1. It sounds like the mechanism for killing cells is very general. Why do histatins not attack somatic cells?
2. Do mouth wounds simply heal faster because the mouth is cleaner?
1. It sounds like the mechanism for killing cells is very general. Why do histatins not attack somatic cells?
2. Do mouth wounds simply heal faster because the mouth is cleaner?
In regard to the second, I can say this: in the ER, a human bite is considered FAR more dangerous than a dog bite, because the human mouth has more — and more dangerous — pathogens. The mouth is much dirtier (not cleaner) than skin.
They semi-specifically target a receptor on C. albicans and other pathogens. They're also cationic [1], so they bind anionic lipids in bacteria and mitochondria that aren't found (in large quantities) on the mammalian cell surface.
> 2. Do mouth wounds simply heal faster because the mouth is cleaner?
From that second abstract:
"..histatins were actively internalized by epithelial cells and specifically used the extracellular signal-regulated kinases 1/2 (ERK1/2) pathway, thereby enhancing epithelial migration."
It's a relatively simple assay: Just grow a lawn of the skin cells, scrape a line down the middle, and see how quickly the line is filled in (with or without exogenous histatin).
So those peptides tend to do both: kill bacteria and lead to wounds healing faster.
[1] http://aps.unmc.edu/AP/database/query_output.php?ID=00505
As for histamines, mast cells are designed to respond to them and rupture as part of your inflammatory cycle. They release more cytokines, recruiting neutrophils and in general telling your immune system to attack.