Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0847097 (acidity)
 15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To examine the effects of acid exposure with moderate acidity (pH 3.0-5.0) on bactericidal activity of airway surface liquid (ASL), ASL was collected by washing the surface of primary cultures of human tracheal epithelial cells 24 h after treatment with phosphate-buffered saline (PBS) adjusted to a pH of 3.0, 4.0, or 5.0. In all ASL, bactericidal activity was sensitive to sodium concentration. Escherichia coli (500 colony forming units [CFU]) was incubated in ASL, and the number of surviving bacteria was examined. The number of surviving bacteria in ASL from cultured cells with acid exposure at pH 3.0-5.0 was significantly higher than that in control ASL. The minimum inhibitory dilution ratio of ASL against 500 CFU of E. coli was also examined by microdilution assays. According to this assay, the bactericidal activity in ASL with acid challenge at a pH of 3.0 was less than half of that in control ASL. Reverse transcription-polymerase chain reaction and Western blot analysis showed that the production of mRNA and protein of human beta-defensin (HBD)-1 were significantly decreased by acid exposure at pH 3.0-5.0. In contrast, acid exposure did not change the production of mRNA and protein of HBD-2 and beta-actin mRNA. These results indicate that acid exposure, even with moderate acidity, may inhibit the production of bactericidal molecules, including HBD-1, in airway epithelial cells. Acid exposure may reduce bactericidal activity of ASL in human airway epithelial cells and may increase susceptibility of the airway to bacterial infection.
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PMID:Acid stimulation reduces bactericidal activity of surface liquid in cultured human airway epithelial cells. 1175 Dec 10

Increased adenosine concentration inhibits gastric acid secretion in rat via adenosine A1 and A2A receptors, whereas achlorhydria suppresses A1 and A2A receptor gene expression. This study aimed to examine the effects of omeprazole-induced achlorhydria on the expression and functional activity of nucleoside transporters in rat gastric mucosa. Wistar rats were treated for either 1 or 3 days with 0.4 mmol/kg omeprazole via gavage; controls were treated with vehicle. The expression of nucleoside transporters at the transcript level was explored by quantitative real-time polymerase chain reaction assays; the functional activity of nucleoside transporters in gastric mucosa was explored by observing [3H]adenosine uptake in vitro. Gastric mucosa expressed rat equilibrative nucleoside transporter (rENT) 1 and 2, and rat concentrative nucleoside transporter (rCNT) 1, 2, and 3 at the transcript level, and the estimated values for the threshold cycles for target amplification (Ct) were 31.5 +/- 2, 28.5 +/- 2.1, 32.9 +/- 2.2, 29.1 +/- 2, and 28.9 +/- 2.5, respectively (n = 3 or 4). The Ct value for rat beta-actin was 21.9 +/- 1.8 (n = 4). In vitro uptake of [3H]adenosine by gastric mucosa samples consisted of Na+-dependent and Na+-independent components. One-day omeprazole treatment caused no change in nucleoside transporter mRNA levels or in [3H]adenosine uptake. Three-day omeprazole treatments, however, led to a 12-fold and 17-fold increase in rENT2 and rCNT1 mRNA levels, respectively. Samples taken after 3 days of treatment also took up significantly more [3H]adenosine than did samples from the corresponding control. In conclusion, the possible modification of nucleoside transport activities by changes in intraluminal acidity may have significance as part of a purinergic regulatory feedback mechanism in the control of gastric acid secretion.
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PMID:Effects of omeprazole treatment on nucleoside transporter expression and adenosine uptake in rat gastric mucosa. 1944 39