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

Abstract

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.

Clinical and microbiological characteristics of cystic fibrosis adults never colonized by Pseudomonas aeruginosa: Analysis of the French CF registry

“…A plausible explanation is the treatment of aspergillosis by glucocorticoids, which could impair internalization and phagocytosis of P . aeruginosa by CF respiratory epithelial cells [12].…”

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

“…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). Nonmucoid P. aeruginosa may hide in epithelial cells to escape the host innate immune defense or secrete toxins to efficiently kill host cells (30).…”

Microbial uptake by the respiratory epithelium: outcomes for host and pathogen

“…Bronchoalveolar lavages of CF patients show elevated levels of IL-6 and IL-8 (Bonfield et al 1995), and pre-treatment of CF AECs with IL-6 or IL-8 increases P. aeruginosa internalisation, suggesting that appropriate inflammatory responsiveness might hamper the establishment of chronic colonisation in CF patients (Hussain et al 2015). Despite controversy, glucocorticoids are used as anti-inflammatory agents; however, it has been shown that concomitant treatment of CF airway cells with glucocorticoids and IL-6 decreases bacterial internalisation, in turn reducing bacterial clearance and possibly increasing the risk of pulmonary infection in CF patients (Hussain et al 2015). Heightened release of IL-1β is also central to the lethal effect of acute P. aeruginosa infection and mice deficient for the IL-1 receptor show improved host defence against infection in the lung (Schultz et al 2002(Schultz et al , 2004.…”