CFTR Maturation.
Abstract S-Nitrosothiols (SNOs) are endogenous signaling compounds with a diverse spectrum of beneficial airway effects that are both cGMP-dependent and -independent. SNOs are present in healthy human airways, but levels are low in the airways of cystic fibrosis (CF) patients. Here, we evaluated the interactions of SNOs with molecular co-chaperone C-terminus Hsc70 interacting protein (CHIP)- an E3 ubiquitin ligase that targets improperly folded CFTR for degradation. CHIP was expressed in primary human bronchial epithelial and CFBE41o - cells expressing either wild type or F508del CFTR. Confocal microscopy and immu...
Source: Am J Respir Cell Mol... - October 8, 2019 Category: Respiratory Medicine Authors: Zaman K, Knight J, Hussain F, Cao R, Estabrooks SK, Altawallbeh G, Holloway K, Jafri A, Sawczak V, Li Y, Getsy P, Sun F, Raffay T, Cotton C, Brodsky JL, Periasamy A, Lewis SJ, Gaston B Tags: Am J Respir Cell Mol Biol Source Type: research

TRPA1 Channels Modulate Inflammatory Response in Respiratory Cells from Cystic Fibrosis Patients.
In conclusion, TRPA1 channels are involved in regulating the extent of airway inflammation driven by CF bronchial epithelial cells. PMID: 27281024 [PubMed - as supplied by publisher]
Source: Am J Respir Cell Mol... - June 8, 2016 Category: Respiratory Medicine Authors: Prandini P, De Logu F, Fusi C, Provezza L, Nassini R, Montagner G, Materazzi S, Munari S, Gilioli E, Bezzerri V, Finotti A, Lampronti I, Tamanini A, Dechecchi M, Lippi G, Ribeiro CM, Rimessi A, Pinton P, Gambari R, Geppetti P, Cabrini G Tags: Am J Respir Cell Mol Biol Source Type: research

Augmentation of CFTR maturation by S-nitrosoglutathione reductase
S-nitrosoglutathione (GSNO) reductase regulates novel endogenous S-nitrosothiol signaling pathways, and mice deficient in GSNO reductase are protected from airways hyperreactivity. S-nitrosothiols are present in the airway, and patients with cystic fibrosis (CF) tend to have low S-nitrosothiol levels that may be attributed to upregulation of GSNO reductase activity. The present study demonstrates that 1) GSNO reductase activity is increased in the cystic fibrosis bronchial epithelial (CFBE41o–) cells expressing mutant F508del-cystic fibrosis transmembrane regulator (CFTR) compared with the wild-type CFBE41o– ce...
Source: AJP: Lung Cellular and Molecular Physiology - February 1, 2016 Category: Respiratory Medicine Authors: Zaman, K., Sawczak, V., Zaidi, A., Butler, M., Bennett, D., Getsy, P., Zeinomar, M., Greenberg, Z., Forbes, M., Rehman, S., Jyothikumar, V., DeRonde, K., Sattar, A., Smith, L., Corey, D., Straub, A., Sun, F., Palmer, L., Periasamy, A., Randell, S., Kelley Tags: CALL FOR PAPERS Source Type: research

Augmentation of CFTR maturation by S-nitrosoglutathione reductase.
Abstract S-Nitrosoglutathione reductase (GSNOR) regulates novel endogenous S-nitrosothiol signaling pathways, and mice deficient in GSNO reductase are protected from airways hyper-reactivity. S-Nitrosothiols are present in the airway, and in patients with cystic fibrosis (CF) tend to have low SNO levels that may be attributed to up-regulation of GSNO reductase activity. The present study demonstrates that (1) GSNO reductase activity is increased in the cystic fibrosis bronchial epithelial (CFBE41o(-) ) cells expressing mutant F508del-CFTR when compared to the wild type CFBE41o(-) cells, (2) GSNO reductase expressi...
Source: Am J Physiol Lung Ce... - December 4, 2015 Category: Respiratory Medicine Authors: Zaman K, Sawczak V, Zaidi A, Butler M, Bennett D, Getsy P, Zeinomar M, Greenberg Z, Forbes MS, Rehman S, Jyothikumar V, DeRonde K, Sattar A, Smith L, Corey DA, Straub A, Sun F, Palmer L, Periasamy A, Randell SH, Kelley TJ, Lewis SJ, Gaston B Tags: Am J Physiol Lung Cell Mol Physiol Source Type: research

Pro-resolving Action of MAG-DHA in Lung Inflammatory Models Related to Cystic Fibrosis.
CONCLUSIONS: MAG-DHA displays anti-inflammatory properties and reduces mucin overexpression in Calu-3 cells and human bronchi untreated or treated with P. aeruginosa LPS, a finding consistent with the effects of ResolvinD1, a known anti-inflammatory mediator. PMID: 25781052 [PubMed - as supplied by publisher]
Source: Am J Respir Cell Mol... - March 17, 2015 Category: Respiratory Medicine Authors: Morin C, Cantin AM, Rousseau É, Sirois M, Sirois C, Rizcallah E, Fortin S Tags: Am J Respir Cell Mol Biol Source Type: research

Impaired TLR4 and HIF expression in cystic fibrosis bronchial epithelial cells downregulates hemeoxygenase-1 and alters iron homeostasis in vitro
In this study, we investigated in vitro the role of Toll-like receptor 4 (TLR4), hypoxia-inducible factor 1α (HIF-1α), and iron on HO-1 expression in cystic fibrosis (CF). Immunohistochemical analysis of TLR4, HO-1, ferritin, and HIF-1α were performed on lung sections of CFTR–/– and wild-type mice. CFBE41o- and 16HBE14o- cell lines were employed for in vitro analysis via immunoblotting, immunofluorescence, real-time PCR, luciferase reporter gene analysis, and iron quantification. We observed a reduced TLR4, HIF-1α, HO-1, and ferritin in CFBE41o- cell line and CF mice. Knockdown studies u...
Source: AJP: Lung Cellular and Molecular Physiology - November 15, 2014 Category: Respiratory Medicine Authors: Chillappagari, S., Venkatesan, S., Garapati, V., Mahavadi, P., Munder, A., Seubert, A., Sarode, G., Guenther, A., Schmeck, B. T., Tummler, B., Henke, M. O. Tags: ARTICLES Source Type: research

Lipoxin A4-mediated KATP potassium channel activation results in cystic fibrosis airway epithelial repair
The main cause of morbidity and mortality in cystic fibrosis (CF) is progressive lung destruction as a result of persistent bacterial infection and inflammation, coupled with reduced capacity for epithelial repair. Levels of the anti-inflammatory mediator lipoxin A4 (LXA4) have been reported to be reduced in bronchoalveolar lavages of patients with CF. We investigated the ability of LXA4 to trigger epithelial repair through the initiation of proliferation and migration in non-CF (NuLi-1) and CF (CuFi-1) airway epithelia. Spontaneous repair and cell migration were significantly slower in CF epithelial cultures (CuFi-1) comp...
Source: AJP: Lung Cellular and Molecular Physiology - July 15, 2013 Category: Respiratory Medicine Authors: Buchanan, P. J., McNally, P., Harvey, B. J., Urbach, V. Tags: ARTICLES Source Type: research