Journal
IMMUNOBIOLOGY
Volume 218, Issue 4, Pages 561-569Publisher
ELSEVIER GMBH
DOI: 10.1016/j.imbio.2012.07.022
Keywords
NKT cells; NK cells; CD1d; Inflammation; Atherosclerosis
Categories
Funding
- Japan Society for the Promotion of Science (JSPS) [20390106, 23370059]
- Global COE Program, Establishment of International Collaboration Center for Zoonosis Control, from the Ministry of Education, Culture, Science, Sports and Technology (MEXT), Japan
- Health and Labor Sciences Research Grant on Intractable Diseases from the Ministry of Health, Labor and Welfare of Japan
- Akiyama Foundation
- Daiwa Securities Health Foundation
- Suhara Memorial Foundation
- BioLegend/Tomy Digital Biology
- Parent's Association (Keyakikai) at Kitasato University School of Medicine
- National Institutes of Health [AI070305, HL089667, DK081536]
- Grants-in-Aid for Scientific Research [23370059, 20390106, 22501024] Funding Source: KAKEN
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Lipopolysaccharide (LPS) has been shown to accelerate atherosclerosis and to increase the prevalence of IL-4-producing natural killer T (NKT) cells in various tissues. However, the role of NKT cells in the development of LPS-induced atherosclerotic lesions has not been fully tested in NKT cell-deficient mice. Here, we examined the lesion development in apolipoprotein E knockout (apoE-KO) mice and apoE-KO mice on an NKT cell-deficient, CD1d knockout (CD1d-KO) background (apoE-CD1d double knockout; DKO). LPS (0.5 mu g/g body weight/wk) or phosphate-buffered saline (PBS) was intraperitoneally administered to apoE-KO and DKO mice (8-wk old) for 5 wk and atherosclerotic lesion areas were quantified thereafter. Consistent with prior reports, NKT cell-deficient DKO mice showed milder atherosclerotic lesions than apoE-KO mice. Notably, LPS administration significantly increased the lesion size in apoE-KO, but not in DKO mice, compared to PBS controls. Our findings suggest that LPS, and possibly LPS-producing bacteria, aggravate the development of atherosclerosis primarily through NKT cell activation and subsequent collaboration with NK cells. (C) 2012 Elsevier GmbH. All rights reserved.
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