The new research uses the common bladder infection-producing uropathogenic E. coli as a model to show how nitric oxide unwittingly assists bacterial uptake and survival.
"In bladder cells, E. coli uses this mechanism to get inside the cells and hide from the antibiotic effect and the immune system," says Dr. Daaka. "We think their hiding is mediated through dynamin. This is not only applicable to this particular pathogen but for many more."
Dr. Daaka, who studies receptor signaling, likens receptors to television antennae that control relay of signals from outside the cell to inside by turning on or off. Although there are no known receptors that have the job of triggering a bad result in the body, receptors that are 'on' too much may end up instructing the cell to do bad things, he says. "The hypothesis is that in cancer, for example, the receptors get stuck on 'on'."
Receptor over-stimulation also helps explain why some drugs stop being effective over time. "What that means is there are no more receptors outside the cells to be affected by the drugs," Dr. Daaka says. "This is a self-regulatory mechanism for cells. You don't want your receptors to always be on."
Interestingly, this self-regulatory mechanism seems to work best when a receptor, not a bacteria, is the instigator. Unlike receptors, bacteria and viruses don't degrade if they stay inside the vesicles because fusion with a second vesicle that enables the degredation doesn't happen, says Dr. Daaka, a Georgia Cancer Coalition Distinguished Cancer Scholar.