A fresh study carried out by researchers from King's College London (KCL) has established a link between a certain form of bacteria present on the skin following a surface wound and a type of white blood cell receptor, that together tip the scale away from the normal healing process and instead encourage the formation of cancerous tumors. The results of the study have the potential to create innovative treatment options for patients suffering from skin diseases, such as those that result in chronic ulcers and severe blistering.
There is a long standing association between tissue damage in patients suffering from chronic skin inflammation and the occurrence of cancerous tumors, however the reasoning behind the phenomenon has never been truly understood. The research carried out by KCL has brought us one step closer by establishing a link between the receptor found on the surface of white blood cells, Toll-like receptor 5 (TLR5), and the bacteria flagellin.
Over the course of the study, mice exhibiting chronic skin inflammation were wounded on their side, resulting in tumors forming around the break in the skin, with heightened levels of the protein HMGB1 being observed.
Ordinarily, the protective characteristics of unbroken skin prevent the flagellin and the white blood cells from interacting. However, when there is a break in the skin, the bacteria come into direct contact with the body's protective white blood cells, and more specifically, the TLR5 receptors that coat the outer layer of the tiny protectors.
When the receptors detect the bacteria, they increase the amount of HMGB1 present around the wound, and it is the heightened concentration of this protein that the team believes is responsible for disrupting the body's ordinary healing process, instead prompting the growth of cancerous tumors.
While the team is as of yet unsure how their findings will translate to human tumor growth, members have drawn a comparison with patients suffering from the disease epidermolysis bullosa, an extremely painful and debilitating condition that manifests itself through fragile skin and painful blisters.
Patients suffering from the disease run an increased risk of tumors forming around the open wounds that are so prevalent with this condition, and researchers have noted that, like the mice afflicted with chronic skin inflammation, sufferers of epidermolysis bullosa exhibit the same increased levels of HMGB1.
"These findings have broad implications for various types of cancers and in particular for the treatment of tumors that arise in patients suffering from chronic ulcers or skin blistering diseases," states lead author and Director of the Center for Stem Cells and Regenerative Medicine at KCL, Professor Fiona Watt. "Our findings raise the possibility that the use of specific antibiotics targeting bacteria in wound-induced malignancies might present an interesting clinical avenue."
The study is available in the online journal Nature Communications.
Source: King's College London
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