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Bacterial killing in gastric juice – effect of pH and pepsin on Escherichia coli and Helicobacter pylori
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Zeitschriftentitel: | Journal of Medical Microbiology |
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Personen und Körperschaften: | , , , |
In: | Journal of Medical Microbiology, 55, 2006, 9, S. 1265-1270 |
Format: | E-Article |
Sprache: | Englisch |
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Microbiology Society
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author_facet |
Zhu, H. Hart, C. A. Sales, D. Roberts, N. B. Zhu, H. Hart, C. A. Sales, D. Roberts, N. B. |
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author |
Zhu, H. Hart, C. A. Sales, D. Roberts, N. B. |
spellingShingle |
Zhu, H. Hart, C. A. Sales, D. Roberts, N. B. Journal of Medical Microbiology Bacterial killing in gastric juice – effect of pH and pepsin on Escherichia coli and Helicobacter pylori Microbiology (medical) General Medicine Microbiology |
author_sort |
zhu, h. |
spelling |
Zhu, H. Hart, C. A. Sales, D. Roberts, N. B. 0022-2615 1473-5644 Microbiology Society Microbiology (medical) General Medicine Microbiology http://dx.doi.org/10.1099/jmm.0.46611-0 <jats:p>The susceptibility of <jats:italic>Escherichia coli</jats:italic> and <jats:italic>Helicobacter pylori</jats:italic> to pH and the effect of pepsin-mediated proteolysis were investigated. This was to establish the relative importance of their bacterial killing properties in gastric juice. Solutions in the pH range 1.5–7.4 with or without pig pepsin A were used, together with seven gastric juice samples obtained from patients undergoing routine gastric collection. <jats:italic>Escherichia coli</jats:italic> C690 (a capsulate strain), <jats:italic>E. coli</jats:italic> K-12 (a rough mutant) and <jats:italic>Helicobacter pylori</jats:italic> E5 were selected as the test organisms. Suspensions of bacteria (1×10<jats:sup>6</jats:sup> <jats:italic>E. coli</jats:italic> ml<jats:sup>−1</jats:sup> and 1×10<jats:sup>8</jats:sup> <jats:italic>H. pylori</jats:italic> ml<jats:sup>−1</jats:sup>) were pre-incubated with test solutions at 37 °C for up to 2 h, and then cultured to establish the effect on subsequent growth. Survival of bacteria was diminished at pHs of less than 3.5, whereas killing required a pH of less than 2.5. Pre-incubation with pig pepsin at 0.5, 1.0 and 2.0 mg ml<jats:sup>−1</jats:sup> at pH 3.5 reduced viable counts by 100 % for <jats:italic>E. coli</jats:italic> 690 and <jats:italic>E. coli</jats:italic> K-12 after 100 min incubation. With <jats:italic>H. pylori</jats:italic>, the viable counts decreased to 50 % of the control after 20 min incubation in 1 mg pepsin ml<jats:sup>−1</jats:sup> at pH 2.5, 3.0 and 3.5. The gastric juices showed bactericidal activity at pH 3.5, and the rate of killing was juice dependent, with complete death of <jats:italic>E. coli</jats:italic> 690 occurring between 5 and 40 min post-incubation. Thus, killing of <jats:italic>E. coli</jats:italic> and <jats:italic>H. pylori</jats:italic> occurs optimally at pHs of less than 2.5. At pH 3.5, little effect is observed, whereas addition of pepsin alone or in gastric juice causes a marked increase in bacterial susceptibility, suggesting an important role for proteolysis in the killing of bacteria.</jats:p> Bacterial killing in gastric juice – effect of pH and pepsin on Escherichia coli and Helicobacter pylori Journal of Medical Microbiology |
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10.1099/jmm.0.46611-0 |
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Biologie |
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Microbiology Society, 2006 |
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title |
Bacterial killing in gastric juice – effect of pH and pepsin on Escherichia coli and Helicobacter pylori |
title_unstemmed |
Bacterial killing in gastric juice – effect of pH and pepsin on Escherichia coli and Helicobacter pylori |
title_full |
Bacterial killing in gastric juice – effect of pH and pepsin on Escherichia coli and Helicobacter pylori |
title_fullStr |
Bacterial killing in gastric juice – effect of pH and pepsin on Escherichia coli and Helicobacter pylori |
title_full_unstemmed |
Bacterial killing in gastric juice – effect of pH and pepsin on Escherichia coli and Helicobacter pylori |
title_short |
Bacterial killing in gastric juice – effect of pH and pepsin on Escherichia coli and Helicobacter pylori |
title_sort |
bacterial killing in gastric juice – effect of ph and pepsin on escherichia coli and helicobacter pylori |
topic |
Microbiology (medical) General Medicine Microbiology |
url |
http://dx.doi.org/10.1099/jmm.0.46611-0 |
publishDate |
2006 |
physical |
1265-1270 |
description |
<jats:p>The susceptibility of <jats:italic>Escherichia coli</jats:italic> and <jats:italic>Helicobacter pylori</jats:italic> to pH and the effect of pepsin-mediated proteolysis were investigated. This was to establish the relative importance of their bacterial killing properties in gastric juice. Solutions in the pH range 1.5–7.4 with or without pig pepsin A were used, together with seven gastric juice samples obtained from patients undergoing routine gastric collection. <jats:italic>Escherichia coli</jats:italic> C690 (a capsulate strain), <jats:italic>E. coli</jats:italic> K-12 (a rough mutant) and <jats:italic>Helicobacter pylori</jats:italic> E5 were selected as the test organisms. Suspensions of bacteria (1×10<jats:sup>6</jats:sup>
<jats:italic>E. coli</jats:italic> ml<jats:sup>−1</jats:sup> and 1×10<jats:sup>8</jats:sup>
<jats:italic>H. pylori</jats:italic> ml<jats:sup>−1</jats:sup>) were pre-incubated with test solutions at 37 °C for up to 2 h, and then cultured to establish the effect on subsequent growth. Survival of bacteria was diminished at pHs of less than 3.5, whereas killing required a pH of less than 2.5. Pre-incubation with pig pepsin at 0.5, 1.0 and 2.0 mg ml<jats:sup>−1</jats:sup> at pH 3.5 reduced viable counts by 100 % for <jats:italic>E. coli</jats:italic> 690 and <jats:italic>E. coli</jats:italic> K-12 after 100 min incubation. With <jats:italic>H. pylori</jats:italic>, the viable counts decreased to 50 % of the control after 20 min incubation in 1 mg pepsin ml<jats:sup>−1</jats:sup> at pH 2.5, 3.0 and 3.5. The gastric juices showed bactericidal activity at pH 3.5, and the rate of killing was juice dependent, with complete death of <jats:italic>E. coli</jats:italic> 690 occurring between 5 and 40 min post-incubation. Thus, killing of <jats:italic>E. coli</jats:italic> and <jats:italic>H. pylori</jats:italic> occurs optimally at pHs of less than 2.5. At pH 3.5, little effect is observed, whereas addition of pepsin alone or in gastric juice causes a marked increase in bacterial susceptibility, suggesting an important role for proteolysis in the killing of bacteria.</jats:p> |
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author | Zhu, H., Hart, C. A., Sales, D., Roberts, N. B. |
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description | <jats:p>The susceptibility of <jats:italic>Escherichia coli</jats:italic> and <jats:italic>Helicobacter pylori</jats:italic> to pH and the effect of pepsin-mediated proteolysis were investigated. This was to establish the relative importance of their bacterial killing properties in gastric juice. Solutions in the pH range 1.5–7.4 with or without pig pepsin A were used, together with seven gastric juice samples obtained from patients undergoing routine gastric collection. <jats:italic>Escherichia coli</jats:italic> C690 (a capsulate strain), <jats:italic>E. coli</jats:italic> K-12 (a rough mutant) and <jats:italic>Helicobacter pylori</jats:italic> E5 were selected as the test organisms. Suspensions of bacteria (1×10<jats:sup>6</jats:sup> <jats:italic>E. coli</jats:italic> ml<jats:sup>−1</jats:sup> and 1×10<jats:sup>8</jats:sup> <jats:italic>H. pylori</jats:italic> ml<jats:sup>−1</jats:sup>) were pre-incubated with test solutions at 37 °C for up to 2 h, and then cultured to establish the effect on subsequent growth. Survival of bacteria was diminished at pHs of less than 3.5, whereas killing required a pH of less than 2.5. Pre-incubation with pig pepsin at 0.5, 1.0 and 2.0 mg ml<jats:sup>−1</jats:sup> at pH 3.5 reduced viable counts by 100 % for <jats:italic>E. coli</jats:italic> 690 and <jats:italic>E. coli</jats:italic> K-12 after 100 min incubation. With <jats:italic>H. pylori</jats:italic>, the viable counts decreased to 50 % of the control after 20 min incubation in 1 mg pepsin ml<jats:sup>−1</jats:sup> at pH 2.5, 3.0 and 3.5. The gastric juices showed bactericidal activity at pH 3.5, and the rate of killing was juice dependent, with complete death of <jats:italic>E. coli</jats:italic> 690 occurring between 5 and 40 min post-incubation. Thus, killing of <jats:italic>E. coli</jats:italic> and <jats:italic>H. pylori</jats:italic> occurs optimally at pHs of less than 2.5. At pH 3.5, little effect is observed, whereas addition of pepsin alone or in gastric juice causes a marked increase in bacterial susceptibility, suggesting an important role for proteolysis in the killing of bacteria.</jats:p> |
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spelling | Zhu, H. Hart, C. A. Sales, D. Roberts, N. B. 0022-2615 1473-5644 Microbiology Society Microbiology (medical) General Medicine Microbiology http://dx.doi.org/10.1099/jmm.0.46611-0 <jats:p>The susceptibility of <jats:italic>Escherichia coli</jats:italic> and <jats:italic>Helicobacter pylori</jats:italic> to pH and the effect of pepsin-mediated proteolysis were investigated. This was to establish the relative importance of their bacterial killing properties in gastric juice. Solutions in the pH range 1.5–7.4 with or without pig pepsin A were used, together with seven gastric juice samples obtained from patients undergoing routine gastric collection. <jats:italic>Escherichia coli</jats:italic> C690 (a capsulate strain), <jats:italic>E. coli</jats:italic> K-12 (a rough mutant) and <jats:italic>Helicobacter pylori</jats:italic> E5 were selected as the test organisms. Suspensions of bacteria (1×10<jats:sup>6</jats:sup> <jats:italic>E. coli</jats:italic> ml<jats:sup>−1</jats:sup> and 1×10<jats:sup>8</jats:sup> <jats:italic>H. pylori</jats:italic> ml<jats:sup>−1</jats:sup>) were pre-incubated with test solutions at 37 °C for up to 2 h, and then cultured to establish the effect on subsequent growth. Survival of bacteria was diminished at pHs of less than 3.5, whereas killing required a pH of less than 2.5. Pre-incubation with pig pepsin at 0.5, 1.0 and 2.0 mg ml<jats:sup>−1</jats:sup> at pH 3.5 reduced viable counts by 100 % for <jats:italic>E. coli</jats:italic> 690 and <jats:italic>E. coli</jats:italic> K-12 after 100 min incubation. With <jats:italic>H. pylori</jats:italic>, the viable counts decreased to 50 % of the control after 20 min incubation in 1 mg pepsin ml<jats:sup>−1</jats:sup> at pH 2.5, 3.0 and 3.5. The gastric juices showed bactericidal activity at pH 3.5, and the rate of killing was juice dependent, with complete death of <jats:italic>E. coli</jats:italic> 690 occurring between 5 and 40 min post-incubation. Thus, killing of <jats:italic>E. coli</jats:italic> and <jats:italic>H. pylori</jats:italic> occurs optimally at pHs of less than 2.5. At pH 3.5, little effect is observed, whereas addition of pepsin alone or in gastric juice causes a marked increase in bacterial susceptibility, suggesting an important role for proteolysis in the killing of bacteria.</jats:p> Bacterial killing in gastric juice – effect of pH and pepsin on Escherichia coli and Helicobacter pylori Journal of Medical Microbiology |
spellingShingle | Zhu, H., Hart, C. A., Sales, D., Roberts, N. B., Journal of Medical Microbiology, Bacterial killing in gastric juice – effect of pH and pepsin on Escherichia coli and Helicobacter pylori, Microbiology (medical), General Medicine, Microbiology |
title | Bacterial killing in gastric juice – effect of pH and pepsin on Escherichia coli and Helicobacter pylori |
title_full | Bacterial killing in gastric juice – effect of pH and pepsin on Escherichia coli and Helicobacter pylori |
title_fullStr | Bacterial killing in gastric juice – effect of pH and pepsin on Escherichia coli and Helicobacter pylori |
title_full_unstemmed | Bacterial killing in gastric juice – effect of pH and pepsin on Escherichia coli and Helicobacter pylori |
title_short | Bacterial killing in gastric juice – effect of pH and pepsin on Escherichia coli and Helicobacter pylori |
title_sort | bacterial killing in gastric juice – effect of ph and pepsin on escherichia coli and helicobacter pylori |
title_unstemmed | Bacterial killing in gastric juice – effect of pH and pepsin on Escherichia coli and Helicobacter pylori |
topic | Microbiology (medical), General Medicine, Microbiology |
url | http://dx.doi.org/10.1099/jmm.0.46611-0 |