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how "good cholesterol" stops inflammation

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How "good cholesterol" stops inflammation

9 December 2013

Larisa Labzin, Prof. Dr. Eicke Latz and Dr. Dominic De
Nardo of the Institute of Innate Immunity. Credit: Barbara
Frommann/Uni Bonn

High-density lipoprotein (HDL), known colloquially
as "good cholesterol", protects against dangerous
deposits in the arteries. An important function of
HDL is its anti-inflammatory properties. An
international research team at the Institute of
Innate Immunity at the University Hospital of Bonn
and the LIMES Institute at the University of Bonn
has identified a central switch by which HDL
controls the inflammatory response. The results
are presented in the current issue of Nature

High cholesterol levels are seen as a cause of
dangerous deposits in the bloodstream, which lead
to hardening of the arteries (atherosclerosis). As a
consequence, thrombosis, strokes, and heart
attacks can develop, which are among the leading
causes of death in Western society. Low-density
lipoprotein (LDL) is commonly referred to as the
"bad cholesterol", because it promotes
atherosclerosis. In contrast, the "good cholesterol,"
high-density lipoprotein (HDL), helps transport
excess cholesterol out of the bloodstream and can
counteract an inflammatory reaction in damaged
vessel walls.

"It has long been known that HDL has a protective

function in cardiovascular diseases that are based

on atherosclerosis," reports Prof. Eicke Latz,
Director of the Institute of Innate Immunity at the
University of Bonn and who is further affiliated with
the German Center for Neurodegenerative
Diseases (DZNE) and the University of
Massachusetts Medical School in the USA. "The
molecular causes to which this protective effect of
HDL can be attributed were unclear until now." For
instance, studies had shown that therapies that
simply increase HDL levels in the blood of patients
are not sufficient to reduce the incidence of
atherosclerosis. HDL has anti-inflammatory effects
on immune cells – however the mechanisms have
remained unclear until now. The research group
has now investigated how HDL acts upon
inflammatory processes.

Bioinformatics approach revealed a candidate

Principle investigators Dr. Dominic De Nardo and
Larisa I. Labzin are both Australians currently
training in the lab of Prof. Eicke Latz. In
collaboration with other working groups of the
University of Bonn, an international research team
from Japan, Australia, China, the USA, and
Germany has identified how HDL acts to prevent
chronic inflammation. In a very extensive study
over a period of about three years, the group
performed experiments in human and mouse cells,
to determine which genes are regulated by high
HDL levels. "At first, we were really just feeling
around in the dark," reports Prof. Latz. Close
cooperation with the working group of Prof.
Joachim L. Schultze of the Life and Medical
Sciences (LIMES) Institute of the University of
Bonn finally got the scientists on the right track.
"With the aid of genomic and bioinformatics
approaches, we were able to filter out a candidate
gene from the wealth of regulated genes", adds
Prof. Schultze.

This gene is found in phagocytes, which act in the

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