Washington, Nov 2 (IANS) Researchers have figured out how cancer-causing bug H. pylori, which infects half the world’s population, attacks a cell’s innards, causing it to die by self-destructing.
The finding potentially opens the way to more effective treatment of degenerative diseases such as Alzheimer’s disease and Parkinson’s, beside cancers.
H. pylori are the only bacteria known to survive in the human stomach, tied with hyperacidity and higher risk of gastric cancer, the second-leading cause of cancer-related deaths worldwide.
‘More than half the world’s population is currently infected with H. pylori,’ said University of Illinois (Urbana-Champaign) microbiology professor Steven Blanke, who led the study.
‘And we’ve known for a long time that the host doesn’t respond appropriately to clear the infection from the stomach, allowing the bacterium to persist as a risk factor for cancer,’ Blanke added, reports the journal Proceedings of the National Academy of Sciences.
Blanke’s study is the first to show how a bacterial toxin can disrupt a cell’s mitochondria – its powerhouse and energy distribution system – to disable the cell and spur apoptosis (programmed cell death), according to an Illinois statement.
‘Hundreds of human diseases and disorders are associated with mitochondrial dysfunction, ranging from cancers to degenerative diseases such as Alzheimer’s disease and Parkinson’s,’ Blanke said.
‘As yet, no one has methodically investigated a potential link between bacterial infections and mitochondrial diseases, despite the fact that several dozen pathogenic bacteria and viruses are known to directly target mitochondria.’
‘One of the hallmarks of long-term infection with H. pylori is an increase in apoptotic cells,’ Blanke said. ‘This may contribute to the development of cancer in several ways.’
Apoptosis can damage the epithelial cells that line the stomach, he said, ‘and chronic damage to any tissue is a risk factor for cancer’.
An increase in apoptotic cells may also spur the hyper-proliferation of stem cells in an attempt to repair the damaged tissue, increasing the chance of mutations that can lead to cancer.
