Cannibalistic process in cells plays a key role in preventing Salmonella infection, according to infectious-disease specialists at UT Southwestern Medical Center.
Salmonella, the causative agent of salmonellosis, causes many of the intestinal infections and food-related illnesses.
The new findings are among the first to demonstrate that a process called autophagy (pronounced "aw-TAH-fah-gee") prevents harmful bacteria, such as Salmonella, from becoming successful pathogens.
"It's known that as you get older you become more susceptible to infectious diseases and also that autophagy decreases. In this paper, we've shown that signaling pathways that extend life and protect against bacterial invaders do so by triggering autophagy. This suggests that therapeutic strategies to increase autophagy may be effective in defeating harmful bacteria that can enter inside cells," said Dr. Beth Levine, senior author of the new study.
Autophagy is the way cells devour their own unwanted or damaged parts. It is a highly regulated and completely normal process by which cells remain healthy by performing "routine housekeeping" and "garbage disposal."
Previous studies have shown that the process appears to be an adaptive response that our bodies employ during times of stress or starvation, and which also helps protect our bodies against cancer and neurodegenerative diseases.
Although it is unclear why older people become more susceptible to infections, research has shown that autophagy does decrease with age.
Levine has said that it is possible that by reversing or regulating this process, researchers could prevent the elderly and others with weakened immune systems from becoming more susceptible to infections.
For this study, the researchers studied the effects of Salmonella infections in two organisms they had genetically engineered to lack active autophagy genes-Caenorhabditis elegans, a common research worm also known as a nematode, and Dictyostelium discoideum, a soil amoeba that functions much like certain cells in the human immune system.
In both cases, the animals with inactive autophagy genes fared far worse than those with active ones.
Instead of being targeted for elimination, the Salmonella bacterium was able to invade the host cells, where it started replicating.
Levine said that the findings indicate that the autophagy process plays an important role in resistance to certain types of pathogens, specifically those that can enter inside our cells.
The next step, Dr. Levine said, is to begin studying the efficacy of a new autophagy-inducing molecule in treating a number of intracellular bacterial infections including salmonellosis, tuberculosis, tularemia and listeriosis.
The study has been published in an upcoming issue of the Proceedings of the National Academy of Sciences.