Weight loss seen during an intestinal worm infection is actually beneficial in fighting off the parasite discovers scientists from the University of Manchester. The findings are from a collaboration between Professor Richard Grencis of the Manchester Immunology Group and Professor John McLaughlin from the School of Translational Medicine. They can be found in the Open Access journal PLOS Pathogens.
The research shows the immune system hijacks our natural feeding pathways causing weight loss, which drives our defense mechanisms down the correct pathway to expel the worms. Nearly one quarter of the world's population are infected with gastrointestinal parasites. These prevalent infections often result in a period of reduced appetite resulting in weight loss; however the factors controlling these feeding alterations and the reason why they occur were unknown.
The research, performed by John Worthington, a post-doctoral research associate within the University of Manchester's Immunology Group, studied mice lacking immune cells and feeding hormones during a Trichinella spiralis worm infection. The T-helper cells of the mouse's immune system responded by increasing levels of the feeding hormone cholecystokinin to cause a reduction in weight and fat deposits. This reduced the levels of the fat produced hormone leptin, which can influence the immune response.
To see if this reduction in leptin was beneficial, the researchers restored leptin levels during worm infection and saw that these treated mice did not make the correct immune response to the parasite resulting in a delayed worm expulsion. This research was confined to mice so any relevance to humans is not clear. However intestinal parasitic worm infections are extremely common throughout the animal kingdom including mice and the authors conclude that the study "provides novel insights into how the immune system interacts with feeding pathways during intestinal inflammation and may help us design new strategies for helping people with parasitic infections of the gut".