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14. 116 Effect of Staphylococcus aureus supernatant on airway epithelium functionality in infants with cystic fibrosis

Author

Bessaci-Kabouya, K., primary, Gaultier, B., additional, Zahm, J.-M., additional, Coraux, C., additional, Mauran, P., additional, Weiss, L., additional, Dalphin, M.-L., additional, Derelle, J., additional, Tatopoulos, A., additional, Huet, F., additional, Perez-Martin, S., additional, Birembaut, P., additional, and Abely, M., additional

Published
2013
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45. [MicroRNA control biosynthesis of motile cilia in vertebrates]

Author

Chevalier B, Kodjabachian L, Coraux C, Pascal Barbry, Marcet B, Institut de Biologie du Développement de Marseille (IBDM), Aix Marseille Université (AMU)-Centre National de la Recherche Scientifique (CNRS), Institut de pharmacologie moléculaire et cellulaire (IPMC), Université Nice Sophia Antipolis (... - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Centre National de la Recherche Scientifique (CNRS), Plasticité de l'épithélium respiratoire dans les conditions normales et pathologiques - UMR-S 903 (PERPMP), SFR CAP Santé (Champagne-Ardenne Picardie Santé), Université de Reims Champagne-Ardenne (URCA)-Université de Picardie Jules Verne (UPJV)-Université de Reims Champagne-Ardenne (URCA)-Université de Picardie Jules Verne (UPJV)-Centre Hospitalier Universitaire de Reims (CHU Reims)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Reims Champagne-Ardenne (URCA), Université Nice Sophia Antipolis (1965 - 2019) (UNS), Université de Reims Champagne-Ardenne (URCA)-Centre Hospitalier Universitaire de Reims (CHU Reims)-Institut National de la Santé et de la Recherche Médicale (INSERM)-SFR CAP Santé (Champagne-Ardenne Picardie Santé), and Université de Reims Champagne-Ardenne (URCA)-Université de Reims Champagne-Ardenne (URCA)

Subjects
MESH: Cystic Fibrosis, Bronchi/cytology/secretion, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, MESH: Receptor, Notch1, MESH: Gene Expression Profiling, Xenopus laevis, Epithelial Cells/secretion/ultrastructure, MESH: Xenopus laevis, MESH: Cilia, MicroRNAs/genetics/*physiology, MESH: Intracellular Signaling Peptides and Proteins, MESH: Mucus, Mucus/secretion, Cell Movement/genetics, Vertebrates/*genetics, Animals, Humans, MESH: Animals, MESH: Vertebrates, MESH: Cell Movement, ComputingMilieux_MISCELLANEOUS, Intracellular Signaling Peptides and Proteins/physiology, MESH: Humans, Cystic Fibrosis/pathology, Nonmammalian, Notch1/physiology, Gene Expression Profiling, Membrane Proteins/physiology, MESH: Bronchi, MESH: Embryo, Nonmammalian, MESH: Epithelial Cells, Embryo, MESH: Membrane Proteins, Cilia/*genetics/metabolism, MESH: Epidermis, Epidermis/embryology/secretion/ultrastructure, MESH: MicroRNAs, Receptor
Abstract

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47. Long acting β2-agonist and corticosteroid restore airway glandular cell function altered by bacterial supernatant

Author

Nawrocki-Raby Béatrice, Toumi Férial, Delavoie Franck, Zahm Jean-Marie, Kileztky Claire, Michel Jean, Balossier Gérard, Johnson Malcolm, Coraux Christelle, and Birembaut Philippe

Subjects
Diseases of the respiratory system, RC705-779
Abstract

Abstract Background Staphylococcus aureus releases virulence factors (VF) that may impair the innate protective functions of airway cells. The aim of this study was to determine whether a long-acting β2 adrenergic receptor agonist (salmeterol hydroxynaphthoate, Sal) combined with a corticosteroid (fluticasone propionate, FP) was able to regulate ion content and cytokine expression by airway glandular cells after exposure to S. aureus supernatant. Methods A human airway glandular cell line was incubated with S. aureus supernatant for 1 h and then treated with the combination Sal/FP for 4 h. The expression of actin and CFTR proteins was analyzed by immunofluorescence. Videomicroscopy was used to evaluate chloride secretion and X-ray microanalysis to measure the intracellular ion and water content. The pro-inflammatory cytokine expression was assessed by RT-PCR and ELISA. Results When the cells were incubated with S. aureus supernatant and then with Sal/FP, the cellular localisation of CFTR was apical compared to the cytoplasmic localisation in cells incubated with S. aureus supernatant alone. The incubation of airway epithelial cells with S. aureus supernatant reduced by 66% the chloride efflux that was fully restored by Sal/FP treatment. We also observed that Sal/FP treatment induced the restoration of ion (Cl and S) and water content within the intracellular secretory granules of airway glandular cells and reduced the bacterial supernatant-dependent increase of pro-inflammatory cytokines IL8 and TNFα. Conclusions Our results demonstrate that treatment with the combination of a corticosteroid and a long-acting β2 adrenergic receptor agonist after bacterial infection restores the airway glandular cell function. Abnormal mucus induced by defective ion transport during pulmonary infection could benefit from treatment with a combination of β2 adrenergic receptor agonist and glucocorticoid.

Published
2010
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48. Long acting beta2-agonist and corticosteroid restore airway glandular cell function altered by bacterial supernatant.

Author

Zahm JM, Delavoie F, Toumi F, Nawrocki-Raby B, Kileztky C, Michel J, Balossier G, Johnson M, Coraux C, Birembaut P, Zahm, Jean-Marie, Delavoie, Franck, Toumi, Férial, Nawrocki-Raby, Béatrice, Kileztky, Claire, Michel, Jean, Balossier, Gérard, Johnson, Malcolm, Coraux, Christelle, and Birembaut, Philippe

Abstract

Background: Staphylococcus aureus releases virulence factors (VF) that may impair the innate protective functions of airway cells. The aim of this study was to determine whether a long-acting beta2 adrenergic receptor agonist (salmeterol hydroxynaphthoate, Sal) combined with a corticosteroid (fluticasone propionate, FP) was able to regulate ion content and cytokine expression by airway glandular cells after exposure to S. aureus supernatant.Methods: A human airway glandular cell line was incubated with S. aureus supernatant for 1 h and then treated with the combination Sal/FP for 4 h. The expression of actin and CFTR proteins was analyzed by immunofluorescence. Videomicroscopy was used to evaluate chloride secretion and X-ray microanalysis to measure the intracellular ion and water content. The pro-inflammatory cytokine expression was assessed by RT-PCR and ELISA.Results: When the cells were incubated with S. aureus supernatant and then with Sal/FP, the cellular localisation of CFTR was apical compared to the cytoplasmic localisation in cells incubated with S. aureus supernatant alone. The incubation of airway epithelial cells with S. aureus supernatant reduced by 66% the chloride efflux that was fully restored by Sal/FP treatment. We also observed that Sal/FP treatment induced the restoration of ion (Cl and S) and water content within the intracellular secretory granules of airway glandular cells and reduced the bacterial supernatant-dependent increase of pro-inflammatory cytokines IL8 and TNFalpha.Conclusions: Our results demonstrate that treatment with the combination of a corticosteroid and a long-acting beta2 adrenergic receptor agonist after bacterial infection restores the airway glandular cell function. Abnormal mucus induced by defective ion transport during pulmonary infection could benefit from treatment with a combination of beta2 adrenergic receptor agonist and glucocorticoid. [ABSTRACT FROM AUTHOR]

Published
2010
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50. The F508del-CFTR trafficking correctors elexacaftor and tezacaftor are CFTR-independent Ca 2+ -mobilizing agonists normalizing abnormal Ca 2+ levels in human airway epithelial cells.

Author

Lévêque M, Mirval S, Barrault C, Fixe I, Coraux C, Sage E, Becq F, and Vandebrouck C

Subjects
Humans, Animals, Cystic Fibrosis metabolism, Cystic Fibrosis drug therapy, Cystic Fibrosis genetics, Cricetulus, Epithelial Cells metabolism, Epithelial Cells drug effects, CHO Cells, Pyrroles pharmacology, Cells, Cultured, Respiratory Mucosa metabolism, Respiratory Mucosa drug effects, Protein Transport drug effects, Pyridines pharmacology, Pyrrolidines, Cystic Fibrosis Transmembrane Conductance Regulator genetics, Cystic Fibrosis Transmembrane Conductance Regulator metabolism, Benzodioxoles pharmacology, Indoles pharmacology, Calcium metabolism, Pyrazoles pharmacology
Abstract

Background: Cystic fibrosis (CF) is caused by mutations in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR) channel. For people with CF (pwCF) affected by the most common pathogenic variant F508del, a tritherapy, named Trikafta/Kaftrio (ETI: elexacaftor (VX-445) /tezacaftor (VX-661) / ivacaftor (VX-770)) was successfully developed. However, in CF airway epithelial cells the calcium homeostasis is also disturbed; it is observed an increased calcium mobilization in CF cells compared to non-CF cells. Here, we studied the effects of ETI on intracellular calcium levels in F508del-CFTR airway epithelial cells to determine whether these compounds, individually or collectively, could normalize intracellular calcium levels., Methods: We measured intracellular calcium variations using human airway epithelial cells (hAEC) from pwCF, human bronchial epithelial CFBE41o- F508del-CFTR cells and Chinese Hamster Ovary (CHO) cells using the fluorescent probe Fluo4-AM, in the presence or absence of extracellular calcium. The rescue to the plasma membrane of F508del-CFTR protein by ETI was determined by western blot. The SarcoEndoplasmic Reticulum Calcium ATPase (SERCA), was also analysed by western blotting and by interference assay., Results: We show that ETI normalizes calcium homeostasis in our cellular models. However, we also found that (1) each ETI-corrector compound is capable of mobilizing calcium acutely in the absence of CFTR, and (2) tezacaftor mobilizes calcium from the endoplasmic reticulum (ER) probably via inhibition of the SERCA pump., Conclusions: We show that ETI not only corrects the abnormal trafficking and function of F508del-CFTR but also normalizes calcium homeostasis in our cellular models. Finally, we identified SERCA as a potential intracellular target for tezacaftor., Competing Interests: Declarations. Ethics approval and consent to participate: Not applicable. Consent for publication: Not applicable. Competing interests: The authors declare no competing interests., (© 2024. The Author(s).)

Published
2024
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