Wound inflammation which results in impaired wound
healing can have serious consequences for patients. Researchers from Charité --
Universitätsmedizin Berlin have discovered a new defensive mechanism which
enables our skin to actively kill bacteria. Central to this mechanism is a
cellular messenger molecule known as 'interleukin 6', whose mode of action may
be used in the future to prevent wound infections.
Skin wound colonization by bacteria or other pathogens
can lead to severe inflammation. In the worst cases, this can result in
septicemia or amputation. Prompt treatment is therefore essential. However,
growing numbers of bacteria developing antibiotic resistance have resulted in
treatment options becoming increasingly limited.
Using an animal model, the researchers studied the
effects of an absence of mast cells on wound healing after infection. The
researchers observed that, on day five after infection, the total number of
bacteria present in the wound was 20 times higher if mast cells were absent.
This resulted in the infected wound taking several days longer to close.
According to the researchers' findings, the mast cells' bacteria-killing effect
is a product of the release of the messenger molecule interleukin 6. This
molecule stimulates cells within the superficial layer of the skin, prompting them
to release 'antimicrobial peptides', short protein chains which kill bacteria,
viruses and fungi.
The study demonstrated the nature and extent of mast
cell involvement in the skin's host defense mechanism against bacteria. Exploiting
their knowledge of interleukin 6 and its key function, the researchers found
that the application of interleukin 6 to the wound prior to infection resulted
in an improved defense against bacteria, even in animals with intact immune
systems.
The researchers were also able to replicate this
effect in human tissue.
See:
Posted by Dr. Tim Sandle, Pharmaceutical Microbiology
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