Allograft inflammatory factor‐1 regulates trinitrobenzene sulphonic acid‐induced colitis

Morohashi, Taiki; Iwabuchi, Kazuya; Watano, Keiko; Dashtsoodol, Nyambayar; Mishima, Tetsuya; Nakai, Yukihito; Shimada, Shigeki; Nishida, Ryutaro; Fujii, Satoshi; Onoé, Kazunori

doi:10.1046/j.1365-2567.2003.01714.x

Cited by 20 publications

(19 citation statements)

References 35 publications

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“…This may be attributed to the prominent atherosclerosis development in ApoE -/-mice compared to the wild-type B6 mice. Another possible explanation may be that AIF-1 overexpression biases the immune response from Th1 to Th2 as we have demonstrated in in vitro experiments (14) and in the trinitrobenzene sulphonateinduced colitis model in mice (15). Since atherosclerosis is aggravated in the Th1 condition, the Th2-biased immune deviation (elevation of IL-6 and IL-10 levels) may exert regulatory influences on atherogenesis in the AIF-1 Tg environment (32)(33)(34)(35)(36).…”

Section: Discussionmentioning

confidence: 91%

“…In our previous study (14,15), we reported that AIF-1 overexpression modulates macrophage functions. To examine whether the phagocytotic activity of macrophages is also modulated by AIF-1 overexpression, AIF-1 transfectants and the vector control were examined for incorporation of FITClabeled latex beads.…”

Section: Increased Incorporation Of Fitc-beads In Aif-1 Transfectantsmentioning

confidence: 89%

“…Since the level of AcLDL uptake by macrophages is directly related to susceptibility to atherosclerosis in mice (30), these results suggest that AIF-1 is involved in the augmented development of atherosclerotic vasculopathy. In addition, the survival and migration of macrophages were affected by AIF-1 expression (14,15), which might alter and modulate the development of atherosclerotic disease.…”

Section: Discussionmentioning

confidence: 99%

“…AIF-1 Tg mice were generated with mouse AIF-1 cDNA construct under the human CD11b promoter as previously described (15), and backcrossed to C57BL/6 (B6; Japan SLC, Hamamatsu, Japan) for more than 9 generations. Nontransgenic litter mates (NTgm) were used as controls.…”

Section: Methodsmentioning

confidence: 99%

“…We previously cloned mouse AIF-1 cDNA and established AIF-1 transfectants and AIF-1 transgenic (AIF-1 Tg ) mice to analyze the effects of AIF-1 overexpression (14,15). AIF-1 overexpression modulates the capability of macrophages to produce various cytokines, which might influence subsequent immune responses.…”

Section: Introductionmentioning

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: Discussionmentioning

confidence: 91%

Section: Increased Incorporation Of Fitc-beads In Aif-1 Transfectantsmentioning

confidence: 89%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

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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Myeloid calcifying cells promote atherosclerotic calcification via paracrine activity and allograft inflammatory factor-1 overexpression

et al. 2013

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Several cell types contribute to atherosclerotic calcification. Myeloid calcifying cells (MCCs) are monocytes expressing osteocalcin (OC) and bone alkaline phosphatase (BAP). Herein, we tested whether MCCs promote atherosclerotic calcification in vivo. We show that the murine spleen contains OC(+)BAP(+) cells with a phenotype similar to human MCCs, a high expression of adhesion molecules and CD11b, and capacity to calcify in vitro and in vivo. Injection of GFP(+) OC(+)BAP(+) cells into 8-or 40-week ApoE(-/-) mice led to more extensive calcifications in atherosclerotic areas after 24 or 4 weeks, respectively, compared to control OC(-)BAP(-) cells. Despite that OC(+)BAP(+) cells had a selective transendothelial migration capacity, tracking of the GFP signal revealed that presence of injected cells within atherosclerotic areas was an extremely rare event and so GFP mRNA was undetectable by qPCR of lesion extracts. By converse, injected OC(+)BAP(+) cells persisted in the bloodstream and bone marrow up to 24 weeks, suggesting a paracrine effect. Indeed, OC(+)BAP(+) cell-conditioned medium (CM) promoted calcification by cultured vascular smooth muscle cells (VSMC) more than CM from OC(-)BAP(-) cells. A genomic and proteomic investigation of MCCs identified allograft inflammatory factor (AIF)-1 as a potential candidate of this paracrine activity. AIF-1 stimulated VSMC calcification in vitro and monocyte-specific (CD11b-driven) AIF-1 overexpression in ApoE(-/-) mice increased calcium content in atherosclerotic areas. In conclusion, we show that murine OC(+)BAP(+) cells correspond to human MCCs and promote atherosclerotic calcification in ApoE(-/-) mice, through paracrine activity and modulation of resident cells by AIF-1 overexpression. BAP-cells. A genomic and proteomic investigation of MCCs identified allograft inflammatory factor (AIF)-1 as a potential candidate of this paracrine activity. AIF-1 stimulated VSMC calcification in vitro and monocyte-specific (CD11b-driven) AIF-1 overexpression in ApoE -/-mice increased calcium content in atherosclerotic areas. In conclusion, we show that murine OC + BAP + cells correspond to human MCCs and promote atherosclerotic calcification in ApoE -/-mice, through paracrine activity and modulation of resident cells by AIF-1 overexpression.

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Allograft inflammatory factor-1 alleviates liver disease of BALB/c mice infected with Schistosoma japonicum

et al. 2014

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Allograft inflammatory factor-1 (AIF-1) plays an important role in various inflammatory conditions. Our previous study demonstrated that AIF-1 was over-expressed in the liver of BALB/c mice infected with Schistosoma japonicum and played significant role in the pathogenesis of schistosomiasis. The aim of this study was to focus on the effect of AIF-1 treatment on liver fibrosis and necrosis of BALB/c mice infected with S. japonicum. Seventy-two BALB/c mice were infected with cercariae of S. japonicum and then divided into three groups: AIF-1-treated group, saline-treated group, and control group. The vital signs, liver function, egg load, and hepatic pathological changes of the mice were assessed, and the levels of AIF-1 and TNF-α in the liver and spleen were measured at 5, 8, and 14 weeks postinfection. The treatment of AIF-1 on the mice infected with S. japonicum suppressed the expression of TNF-α and increased the effectiveness of AIF-1 in the liver and spleen at 14 weeks postinfection. Histopathological analysis and Masson trichrome staining for the liver tissues showed that the liver fibrosis and necrosis were alleviated previously compared with other infected mice at 14 weeks postinfection. The treatment of AIF-1 on the mice infected with S. japonicum can alleviate hepatic fibrosis and necrosis which indicate that AIF-1 use may prevent and cure the liver fibrosis.

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Allograft inflammatory factor‐1 regulates trinitrobenzene sulphonic acid‐induced colitis

Cited by 20 publications

References 35 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

Myeloid calcifying cells promote atherosclerotic calcification via paracrine activity and allograft inflammatory factor-1 overexpression

Allograft inflammatory factor-1 alleviates liver disease of BALB/c mice infected with Schistosoma japonicum

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