|  Help  |  About  |  Contact Us

Publication : Hypercholesterolemia Induced Immune Response and Inflammation on Progression of Atherosclerosis in Apob(tm2Sgy) Ldlr(tm1Her)/J Mice.

First Author  Rao LN Year  2015
Journal  Lipids Volume  50
Issue  8 Pages  785-97
PubMed ID  26178198 Mgi Jnum  J:314827
Mgi Id  MGI:6765074 Doi  10.1007/s11745-015-4046-4
Citation  Rao LN, et al. (2015) Hypercholesterolemia Induced Immune Response and Inflammation on Progression of Atherosclerosis in Apob(tm2Sgy) Ldlr(tm1Her)/J Mice. Lipids 50(8):785-97
abstractText  The effect of hypercholesterolemia induced immune response and inflammation on progression of atherosclerosis in ApoB(tm25gy) LDLr(tm1Her) mice, expressing only ApoB100 and deficient in the low density lipoprotein (LDL) receptor, thus closely resembling human cholesterol transport is not well defined. Atherosclerosis was induced by a high cholesterol diet and its progression was studied at 8, 14 and 20 weeks. Antibody response was determined by ELISA. Lymphocytes in spleen and aortic expression of inflammatory markers were studied by flow cytometry, and immunohistochemistry respectively. A rapid increase in plasma LDL levels in the first 8 weeks was followed by the exponential development of atherosclerosis between 8 and 14 weeks. Progression of the disease was accompanied by an accumulation of macrophages and increased expression of IL17 and IFN-gamma in the aorta. Hypercholesterolemia resulted in increased immune response to modified lipids and aortic inflammation, with an expansion of Th17 cells in the spleen. Progression of atherosclerosis showed a positive correlation (r = 0.84, P < 0.001) with Th17 cells and a negative correlation with Treg cells (r = 0.83, P < 0.001). IgM antibodies to Ox-LDL and Th17 cells in spleen showed greatest association with disease development. Our results suggest that anti Ox-LDL IgM antibodies, Th17 cells could be developed as a potential marker to study disease progression and to study the effect of therapeutic regulation of inflammation.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

5 Bio Entities

0 Expression