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Interleukin-25 (IL-25) has a protective role in atherosclerosis development in the aortic arch in mice

Mantani, Polyxeni T. LU ; Dunér, Pontus LU ; Bengtsson, Eva LU orcid ; Ljungcrantz, Irena LU ; Sundius, Lena LU ; To, Fong LU ; Nilsson, Jan LU ; Björkbacka, Harry LU orcid and Fredrikson, Gunilla Nordin LU (2018) In Journal of Biological Chemistry 293(18). p.6791-6801
Abstract

Atherosclerosis is a chronic inflammatory disease characterized by the entrapment of apolipoprotein B– containing lipoproteins in the arterial intima, leading to local inflammation. T helper (Th) cell 1–mediated immune responses have been associated with atherosclerosis, and the cytokine interleukin-25 (IL-25 or IL-17E) has been reported to potentially regulate Th1 cell– and Th17 cell–related immune responses. In this study, we evaluated the effects of complete IL-25 deficiency or of a temporal IL-25 blockade on atherosclerosis development in apolipoprotein E– deficient (Apoe/) mice. Mice deficient in both apolipoprotein E and IL-25 (Apoe//IL-25/) had more Th1 cells in the spleen, along with elevated plasma levels of IL-17 and an... (More)

Atherosclerosis is a chronic inflammatory disease characterized by the entrapment of apolipoprotein B– containing lipoproteins in the arterial intima, leading to local inflammation. T helper (Th) cell 1–mediated immune responses have been associated with atherosclerosis, and the cytokine interleukin-25 (IL-25 or IL-17E) has been reported to potentially regulate Th1 cell– and Th17 cell–related immune responses. In this study, we evaluated the effects of complete IL-25 deficiency or of a temporal IL-25 blockade on atherosclerosis development in apolipoprotein E– deficient (Apoe/) mice. Mice deficient in both apolipoprotein E and IL-25 (Apoe//IL-25/) had more Th1 cells in the spleen, along with elevated plasma levels of IL-17 and an increased release of splenic interferon- (INF-). In support of this observation, a 4-week-long treatment of young Apoe/ mice (at 10 –14 weeks of age) with an IL-25– blocking antibody increased the release of Th1/Th17-associated cytokines in the spleen. In both mouse models, these findings were associated with increased atherosclerotic plaque formation in the aortic arch. We conclude that complete IL-25 deficiency and a temporal IL-25 blockade during early plaque development aggravate atherosclerosis development in the aortic arch of Apoe/ mice, accompanied by an increase in Th1/Th17-mediated immune responses. Our finding that endogenous IL-25 has an atheroprotective role in the murine aortic arch has potential implications for atherosclerosis development and management in humans.

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author
; ; ; ; ; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Journal of Biological Chemistry
volume
293
issue
18
pages
11 pages
publisher
American Society for Biochemistry and Molecular Biology
external identifiers
  • scopus:85046623740
  • pmid:29572351
ISSN
0021-9258
DOI
10.1074/jbc.RA117.000292
language
English
LU publication?
yes
id
90e07bdf-1bdd-4650-977c-a11c9433a25d
date added to LUP
2018-05-25 12:57:55
date last changed
2024-03-18 10:07:04
@article{90e07bdf-1bdd-4650-977c-a11c9433a25d,
  abstract     = {{<p>Atherosclerosis is a chronic inflammatory disease characterized by the entrapment of apolipoprotein B– containing lipoproteins in the arterial intima, leading to local inflammation. T helper (Th) cell 1–mediated immune responses have been associated with atherosclerosis, and the cytokine interleukin-25 (IL-25 or IL-17E) has been reported to potentially regulate Th1 cell– and Th17 cell–related immune responses. In this study, we evaluated the effects of complete IL-25 deficiency or of a temporal IL-25 blockade on atherosclerosis development in apolipoprotein E– deficient (Apoe/) mice. Mice deficient in both apolipoprotein E and IL-25 (Apoe//IL-25/) had more Th1 cells in the spleen, along with elevated plasma levels of IL-17 and an increased release of splenic interferon- (INF-). In support of this observation, a 4-week-long treatment of young Apoe/ mice (at 10 –14 weeks of age) with an IL-25– blocking antibody increased the release of Th1/Th17-associated cytokines in the spleen. In both mouse models, these findings were associated with increased atherosclerotic plaque formation in the aortic arch. We conclude that complete IL-25 deficiency and a temporal IL-25 blockade during early plaque development aggravate atherosclerosis development in the aortic arch of Apoe/ mice, accompanied by an increase in Th1/Th17-mediated immune responses. Our finding that endogenous IL-25 has an atheroprotective role in the murine aortic arch has potential implications for atherosclerosis development and management in humans.</p>}},
  author       = {{Mantani, Polyxeni T. and Dunér, Pontus and Bengtsson, Eva and Ljungcrantz, Irena and Sundius, Lena and To, Fong and Nilsson, Jan and Björkbacka, Harry and Fredrikson, Gunilla Nordin}},
  issn         = {{0021-9258}},
  language     = {{eng}},
  month        = {{01}},
  number       = {{18}},
  pages        = {{6791--6801}},
  publisher    = {{American Society for Biochemistry and Molecular Biology}},
  series       = {{Journal of Biological Chemistry}},
  title        = {{Interleukin-25 (IL-25) has a protective role in atherosclerosis development in the aortic arch in mice}},
  url          = {{http://dx.doi.org/10.1074/jbc.RA117.000292}},
  doi          = {{10.1074/jbc.RA117.000292}},
  volume       = {{293}},
  year         = {{2018}},
}