Natural killer T cells are required for lipopolysaccharide-mediated enhancement of atherosclerosis in apolipoprotein E-deficient mice

Yasuhiro Andoh, Hisako Ogura, Masashi Satoh, Kentaro Shimano, Hironori Okuno, Satoshi Fujii, Naoki Ishimori, Koji Eshima, Hidekazu Tamauchi, Tatsuro Otani, Yukihito Nakai, Luc Van Kaer, Hiroyuki Tsutsui, Kazunori Onoé, Kazuya Iwabuchi

研究成果: ジャーナルへの寄稿記事

11 引用 (Scopus)

抄録

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 μg/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.

元の言語英語
ページ(範囲)561-569
ページ数9
ジャーナルImmunobiology
218
発行部数4
DOI
出版物ステータス出版済み - 4 1 2013
外部発表Yes

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Natural Killer T-Cells
Apolipoproteins E
Lipopolysaccharides
Atherosclerosis
Knockout Mice
Phosphates
Natural Killer Cells
Interleukin-4
Body Weight
Bacteria

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology
  • Hematology

これを引用

Natural killer T cells are required for lipopolysaccharide-mediated enhancement of atherosclerosis in apolipoprotein E-deficient mice. / Andoh, Yasuhiro; Ogura, Hisako; Satoh, Masashi; Shimano, Kentaro; Okuno, Hironori; Fujii, Satoshi; Ishimori, Naoki; Eshima, Koji; Tamauchi, Hidekazu; Otani, Tatsuro; Nakai, Yukihito; Van Kaer, Luc; Tsutsui, Hiroyuki; Onoé, Kazunori; Iwabuchi, Kazuya.

:: Immunobiology, 巻 218, 番号 4, 01.04.2013, p. 561-569.

研究成果: ジャーナルへの寄稿記事

Andoh, Y, Ogura, H, Satoh, M, Shimano, K, Okuno, H, Fujii, S, Ishimori, N, Eshima, K, Tamauchi, H, Otani, T, Nakai, Y, Van Kaer, L, Tsutsui, H, Onoé, K & Iwabuchi, K 2013, 'Natural killer T cells are required for lipopolysaccharide-mediated enhancement of atherosclerosis in apolipoprotein E-deficient mice', Immunobiology, 巻. 218, 番号 4, pp. 561-569. https://doi.org/10.1016/j.imbio.2012.07.022
Andoh, Yasuhiro ; Ogura, Hisako ; Satoh, Masashi ; Shimano, Kentaro ; Okuno, Hironori ; Fujii, Satoshi ; Ishimori, Naoki ; Eshima, Koji ; Tamauchi, Hidekazu ; Otani, Tatsuro ; Nakai, Yukihito ; Van Kaer, Luc ; Tsutsui, Hiroyuki ; Onoé, Kazunori ; Iwabuchi, Kazuya. / Natural killer T cells are required for lipopolysaccharide-mediated enhancement of atherosclerosis in apolipoprotein E-deficient mice. :: Immunobiology. 2013 ; 巻 218, 番号 4. pp. 561-569.
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abstract = "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 μg/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.",
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AU - Ogura, Hisako

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AU - Shimano, Kentaro

AU - Okuno, Hironori

AU - Fujii, Satoshi

AU - Ishimori, Naoki

AU - Eshima, Koji

AU - Tamauchi, Hidekazu

AU - Otani, Tatsuro

AU - Nakai, Yukihito

AU - Van Kaer, Luc

AU - Tsutsui, Hiroyuki

AU - Onoé, Kazunori

AU - Iwabuchi, Kazuya

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