Happy New Year!

I felt to check PubMed on new findings concerning GSH and CF, and here's a few:

Sci China C Life Sci. 2009 Jun;52(6):501-5. Epub 2009 Jun 26.
Glutathione exhibits antibacterial activity and increases tetracycline efficacy against Pseudomonas aeruginosa.
ZHANG Y, DUAN K.

Molecular Microbiology Laboratory, the College of Life Sciences, Northwest University, Xi'an 710069, China.
Glutathione (GSH) plays important roles in pulmonary diseases, and inhaled GSH therapy has been used to treat cystic fibrosis (CF) patients in clinical trials. The results in this report revealed that GSH altered the sensitivity of Pseudomonas aeruginosa to different antibiotics through pathways unrelated to the oxidative stress as generally perceived. In addition, GSH and its oxidized form inhibited the growth of P. aeruginosa.

PMID: 19557326 [PubMed - indexed for MEDLINE]

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Cell Biol Int. 2009 Oct 20. [Epub ahead of print]
The effect of N-acetylcysteine on chloride efflux from airway epithelial cells.
Varelogianni G, Oliynyk I, Roomans GM, Johannesson M.

Defective chloride transport in epithelial cells increases mucus viscosity and leads to recurrent infections with high oxidative stress in patients with cystic fibrosis (CF). N-acetylcysteine (NAC) is a well known mucolytic and antioxidant drug, and an indirect precursor of glutathione. Since S-nitrosoglutathione (GSNO) previously has been shown to be able to promote Cl- efflux from CF airway epithelial cells, it was investigated whether NAC also could stimulate Cl- efflux from CF and non-CF epithelial cells and through which mechanisms. CF bronchial epithelial cells (CFBE) and normal bronchial epithelial cells (16HBE) were treated with 1mM, 5mM, 10mM or 15mM NAC for 4h at 37 degrees C. The effect of NAC on Cl- transport was measured by Chloride efflux measurements and by X-ray microanalysis. Cl- efflux from CFBE cells was stimulated by NAC in a dose dependent manner, with 10mM NAC causing a significant increase in Cl- efflux with nearly 80% in CFBE cells. The intracellular Cl- concentration in CFBE cells was significantly decreased up to 60 % after 4h treatment with 10mM NAC. Moreover immunocytochemistry and Western Blot experiments revealed expression of CFTR channel on CFBE cells after treatment with 10mM NAC. The stimulation of Cl- efflux by NAC in CF airway epithelial cells may improve hydration of the mucus and thereby be beneficial for CF patients.

PMID: 19947928 [PubMed - as supplied by publisher]

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Respir Res. 2009 Mar 13;10:23.
Mechanisms of the noxious inflammatory cycle in cystic fibrosis.
Rottner M, Freyssinet JM, Martínez MC.

1INSERM U 770; Université Paris-Sud 11, Faculté de Médecine, Hôpital de Bicêtre, Le Kremlin-Bicêtre, France. mathilde.rottner@hemato-ulp.u-strasbg.fr
Multiple evidences indicate that inflammation is an event occurring prior to infection in patients with cystic fibrosis. The self-perpetuating inflammatory cycle may play a pathogenic part in this disease. The role of the NF-kappaB pathway in enhanced production of inflammatory mediators is well documented. The pathophysiologic mechanisms through which the intrinsic inflammatory response develops remain unclear. The unfolded mutated protein cystic fibrosis transmembrane conductance regulator (CFTRDeltaF508), accounting for this pathology, is retained in the endoplasmic reticulum (ER), induces a stress, and modifies calcium homeostasis. Furthermore, CFTR is implicated in the transport of glutathione, the major antioxidant element in cells. CFTR mutations can alter redox homeostasis and induce an oxidative stress. The disturbance of the redox balance may evoke NF-kappaB activation and, in addition, promote apoptosis. In this review, we examine the hypotheses of the integrated pathogenic processes leading to the intrinsic inflammatory response in cystic fibrosis.

PMID: 19284656 [PubMed - indexed for MEDLINE]