Journal
JOURNAL OF INTERFERON AND CYTOKINE RESEARCH
Volume 39, Issue 9, Pages 564-571Publisher
MARY ANN LIEBERT, INC
DOI: 10.1089/jir.2019.0050
Keywords
interleukin-23 (IL-23); inflammation; atherosclerosis; mice
Funding
- National Natural Science Foundation of China [81470381, 81770262]
- Natural Science Foundation of Yangzhou [YZ2015115]
- Jiangsu Key R&D Project in Social Development [BE2015663]
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The aim of this study is to detect the dynamic expression of interleukin-23 (IL-23) in ApoE(-/-) mice at different ages and to further examine the effects of anti-IL-23 therapy on atherosclerosis development. The levels of IL-23 in the sera, aortas, and lymph nodes of ApoE(-/-) mice were significantly increased compared with those of age-matched controls at 8, 12, 16, 20, and 24 weeks of age. Then, 12-week-old ApoE(-/-) mice were intraperitoneally injected with anti-IL-23p19 neutralizing antibodies, isotype controls, and phosphate-buffered saline for 8 weeks. The proinflammatory and anti-inflammatory mediators in atherosclerotic aortas, plaque areas, plaque necrotic cores, and the contents of major inflammatory cells in plaques were subsequently determined. The results showed that anti-IL-23p19 treatment significantly decreased the expression of IL-17A, IL-6, and TNF-alpha in the aortas of ApoE(-/-) mice, but had no obvious effect on the plaque area, plaque necrotic core, or content of major inflammatory cells in atherosclerotic plaques. Although anti-IL-23p19 therapy reduces the expression of several proinflammatory cytokines, it does not significantly suppress the progression of atherosclerosis in ApoE(-/-) mice.
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