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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 J+Leukoc+Biol
2015 ; 98
(5
): 837-50
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Adipose triglyceride lipase acts on neutrophil lipid droplets to regulate
substrate availability for lipid mediator synthesis
#MMPMID26109679
Schlager S
; Goeritzer M
; Jandl K
; Frei R
; Vujic N
; Kolb D
; Strohmaier H
; Dorow J
; Eichmann TO
; Rosenberger A
; Wölfler A
; Lass A
; Kershaw EE
; Ceglarek U
; Dichlberger A
; Heinemann A
; Kratky D
J Leukoc Biol
2015[Nov]; 98
(5
): 837-50
PMID26109679
show ga
In humans, mutations in ATGL lead to TG accumulation in LDs of most tissues and
cells, including peripheral blood leukocytes. This pathologic condition is called
Jordans' anomaly, in which functional consequences have not been investigated. In
the present study, we tested the hypothesis that ATGL plays a role in leukocyte
LD metabolism and immune cell function. Similar to humans with loss-of-function
mutations in ATGL, we found that global and myeloid-specific Atgl(-/-) mice
exhibit Jordans' anomaly with increased abundance of intracellular TG-rich LDs in
neutrophil granulocytes. In a model of inflammatory peritonitis, lipid
accumulation was also observed in monocytes and macrophages but not in
eosinophils or lymphocytes. Neutrophils from Atgl(-/-) mice showed enhanced
immune responses in vitro, which were more prominent in cells from global
compared with myeloid-specific Atgl(-/-) mice. Mechanistically, ATGL(-/-) as well
as pharmacological inhibition of ATGL led to an impaired release of lipid
mediators from neutrophils. These findings demonstrate that the release of lipid
mediators is dependent on the liberation of precursor molecules from the TG-rich
pool of LDs by ATGL. Our data provide mechanistic insights into Jordans' anomaly
in neutrophils and suggest that ATGL is a potent regulator of immune cell
function and inflammatory diseases.
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