Bioscientists have found a direct link between vitamin B12 deficiency and an increased risk of infection by potentially deadly pathogens…

Using roundworms, Rice University bioscientists have found the first direct link between a diet with too little vitamin B12 and an increased risk of infection by two potentially deadly pathogens.

What we have in common with roundworms

Despite their simplicity, 1-millimetre-long nematodes called Caenorhabditis elegans (C. elegans) share an important limitation with humans: They cannot make B12 and must get all they need from their diet.

Vitamin B12 deficiency leads to a toxic build-up

According to Rice biochemists and cancer researcher Natasha Kirienko, a B12-deficient diet harms C. elegans‘ health at a cellular level, reducing the worms’ ability to metabolise branched-chain amino acids (BCAA).

The research showed that the reduced ability to break down BCAAs led to a toxic build-up of partially metabolised BCAA by-products that damaged mitochondrial health.

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Bioscientists have found the first direct link between a diet with too little vitamin B12 and an increased risk of infection by two potentially deadly pathogens

The study

Researchers studied the health of two populations of worms, one with a diet sufficient in B12 and another that got too little B12 from its diet.

Like the second population of worms, at least 10 percent of U.S. adults get too little B12 in their diet, a risk that increases with age.

The lead scientist and co-author of the study, Kirienko said the B12 finding came as a surprise to her team, which first noticed the effect in experiments designed to investigate the mechanisms of pathogenesis of Pseudomonas aeruginosa (P. aeruginosa), a potentially deadly disease in both worms and humans that infects some 51 000 U.S. hospital patients each year, according to the Centres for Disease Control.

Feeding the gut

In many C. elegans research labs worms are fed Escherichia coli (E. coli), a common human gut bacteria that is itself a model organism.

“We found that switching between E. coli strain OP50 and strain HT115 dramatically altered the worm’s stress tolerance,” Kirienko said. She said it took about two years of follow-up studies to isolate the biochemical mechanism of stress and pathogen resistance.

“The key difference between the two diets is the ability of HT115 and OP50 to acquire B12 from the environment,” said lead co-author Alexey Revtovich, a research scientist. “We showed that HT115 is far more efficient at this, making about eight times as much of the protein that it needs to harvest B12 as compared to OP50.”

The researchers used numerous tests to confirm their results and rule out other possible mechanisms for the effect. They also found that C. elegans on an HT115 diet had the ability to resist infection by another deadly human pathogen, Enterococcus faecalis.

“This work is related in the sense that it focuses on mitochondrial health,” Kirienko said. “In this case, we are working to improve mitochondrial health to help fight infections. For CPRIT, we’re trying to do the opposite. We want to damage mitochondria in cancer cells to kill them. So, actually, now that we know this is important, it gives us another potential target in cancer cells.”

Source: Rice University via www.sciencedaily.com

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