According to Rice University, USA, bio-scientists have discovered the first direct link between a diet with vitamin B12 deficiency and an increased risk of infection deadly pathogens.
To test vitamin B12 deficiency, scientists used roundworms, one of Earth’s simplest animals, and uncovered the first direct link between a diet with too little vitamin B12 and an increased risk of infection by two potentially deadly pathogens.
Vitamin B12 deficiency
Despite their simplicity, 1-millimeter-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.
In a study published in PLOS Genetics, researchers from the lab of Rice biochemist and cancer researcher Natasha Kirienko describe how a diet with vitamin B12 deficiency 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.
Researchers studied the health of two populations of worms, one with a diet enough in B12 and another that had vitamin B12 deficiency in its diet.
Using C. elegans
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 Centers for Disease Control.
Her lab, like thousands of others worldwide, uses C. elegans as a model organism to study the effects of disease, drugs, toxins and other processes that affect humans and animals. In many C. elegans research labs worms are fed Escherichia coli (E. coli), a common human gut bacterium 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.
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.
Is there a potential to target cancer cells?
Lee, an undergraduate explained how the study highlights the need for C. elegans labs worldwide to pay attention to the possible differential impacts of diet on experimental outcomes.
“Some labs use OP50 as their standard food, and others use HT115 or even another strain of E. coli,” Lee added.
“Our results show there are significant metabolic differences between these diets, and it’s likely those differences could contribute to substantial uncertainty in research outcomes.”
“This work is related in the sense that it focuses on mitochondrial health,” Kirienko concludes.
“In this case, we are working to improve mitochondrial health to help fight infections. For CPRIT (Cancer Prevention and Research Institute of Texas), 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.”