LeGrand and Alcock offer some answers. For an infection to spread, pathogens need to multiply, whereas host cells can defer replication. Replication makes DNA and newly forming proteins much more susceptible to damage. It also requires energy and nutrientswhich helps explain the benefits of restricting food and sequestering nutrients.
The act of invading a body also requires bacteria to alter their metabolism, which can make them more vulnerable to all kinds of stress, including heat.
Another reason pathogens are more vulnerable to stress is that the immune system is already pummeling them with white blood cells and related stressors at the site of the infection. That means that pathogens are already under local stress when systemic stressors are piled on. "In many ways, the acute-phase response reinforces the stress inflicted on pathogens locally at the infection site," LeGrand said.
As the term "brinksmanship" implies, there's an inherent risk in a strategy that involves harming oneself to hurt the enemy within. This self-harm leaves the body more vulnerable to other dangers, including other infections. Additionally, it is possible for the immune stressors to do more damage than required to control the pathogens.
"But in general, systemic stressors when properly regulated do preferential harm to invaders," LeGrand said. Viewed this way, it's not surprising that natural selection has utilized the stressful parts of the acute-phase response in mammals, reptiles, fish, and even invertebrates.
|Contact: Kevin Stacey|
University of Chicago Press Journals