Delayed Clearance of Zymosan-induced Granuloma and Depressed Phagocytosis of Macrophages with Concomitant Up-regulated Kinase Activities of Src-family in a Human Monocyte ChemoaHractant Protein-1 Transgenic Mouse

Ato, Manabu; Iwabuchi, Kazuya; Matsuki, Naoto; Mukaida, Naofumi; Iwabuchi, Chikako; Takahashi, Akio; Takahashi, Toshiaki; Dondog, Enkh-Amar; Hatakeyama, Susumi; Ishikura, Hiroshi; Kato, Masahito; Negishi, Izumi; Nishihori, H.; Watano, Keiko; Ogasawara, Kunio; Matsushima, Kouji; Onoé, Kazunori

doi:10.1016/s0171-2985(00)80096-0

Cited by 7 publications

(10 citation statements)

References 31 publications

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“…Resident PEC were prepared by washing the peritoneal cavity of AIF-1 Tg mice or NTgm at 8-10 weeks of age with phosphate-buffered saline (PBS) and cells were collected without stimulation. In some experiments, 4% (w/v) thioglycolate broth (2 ml) was intraperitoneally injected and the elicited PEC were collected 4 days later (20).…”

Section: Methodsmentioning

confidence: 99%

“…Wild-type RAW 264.7, three lines of AIF-1 transfectants with different AIF-1 levels, vector control and PEC obtained from NTgm or AIF-1 Tg mice were subjected to phagocytotic assay as previously described (20). In brief, the cells (1x10 6 /tube) were incubated with 10X FITCmicrobeads (f=2.00 μm; Polysciences, Warrington, PA) at 37˚C for 2 h. After the reaction, the cells were extensively washed three times with cold FACS buffer (0.1% bovine serum albumin (BSA), 0.1% NaN 3 in PBS) containing 1.5 mM ethylenediaminetetraacetic acid (EDTA).…”

Section: Methodsmentioning

confidence: 99%

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Allograft inflammatory factor-1 augments macrophage phagocytotic activity and accelerates the progression of atherosclerosis in ApoE−/− mice

Mishima

Iwabuchi²,

Fujii

et al. 2008

Int J Mol Med

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Abstract. Allograft inflammatory factor (AIF)-1, originally cloned from a rat heart allograft under chronic rejection, is induced in various inflammatory conditions including atherosclerosis. Using mouse AIF-1 transfected macrophages and AIF-1 transgenic (AIF-1 Tg ) mice, we analyzed the influence of AIF-1 overexpression on macrophage phagocytosis and the development of atherosclerosis. The AIF-1 transfectants showed significantly increased phagocytosis of latex beads and E. coli BioParticles as well as incorporation of acetylated low-density lipoprotein (LDL) compared to those of vector controls. Concordant results were obtained with elicited peritoneal exudate cells from AIF-1 Tg mice. When AIF-1 Tg mice were crossbred with apolipoprotein E knockout mice (ApoE -/-), these AIF-1 Tg ApoE -/-mice developed significantly increased atherosclerotic lesions compared to ApoE -/-mice. These results suggest that enhanced AIF-1 expression leads to augmented incorporation of degenerated LDL by macrophages and promotes development of atherosclerotic vasculopathy.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Allograft inflammatory factor-1 augments macrophage phagocytotic activity and accelerates the progression of atherosclerosis in ApoE−/− mice

Mishima

Iwabuchi²,

Fujii

et al. 2008

Int J Mol Med

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“…We have established a human (h) MCP‐1 transgenic mouse (Tgm) line that constitutively produces a large amount of hMCP‐1 in the serum 11 . Although the expression of transgenes was detected in various tissues by reverse transcriptase–polymerase chain reaction (RT–PCR), an accumulation of Mφ was detected only in lymphoid organs.…”

Section: Introductionmentioning

confidence: 90%

“…C57BL/6 (B6)‐hMCP‐1 Tgm were produced by backcrossing B6 mice into hMCP‐1 Tgm as described 11 . B6 mice were purchased from Japan SLC (Hamamatsu, Japan).…”

Section: Methodsmentioning

confidence: 99%

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Augmented expression of tumour necrosis factor‐α induced by lipopolysaccharide in spleen of human monocyte chemoattractant protein‐1 transgenic mouse enhances the lipopolysaccharide sensitivity of the marginal zone macrophages

et al. 2002

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SUMMARYMonocyte chemoattractant protein-1 (MCP-1) is a protective cytokine in murine endotoxaemia induced by lipopolysaccharide (LPS). In this study, LPS-induced pathophysiology in the human (h) MCP-1 transgenic mouse (Tgm) line was investigated. The hMCP-1 Tgm showed a marked increase in the mortality and weight loss following LPS administration. In the Tgm spleens, disappearance of marginal zone macrophages (MZMw) and dendritic cells (DC) was induced by a smaller amount of LPS than that required for the disappearance in non-transgenic littermates. A significant number of apoptotic cells were seen in these areas. Furthermore, expressions of tumour necrosis factor-a (TNF-a), interleukin-1a (IL-1a), and IL-6 mRNA were enhanced and sustained in the LPS-treated Tgm. Neutralization of TNF-a considerably depressed the LPS-sensitivity of Tgm. These findings demonstrate that the continuous and systemic presence of MCP-1 is no more protective toward endotoxaemia and suggest that the high sensitivity of the MZMw and DC to LPS is attributed to the enhanced TNF-a production in the hMCP-1 Tgm.

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

et al. 2013

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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 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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Delayed Clearance of Zymosan-induced Granuloma and Depressed Phagocytosis of Macrophages with Concomitant Up-regulated Kinase Activities of Src-family in a Human Monocyte ChemoaHractant Protein-1 Transgenic Mouse

Cited by 7 publications

References 31 publications

Allograft inflammatory factor-1 augments macrophage phagocytotic activity and accelerates the progression of atherosclerosis in ApoE−/− mice

Allograft inflammatory factor-1 augments macrophage phagocytotic activity and accelerates the progression of atherosclerosis in ApoE−/− mice

Augmented expression of tumour necrosis factor‐α induced by lipopolysaccharide in spleen of human monocyte chemoattractant protein‐1 transgenic mouse enhances the lipopolysaccharide sensitivity of the marginal zone macrophages

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

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