This is an update of a talk about bacterial activation of epithelial signalling.
In the earlier material I reviewed how bacterial components stimulate
the airway epithelium, to activate inflammation, and to
start the clearance of infection in the human lung and the airway.
In the next few slides, I'd like to go over some newer information
as to how bacteria interact with the epithelium,
particularly how they activate immunometabolites, and how this is important in infection.
We're going to use cystic fibrosis as a model, because this is
a very well-known disease that affects airway epithelial cells as well as immune cells.
There's an abnormal chloride channel that affects the milieu of the human airway.
We want to know how this epithelial signaling and how these changes in
epithelial metabolism impact upon the pathogenesis of infection.
How do bacteria adapt to the airway epithelium?
They're inhaled and they can adapt due to immune pressure,
the macrophages that try to remove them,
we know from looking at colonies of bacteria from the lungs, we often see small colony variants,
where we see grossly mucoid strains that we only see in this one situation.
The other question is: is it metabolic pressure that is causing
these organisms to change their surface characteristics?
It's felt that these surface components make the organisms more resistant to phagocytosis,
but they could also be protecting the organisms from other things, like oxidative stress.
Again, cystic fibrosis is a great model because it's very well known that cystic fibrosis
isolates of organisms such as Pseudomonas aeruginosa are often mucoid,
or we see these small colony variants, so they have adapted to their long-term residence in the lung.