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Immune system's distress signal tells bacteria when to strike back

barrier cells that line the host's bowel to become more permeable, which renders them more susceptible to the microbe's toxins. Pyocyanin enhances the germ's ability to pass through the weakened bowel wall, enter the bloodstream and invade tissue.

"Our goal," Alverdy said, "is to understand the many steps in this process and use that knowledge to find novel ways to intervene, to stop the infection before it starts rather than trying to kill all the germs."

Many harmful bacteria have already learned how to resist the drugs developed to treat them. Scientists are now looking at alternatives, such as ways to block or scramble the chemical messages that allow microbes to eavesdrop on their hosts or to conspire together to mount an attack.

"We chose to study this in Pseudomonas because it is one of the deadliest infections for patients who undergo major surgery," said Alverdy. "We suspect something very similar, however, occurs in all sorts of infections."

Inflammatory bowel disease patients, for example, have elevated cytokines ?the chemical messengers that trigger an immune response ?in the bowel. "These could signal the bug," said Alverdy, "then the bug strikes back and then the inflammation process snowballs." Because the bacteria in this case are "normal flora," people with no real infection develop a chronic disease.

The battles between pathogens and their hosts have been going on for millions of years, Alverdy said, with each side constantly devising novel measures, countermeasures, and counter-countermeasures, including sophisticated mutual espionage.

The discovery of antibiotics gave human hosts a temporary advantage, "but that seems to be waning a bit," he added. "We need to learn new ways to understand our germs and think about how to placate rather than annihilate them."


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Source:University of Chicago Medical Center


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