Differential effects of interleukin-1 receptor antagonist and tumor necrosis factor binding protein on fatty-streak formation in apolipoprotein E–deficient mice
R Elhage, A Maret, MT Pieraggi, JC Thiers, JF Arnal… - Circulation, 1998 - Am Heart Assoc
R Elhage, A Maret, MT Pieraggi, JC Thiers, JF Arnal, F Bayard
Circulation, 1998•Am Heart AssocBackground—The cytokines interleukin 1 (IL-1) and tumor necrosis factor (TNF) are secreted
by the different cell populations of the vascular wall and have been suggested to promote
atherosclerosis. Methods and Results—Their respective roles in fatty-streak formation in
apolipoprotein E–deficient mice were investigated by use of IL-1 receptor antagonist and
TNF binding protein. Estradiol-17β was used as a positive control. Blocking TNF seemed to
be active in female animals but not in males. IL-1 receptor antagonist was as effective as or …
by the different cell populations of the vascular wall and have been suggested to promote
atherosclerosis. Methods and Results—Their respective roles in fatty-streak formation in
apolipoprotein E–deficient mice were investigated by use of IL-1 receptor antagonist and
TNF binding protein. Estradiol-17β was used as a positive control. Blocking TNF seemed to
be active in female animals but not in males. IL-1 receptor antagonist was as effective as or …
Background—The cytokines interleukin 1 (IL-1) and tumor necrosis factor (TNF) are secreted by the different cell populations of the vascular wall and have been suggested to promote atherosclerosis.
Methods and Results—Their respective roles in fatty-streak formation in apolipoprotein E–deficient mice were investigated by use of IL-1 receptor antagonist and TNF binding protein. Estradiol-17β was used as a positive control. Blocking TNF seemed to be active in female animals but not in males. IL-1 receptor antagonist was as effective as or more effective than estradiol in both sexes.
Conclusions—IL-1 plays a crucial role in the initial step of the atherosclerotic process in this animal model, and blocking the activity of this cytokine should be considered as a therapeutic possibility.
Am Heart Assoc
