Abstract
We investigated the effects of bicarbonate on the growth of several different bacteria as well as its effects on biofilm formation and intracellular cAMP concentration in Pseudomonas aeruginosa. Biofilm formation was examined in 96-well plates, with or without bicarbonate. The cAMP production of bacteria was measured by a commercial assay kit. We found that NaHCO3 (100 mmol l-1) significantly inhibited, whereas NaCl (100 mmol l-1) did not influence the growth of planktonic bacteria. MIC and MBC measurements indicated that the effect of is bacteriostatic rather than bactericidal. Moreover, NaHCO3 prevented biofilm formation as a function of concentration. Bicarbonate and alkalinization of external pH induced a significant increase in intracellular cAMP levels. In conclusion, impedes the planktonic growth of different bacteria and impedes biofilm formation by P. aeruginosa that is associated with increased intracellular cAMP production. These findings suggest that aerosol inhalation therapy with solutions may help improve respiratory hygiene in patients with cystic fibrosis and possibly other chronically infected lung diseases.
Highlights
Cystic fibrosis (CF) is caused by mutations in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR) protein (Riordan et al, 1989)
Glucose starvation leads to impaired biofilm formation associated with elevated cAMP levels (Huynh et al, 2012), glucose is required for optimal biofilm formation
Since we found that increased HCO−3 impedes the growth and biofilm formation of several pulmonary bacterial pathogens, we expect that increasing HCO−3 in the airways may reduce infection, inflammation, and a consequent tissue damage in the lungs
Summary
Cystic fibrosis (CF) is caused by mutations in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR) protein (Riordan et al, 1989). CFTR is a cAMP/protein kinase A (PKA)-dependent epithelial anion channel that conducts both chloride and bicarbonate (Linsdell et al, 1997; Reddy and Quinton, 2003). Defective transepithelial anion transport impairs mucociliary clearance (MCC) leading to the retention of thick, viscid mucus in the airways (Quinton, 2007a, 2010). The poor clearance of viscous CF mucus contributes to a vicious cycle of airway obstruction, infection, and inflammation (Hoffman and Ramsey, 2013). The links between the primary defect in anion transport and CF lung disease appear to be multifactorial. It was recently shown that impaired HCO−3 secretion is likely responsible for aggregated mucus in CF mice (Garcia et al, 2009; Gustafsson et al, 2012) and pigs (Birket et al, 2014)
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