Cystic fibrosis is characterized in the lungs by neutrophil-dominated inflammation mediated significantly by neutrophil elastase (NE). Previous work has shown that

Lactobacillus plantarum P5 grew aerobically in rich media at the expense of lactate; no growth was observed in the absence of aeration. The oxygen-dependent growth was accompanied by the conversion of lactate to acetate which accumulated in the growth medium. Utilization of oxygen with lactate as substrate was observed in buffered suspensions of washed whole cells and in cell-free extracts. A pathway which accounts for the generation of adenosine triphosphate during aerobic metabolism of lactate to acetate via pyruvate and acetyl phosphate is proposed. Each of the enzyme activities involved, nicotinamide adenine dinucleotide independent lactic dehydrogenase, nicotinamide adenine dinucleotide dependent lactic dehydrogenase, pyruvate oxidase, acetate kinase and NADH oxidase were demonstrated in cell-free extracts. The production of pyruvate, acetyl phosphate and acetate was demonstrated using cell-free extracts and cofactors for the enzymes of the proposed pathway.

A non‐genomic antisecretory role for dexamethasone at low concentrations (0.1 nm to1 μm) is described in monolayers of human bronchial epithelial cells in primary culture and in a continuous cell line (16HBE14o‐ cells). Dexamethasone produced a rapid decrease of [Ca2+]i (measured with fura‐2 spectrofluorescence) to a new steady‐state concentration. After 15 min exposure to dexamethasone (1 nm), [Ca2+]i was reduced by 32 ± 11 nm (n= 7, P < 0.0001) from a basal value of 213 ± 36 nm (n= 7). We have shown previously that aldosterone (1 nm) also produces a rapid fall in [Ca2+]i; however, after the decrease in [Ca2+]i induced by dexamethasone, subsequent addition of aldosterone did not produced any further lowering of [Ca2+]i. The rapid response to dexamethasone was insensitive to pretreatment with cycloheximide and unaffected by the glucocorticoid type II and mineralocorticoid receptor antagonists RU486 and spironolactone, respectively. The rapid [Ca2+]i decrease induced by dexamethasone was inhibited by the Ca2+‐ATPase pump inhibitor thapsigargin (1 μm), the adenylate cyclase inhibitor MDL hydrochloride (500 μm) and the protein kinase A inhibitor Rp‐adenosine 3′,5′‐cyclic monophosphorothioate (200 μm), but was not affected by the protein kinase C inhibitor, chelerythrine chloride (0.1 μm). Treatment of 16HBE14o‐ cell monolayers with dexamethasone (1 nm) inhibited the large and transient [Ca2+]i increase induced by apical exposure to ATP (10−4m). Dexamethasone (1 nm) also reduced by 30 % the Ca2+‐dependant Cl− secretion induced by apical exposure to ATP (measured as the Cl−‐sensitive short‐circuit current across monolayers mounted in Ussing chambers). Our results demonstrate, for the first time, that dexamethasone at low concentrations inhibits Cl− secretion in human bronchial epithelial cells. The rapid inhibition of Cl− secretion induced by the synthetic glucocorticoid is associated with a rapid decrease in [Ca2+]i via a non‐genomic mechanism that does not involve the classical glucocorticoid or mineralocorticoid receptor. Rather, it is a result of rapid non‐genomic stimulation of thapsigargin‐sensitive Ca2+‐ATPase, via adenylate cyclase and protein kinase A signalling.