How "good cholesterol" stops inflammation - Medical Xpress (3 pages)

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body like police on the beat and, as part of the

innate immune defense system, arrest intruders.
These patrolmen are supported by a kind of
"criminal file," the so-called Toll-like receptors
(TLR). With their help, the phagocytes can
distinguish between "good" and "bad." If it is a
dangerous intruder, the TLR can also trigger the
release of inflammatory substances via biochemical
signaling pathways. The transcriptional regulator,
ATF3, plays a key role in this process. "It reduces
the transcription of the inflammatory genes and
prevents further stimulation of inflammatory
processes via the Toll-like receptors," explains Dr.
Dominic De Nardo.

Sustained inflammatory reactions can lead to
organ failure

The immune system uses inflammatory processes
to keep pathogens in check, to detect damaged
tissue, and then repair it. In sustained inflammatory
reactions, however, there are dangerous
consequences –including blood poisoning or organ
failure. "The transcriptional regulator ATF3 acts to
reduce these inflammatory reactions by
suppressing the activation of inflammatory genes
following excessive stimulation of
immunoreceptors", reports Dr. De Nardo. In the
end, high-density lipoprotein (HDL) is responsible
for down regulating the inflammatory reactions, via
the activation of ATF3. "To put it simply, high HDL
levels in blood are an important protective factor
against sustained inflammation," says Prof. Latz.

"Our studies also indicate that the amount of HDL
in blood alone is not decisive for the protective
function of HDL, but that the anti-inflammatory
function is probably more important. These results
also suggest a molecular approach for treating
inflammation in other widespread diseases, such as
diabetes," says Prof. Latz.

More information: High-density lipoprotein
mediates anti-inflammatory reprogramming of
macrophages via the transcriptional regulator
ATF3, Nature Immunology,

DOI: 10.1038/ni.2784

Provided by University of Bonn

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