Disease-causing stomach bug attacks energy generation in host cells

May 30, 2018 by Steph Adams, University of Illinois at Urbana-Champaign
Microbiology professor Steven Blanke, graduate student Ik-Jung Kim and their colleagues discovered how a disease-causing bacterium, Helicobacter pylori, undermines the body's immune defenses. Credit: L. Brian Stauffer

Researchers report in a new study that the bacterium Helicobacter pylori - a major contributor to gastritis, ulcers and stomach cancer—resists the body's immune defenses by shutting down energy production within the cells of the stomach lining that serve as a barrier to infection.

The new findings, reported in the journal Cell Microbe & Host, will aid efforts to better understand and combat H. pylori infections, the researchers said.

"H. pylori infects and causes gastritis in half the world's population. It is transmitted from person to person, usually during the first two years of life," said University of Illinois microbiology professor Steven Blanke, who led the new research. "Long-term infection can extend over decades, and most people never experience any symptoms of infection until the disease has progressed to an advanced state."

The human stomach is the only known environment where H. pylori exists, Blanke said.

"When any barrier in the human body is colonized by a pathogen, the immune system sets off a series of predictable counterattacks to reclaim the infected space," he said. "H. pylori cripples these immune counterattacks by going straight to the source of a host cell's power to shut down energy production."

Using and tissues, the team found that H. pylori manipulates the cell from the outside by sending in a toxin to directly target the mitochondria, which serves as the powerhouse where the cell's energy is produced.

"The toxin disables the mitochondria, resulting in a loss of ," Blanke said. "When the cell tries to compensate by reallocating resources from other parts of the cell, a signal is triggered directing the cell to stop production and start breaking things down."

Disabled but still alive, the cell eventually loses its ability to fend off .

"The results of these studies provide an important example of how pathogens effectively target host metabolism in an effort to establish an enduring foothold within the ," Blanke said.

Explore further: A new strategy used by Helicobacter pylori to target mitochondria

More information: Ik-Jung Kim et al, Helicobacter pylori Infection Modulates Host Cell Metabolism through VacA-Dependent Inhibition of mTORC1, Cell Host & Microbe (2018). DOI: 10.1016/j.chom.2018.04.006

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not rated yet May 31, 2018
Maybe that is the reason why it causes disease: it establishes an enduring foothold. Until then it can live inside the stomach without bad consequences.

Now the question is: what would help/direct the microbe to establish a foothold? Probably large numbers of it would work. But I'm thinking of something having to do with its environment and the food we eat. Maybe the large quantities of sugars we eat or the fact we eat each time when we are hungry which cuts out acidity.

I had ulcer once but I got rid of it quite quickly. After that I didn't get it again; I did get some starting gastritis, but got rid of it too in the same way. That would match my idea that there is a transition point between non-pathogenic and disease-causing state in H. pylori. I don't know for sure I had the microbe though.

not rated yet May 31, 2018

How I got rid of the ulcer/gastritis... it was a risky procedure. I acidified the stomach.

If I'd do it again I could eat some yogurt or other fermented milk. I've read once fermented milk foods control the population of H. pylori.

But first I'd do a tolerance test: during the day (but a long time before going to bed in order for the stomach to get rid of it) I'd eat some yogurt and see whether the stomach can tolerate it. If not, then I'd eat some food or an antiacid and I'd quit it.

Again, it may be a dangerous procedure, you should not try it unless you know it doesn't harm you. And it's unsure and experimental; except for my case (where I don't even know that I had the H. pylori microbe) I don't know of it working in any other case. So it may not work at all; or it could even do harm.

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