Pylori bacteria can lead to ulcers

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A cocktail of populating bacteria can lead to ulcer formation

 

Helicobacter pylori have long been considered a major culprit of stomach

ulcers. A report from the Howard Hughes Medical Institute, Michigan, USA

demonstrated that a range of different bacteria could prove equally

responsible.

Posted: 24-Jan-02

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Juanita Merchant and colleagues embarked on a study to investigate the

action of gastrin, a hormone instrumental in controlling acid production

from parietal cells in the stomach. The hormone is released in response to

an alkaline environment and serves as a means of re-establishing the acid

pH. To prevent excessive production, a feedback mechanism comes into play

whereby another hormone - somatostatin - is released.

To determine whether a breakdown in this feedback control mechanism was

responsible for the elevated levels of gastrin observed during bacterial

infections, the researchers examined gastrin-knockout mice, in which acid

production was severely impaired leading to stomach inflammation,

characterized by increased numbers of G-cells and parietal cells.

Surprisingly, the researchers found that they were unable to infect these

mice with Helicobacter as they already harboured a large number of other

bacteria. The group hypothesized that the pH served to control the types of

bacteria inhabiting the stomach, with low pH favouring Helicobacter and high

pH favouring an array of different bacteria.

Additional studies demonstrated that administration of antibiotics into

gastrin-knockout mice resulted in a reduction in stomach inflammation and

was accompanied by a fall in the number of monopolizing bacteria. When

omeprazole - a proton pump inhibitor - was administered, inflammation was

exacerbated, owing to bacteria overgrowth.

'A key finding is that we showed that these abnormal gastrin levels dropped

down in omeprazole-treated mice just by giving them antibiotics,' said

Merchant. 'The question has always been whether this elevation and

regulation of gastrin levels was because the secreting cells were regulated

by the acid concentration. It turns out that's not the case, because

treating these animals with antibiotics caused their gastrin and parietal

cells to return to baseline levels. The elevation was due to inflammation.'

Taken together, the studies highlighted the role of organisms, other than

Helicobacter, in inducing chronic inflammation and conclude that the use of

certain protein pump inhibitors should be treated with caution.

Source: http://www.hhmi.org

Gastroenterology 2002; 122:119-133

American Journal of Physiology - Gastrointestinal and Liver Physiology 2002;

282: 175-183