How E.coli could aid in fight against anaemia

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New York, Aug 24 (IANS) Researchers have found that Escherichia coli (E. coli) — the most prevalent bacterium in the human and animal gut — plays a critical role in promoting health by boosting iron absorption, challenging the previous held notion that it causes food poisoning or steals nutrients from its host.

The study, published in the journal Cell, shed new light on the mechanism by which E. coli benefits its host and could ultimately lead to more effective therapies for iron deficiency anaemia, which impacts more than 1 billion people worldwide.

Scientists have long known that E.coli produces a compound called enterobactin to scavenge iron for its own survival and propagation.

But they presumed that in doing so, it stole iron from its host in what is often referred to as an “iron tug of war.”

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This new study challenged that paradigm, suggesting that enterobactin also binds to a protein called ATP synthase inside the host’s mitochondria, drawing iron into the host’s cells too, the researchers explained.

“In recent years, we have begun to realise that many microorganisms populating the human gastrointestinal tract are good for us, but we are only beginning to discover exactly what benefits they offer and how,” said Min Han, Professor at the University of Colorado (CU) – Boulder in the US.

“This new finding identifies one key role of E.coli and that is to help cells absorb iron,” he added.

In the study, the team started with a series of experiments using Caenorhabditis elegans (C. elegans) — a roundworm naturally rich in E. coli.

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When the young worms genetically altered to lack the ability to produce a compound called enterobactin were fed E. coli, they grew slowly and their iron levels were low.

When enterobactin was re-introduced into the worms, natural growth resumed and iron levels rose.

Subsequent experiments in human cells showed that supplementing the diet with enterobactin, even without the addition of iron, prominently boosted iron levels in cells.–IANS

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