Recent research suggests some people may actually be born with a heightened resistance to H. pylori’s harmful effects, so while they may have the bacteria, they probably will never get sick from it.
In those who are not as lucky, the bacterium can persist as a long-term infection that damages the stomach lining and increasing the person’s chance for cell mutations that can lead to several types of cancer.
A new study led by Steven Blanke, a microbiologist at University of Illinois, and published in Proceedings of the National Academy of Sciences, is the first to show how H. pylori toxin can disrupt a healthy cell's mitochondria, the cell’s internal energy-generation and distribution system. It turns out the toxin disables the otherwise healthy cell's internal mechanism and speeds up its programmed death.
This cell death, called apoptosis, can cause long-term damage to the stomach lining, a known risk factor for cancer. An increase in apoptotic cells can also cause a hyper-proliferation of stem cells dispatched to the damaged area in an attempt to repair the tissue. Too many stem cells can increase a person’s chance of cell mutations that can also lead to cancer, Blanke said in a written statement.
Previous studies had shown that VacA, a protein toxin produced by H. pylori, regulates host cell death by targeting the mitochondria, but exactly how it did it was not understood.
In healthy cells, mitochondria fuse to form elaborate energy-generating networks in response to the cell’s needs. However, if this process becomes dysfunctional illness can follow. According to Blanke, mitochondrial dysfunction is associated with hundreds of diseases and disorders, including cancer and degenerative diseases like Alzheimer's disease and Parkinson's disease.
"To us, finding that a pathogen can disrupt mitochondria in a manner that has striking similarities to what has been observed in known mitochondrial diseases is potentially very exciting and opens a new avenue of investigation of diseases linked to impaired mitochondrial function, ” he said.