Reduced expression of psoriasin in human airway cystic fibrosis epithelia

Li, Tiesong; Cowley, Elizabeth A.

doi:10.1016/j.resp.2012.06.028

Cited by 3 publications

(3 citation statements)

References 32 publications

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“…The present study does not aim to see if the effects of GCs on the internalization of P. aeruginosa vary with the presence of wild type and/or mutant CFTR. It is well described from the in vitro and in vivo studies that CF cells do show P. aeruginosa internalization [16][17][18]29].…”

Section: Introductionmentioning

confidence: 95%

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Glucocorticoids can affectPseudomonas aeruginosa(ATCC 27853) internalization and intracellular calcium concentration in cystic fibrosis bronchial epithelial cells

Hussain

Shahror

Karpati

et al. 2015

Experimental Lung Research

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These findings suggest that if internalization of P. aeruginosa reduces infection, GC therapy would increase the risk of pulmonary infection by decreasing the internalization of P. aeruginosa in CF cells, but GCs may improve airway hydration by increasing the intracellular Ca(2+) concentration. Whether the benefits of GC treatment outweigh the negative effects is questionable, and further clinical studies need to be carried out.

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Section: Introductionmentioning

confidence: 95%

“…However, the exact effects of GCs on the nonmucoid P. aeruginosa internalization in CF bronchial epithelial cells are unknown. A recent study has shown that stimulation of bronchial epithelial cells with IL-22 and a cytomix (IL-1β, TNF-α, and IFN-γ ) decreases P. aeruginosa internalization in both CF and nonCF cells [29].…”

Section: Introductionmentioning

confidence: 99%

Glucocorticoids can affectPseudomonas aeruginosa(ATCC 27853) internalization and intracellular calcium concentration in cystic fibrosis bronchial epithelial cells

Hussain

Shahror

Karpati

et al. 2015

Experimental Lung Research

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“…Some studies have indicated that P. aeruginosa can employ CFTR as a receptor for its internalization (35,39), whereas others do not support this mechanism of bacterial internalization (11). Irrespective of whether or not CFTR is a receptor for P. aeruginosa, it is well described from in vitro and in vivo studies that CF cells do show P. aeruginosa internalization (4,29,35,39). More recent studies have shown that stimulation of bronchial epithelial cells with IL-22 and a cytomix (IL-1␤, TNF-␣, and IFN-␥) decreases P. aeruginosa internalization in both CF and non-CF cells (24) and that glucocorticoids can reduce P. aeruginosa internalization in cystic fibrosis bronchial epithelial cells (27).…”

Section: Lxa 4 Reduces P Aeruginosa Intracellular Invasion and Transmentioning

confidence: 99%

Lipoxin A₄prevents tight junction disruption and delays the colonization of cystic fibrosis bronchial epithelial cells byPseudomonas aeruginosa

Higgins

Fustero-Torre

Tyrrell

et al. 2016

American Journal of Physiology-Lung Cellular and Molecular Phys

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The specialized proresolution lipid mediator lipoxin A4 (LXA4) is abnormally produced in cystic fibrosis (CF) airways. LXA4 increases the CF airway surface liquid height and stimulates airway epithelial repair and tight junction formation. We report here a protective effect of LXA4 (1 nM) against tight junction disruption caused by Pseudomonas aeruginosa bacterial challenge together with a delaying action against bacterial invasion in CF airway epithelial cells from patients with CF and immortalized cell lines. Bacterial invasion and tight junction integrity were measured by gentamicin exclusion assays and confocal fluorescence microscopy in non-CF (NuLi-1) and CF (CuFi-1) bronchial epithelial cell lines and in primary CF cultures, grown under an air/liquid interface, exposed to either a clinical or laboratory strains of P. aeruginosa LXA4 delayed P. aeruginosa invasion and transepithelial migration in CF and normal bronchial epithelial cell cultures. These protective effects of LXA4 were inhibited by the ALX/FPR2 lipoxin receptor antagonist BOC-2. LXA4 prevented the reduction in mRNA biosynthesis and protein abundance of the tight junction protein ZO-1 and reduced tight junction disruption induced by P. aeruginsosa inoculation. In conclusion, LXA4 plays a protective role in bronchial epithelium by stimulating tight junction repair and by delaying and reducing the invasion of CF bronchial epithelial cells by P. aeruginsosa.

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N-acetylcysteine and azithromycin affect the innate immune response in cystic fibrosis bronchial epithelial cells in vitro

Hussain

Varelogianni

Särndahl

et al. 2014

Experimental Lung Research

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Reduced expression of psoriasin in human airway cystic fibrosis epithelia

Cited by 3 publications

References 32 publications

Glucocorticoids can affectPseudomonas aeruginosa(ATCC 27853) internalization and intracellular calcium concentration in cystic fibrosis bronchial epithelial cells

Glucocorticoids can affectPseudomonas aeruginosa(ATCC 27853) internalization and intracellular calcium concentration in cystic fibrosis bronchial epithelial cells

Lipoxin A₄prevents tight junction disruption and delays the colonization of cystic fibrosis bronchial epithelial cells byPseudomonas aeruginosa

N-acetylcysteine and azithromycin affect the innate immune response in cystic fibrosis bronchial epithelial cells in vitro

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Reduced expression of psoriasin in human airway cystic fibrosis epithelia

Cited by 3 publications

References 32 publications

Glucocorticoids can affectPseudomonas aeruginosa(ATCC 27853) internalization and intracellular calcium concentration in cystic fibrosis bronchial epithelial cells

Glucocorticoids can affectPseudomonas aeruginosa(ATCC 27853) internalization and intracellular calcium concentration in cystic fibrosis bronchial epithelial cells

Lipoxin A4prevents tight junction disruption and delays the colonization of cystic fibrosis bronchial epithelial cells byPseudomonas aeruginosa

N-acetylcysteine and azithromycin affect the innate immune response in cystic fibrosis bronchial epithelial cells in vitro

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Lipoxin A₄prevents tight junction disruption and delays the colonization of cystic fibrosis bronchial epithelial cells byPseudomonas aeruginosa