LUND UNIVERSITY
MARCH 6, 2015
Inflammatory processes occur in the brain in
conjunction with stroke and neurological diseases such as Alzheimer's and Parkinson's
disease. Researchers from Lund University and Karolinska Institutet in Sweden,
in close cooperation with a group led by Professor José L. Venero at the
University of Seville, have presented new findings about some of the 'key
players' in inflammation. In the long term, these findings could lead to new
treatments.
One of these key players is a receptor called TLR4.
The receptor plays such an important role in the body's innate immune system
that the researchers who discovered it were awarded the 2011 Nobel Prize in
Physiology or Medicine. The other key player is a protein called galectin-3,
which is absent in healthy brains but present in a brain suffering ongoing
inflammation.
"We have demonstrated that galectin-3 is
secreted by microglial cells, a type of immune cell in the brain. The protein
binds to the TLR4 receptor and amplifies the reactions that lead to
inflammation. More galectin-3 is produced and binds to the immune cells, and
the immune response is further intensified in a self-sustaining process",
explained Tomas Deierborg, associate professor at Lund University.
The researchers have demonstrated the importance of
the link between the two 'key players' using various different methods and in
laboratory tests, animal experiments and human trials. They have shown that
mice genetically modified to be incapable of synthesising galectin-3 show a
lower inflammatory response and less brain damage after a heart attack. Mice
with a model of Parkinson's disease also suffer less brain damage if they do not
have the gene for galectin-3.
The researchers have also observed the interaction
between galectin-3 and TLR4 in the brains of people who died of a stroke.
"We believe that this link could be part of
the explanation for the residual disability that stroke patients often
experience. High levels of galectin-3 remain in the brains of these patients
long after the stroke, which may explain why the inflammatory response
continues to cause damage and does not subside", said Miguel Angel
Burguillos, currently working at Queen Mary University of London.
Galectin-3 is already a target for pharmaceutical
companies trying to develop agents that hinder the harmful effects of the
protein in neuroinflammatory diseases. The new findings on the effects and role
of the protein in a diseased or damaged brain should provide important input to
this work.
"Previously, it was acknowledged that
galectin-3 contributed to the inflammatory response but the mechanism wasn't
clear. The protein is not present in a healthy brain, only in one that is
suffering an inflammatory response. Now that we understand the mechanism, this
will make it easier to develop more effective treatments", said Dr
Deierborg.
###
About the study:
Dr Burguillos is currently working at Queen Mary
University of London, but carried out the work on galectin-3 and TLR4 during
his time as a postdoctoral fellow at Lund University and Karolinska Institutet.
The research in Lund has been led by Tomas Deierborg and at KI by Bertrand
Joseph. The University of Seville also participated in the research, led by
José L. Venero. The results have recently been published in the journal Cell Reports.
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of any information through the EurekAlert system.
http://health.einnews.com/article/253430264/f-WgiFh0vGCoP81B
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