Researchers search for a link between heart disease, psoriasis

Psoriasis elevates the number of skin cells on the elbows, knees and across the body. And according to a new study, it can also elevates the risk of heart disease.

Case Western Reserve University of Medicine in Cleveland published two studies describing how the inflammatory response to psoriasis can alter levels of several immune system modules, which increases the risk of thrombosis and consequently induce fatal blood clots.

The studies focused on a molecule called interleukin 6, or IL-6, which is found in high concentrations in psoriasis patients.

"We wanted to pursue the mechanisms by which skin inflammation contributes to cardiovascular disease," said Nicole Ward, associate professor of dermatology at Case Western Reserve University School of Medicine. "In multiple mouse models, we showed removing IL-6 reduced cardiovascular risk, but did not get rid of psoriasis unless combined with other interventions."

But trials looking at blocking IL-6 alone hasn’t been successful.

"Eliminating this one molecule just isn't good enough,” Ward said.

With that in mind, Ward turned her attention to a protein called MRP14, which predicts heart attack risks in certain populations. People with autoimmune diseases like psoriasis have high levels of MRP14 in their blood, and the gene encoding MRP14 is located near psoriasis genes. Ward and colleagues suspected MRP14 could be contributing to both skin inflammation and cardiovascular disease comorbidities in psoriasis patients. The researchers deleted the gene encoding MRP14 in mice with psoriasis, hoping it would reduce thrombosis.

"The disappointing result was that after two years of work, it had no effect on skin inflammation or cardiovascular comorbidities," said Ward. "The MRP14-deficient psoriasis mice were completely the same as the regular psoriasis mice - they all had similar levels of skin inflammation and thrombosis."

These results forced researchers to consider different mechanisms that could explain these findings. Ward hypothesized that IL-23 and IL-17 could be part of a “workaround” mechanism in mice that compensated for a lack of MRP14 and sustained skin inflammation.

The team had successfully separated psoriasis and cardiovascular disease outcomes. Ward concluded that while blocking IL-6 may not prevent psoriasis on its own, its levels are central to thrombosis events triggered by skin inflammation. The findings may also help explain how alternative immune system molecules could circumvent certain psoriasis treatments.