Scientists from the University of Bonn and Freie Universität Berlin believe they have discovered why beta-blockers trigger and exacerbate psoriasis.
According to their findings, beta-blockers have the ability to interfere with the breakdown of defective cell components, which cause cells to release messengers that trigger immune-mediated inflammatory reactions.
The reason for this could be due to the propranolol medication that is used in beta-blockers, which is slightly alkaline and fat-soluble.
Propranolol's fat solubility enables the active substance to cross biomembranes that enclose cells and some of their components.
The second aspect, however, ensures that propranolol becomes positively charged in an acidic environment, meaning the substance can no longer return through the membrane.
This becomes problematic in the autophagy process if a propranolol molecule randomly finds its way through the membrane into cells' ‘trash bags’, a kind of bubble, when it is positively charged.
The molecule will then become trapped and, over time, causes more and more propranolol to accumulate in the lysosome.
“This process apparently disrupts the autophagy,” says Günther Weindl from the Pharmaceutical Institute at the University of Bonn.
“This in turn alters a number of processes in the cell. As a result, it releases inflammatory messengers, in particular the so-called interleukin-23, which is mainly secreted by immune cells. The consequences are the observed skin problems.”
The scientists hope to use their findings to investigate how these processes are related at molecular level further.