The investigation of the role of cytokine from derived epithelial cell for activation γδ T cells in mucosal infection
The investigation of the role of cytokine from derived epithelial cell for activation γδ T cells in mucosal infection
批准号:
12470473
负责人:
NOGUCHI Toshihide
金额:
$6.98万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (B)
财政年份:
2000
资助国家:
日本
项目状态:
已结题
起止时间:
2000 至 2002
中文摘要
为了解上皮内淋巴细胞在牙周病发病中的作用,本研究以C57 BL/6小鼠和BALB/c小鼠为研究对象,通过比较口腔感染单核细胞增生李斯特菌(Listeria monocytogenes)后小鼠肠上皮细胞(i-EC)早期IL-15的产生,探讨其在牙周病发病中的作用机制。活的L。单核细胞增多症,在第1、3或5天计数肝、脾、肠系膜淋巴结(MLN)和派尔集合淋巴结(PP)中的细菌。C57 BL/6小鼠的所有器官均表现出比BALB/c小鼠更高的抵抗力水平。要知道这些阻力的差异,我们调查的肠上皮内淋巴细胞(i-IEL)在口腔感染单核细胞增生李斯特菌的动力学。口腔感染后第1、3、5天,i-IEL中携带CD 8 αα和CDαβ或TCRαβ和γδ的亚群的绝对数量和比例均无显著性差异。因此,这些结果表明,口腔感染单核细胞增多性李斯特菌可能不会影响亚群, 关于我们 i-IEL的形成。接下来,我们研究了口腔感染后i-EC和i-IEL中细胞因子产生的差异。C57 BL/6小鼠i-EC感染单核细胞增生李斯特菌后第1天IL-15 mRNA和IL-15蛋白表达水平较高,而BALB/c小鼠i-EC中IL-15 mRNA和IL-15蛋白表达水平较低。同时,C57 BL/6小鼠i-IEL对CD 3刺激产生的IFN-γ量高于BALB/c小鼠。而BALB/c小鼠的i-IEL在CD 3刺激下产生的IL-4水平高于C57 BL/6小鼠。Toll样受体(TLR)2已被认为是来自分枝杆菌或革兰氏阳性细菌的细菌脂蛋白的受体。C57 BL/6小鼠感染单核细胞增生李斯特菌后第1天,i-EC中TLR 2 mRNA表达水平升高,提示TLR 2表达与IL-15产生的差异有关,并且i-EC早期产生IL-15的差异可能至少部分是C57 BL/6和BALB/c小鼠对单核细胞增生李斯特菌易感性差异的基础。少
英文摘要
To know the role of intraepithelial lymphocyte as an etiology of periodontal disease, the mechanism responsible for C57BL/6 as resistance mice and BALB/c as susceptibility mice to oral infection with Listeria monocytogenes were studied by comparing early IL-15 production in intestinal epithelial cells (i-EC).After mice were inoculated p.o. with viable L. monocytogenes, the bacteria in liver, spleen, mesenteric lymph nodes (MLN) and Peyer's patch (PP) were counted on day 1, 3 or 5. C57BL/6 mice were shown higher level of resistance than BALB/c in all organs. To know the difference of these resistance, we investigate kinetics of the intestinal intraepithelial lymphocytes (i-IEL) during oral infection with L.monocytogenes. There were no significant difference in the absolute : nmber and the ratio of i-IEL subpopulations bearing CD8αα and CDαβ or TCRαβ and γδ on day 1, 3 and 5 after oral infection. Thus, these results suggest that oral infection with L.monocytogenes may not affect the subp … More opulation of i-IEL in each mice. Next, we investigate the difference of cytokines production in i-EC and i-IEL after oral infection. High levels of IL-15 mRNA and IL-15 protein in i-EC from C57BL/6 mice were expressed on day 1 after L.monocytogenes infection, whereas in i-EC from BALB/c mice, those were expressed very low. Concurrently, a amount of IFN-γ which was produced by i-IEL from C57BL/6 mice in response to CD3 stimulation were higher than by that from BALB/c mice. While the i-IEL from BALB/c mice produced a higher level of IL-4 upon CD3 stimulation than that of C57BL/6 mice. The toll-like receptor (TLR) 2 has been suggested as a receptor for bacterial lipoproteins from Mycobacteria or Gram-positive bacteria. The mRNA expression level of TLR2, which is recognized to mediate a partly signaling for IL-15 gene transcription, was increased in i-EC from C57BL/6 mice on day 1 after L.monocytogenes infection.These results suggest that TLR2 expression regards difference of IL-15 production, and that the difference in early production of IL-15 by i-EC may at least partly underlie the difference in susceptibility to L.monocytogenes between C57BL/6 and BALB/c mice. Less
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Mitani A. et al.: "Interleukin-15 production at the early stage after oral infection with Listeria monocytogenes in mice"Immunology. 97(1). 92-99 (1999)
Mitani A. 等人:“小鼠口腔感染单核细胞增生李斯特氏菌后早期白细胞介素 15 的产生”免疫学。
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Noguchi T. et al.: "Activation of T cells recognizing an epitope of heat shock protein (HSP)70 can protect against rat adjuvant arthritis"J.Immunol. 163. 5560-5565 (1999)
Noguchi T. 等人:“识别热休克蛋白 (HSP)70 表位的 T 细胞的激活可以预防大鼠佐剂关节炎”J.Immunol。
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Noguchi T. et al.: "Activation of T cells recognizing an epitope of heat shock protein (HSP)70 can protect against rat adjuvant arthritis"J. Immunol. 163. 5560-5565 (1999)
Noguchi T. 等人:“激活识别热休克蛋白 (HSP)70 表位的 T 细胞可以预防大鼠佐剂性关节炎”。
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Noguchi T. et al.: "Gene expression of osteoclast differentiation factor is induced by lipopolysaccharide in mouse osteoblasts via toll-like receptors"J. Immunol. 166(5). 3574-3579 (2001)
Noguchi T.等人:“小鼠成骨细胞中脂多糖通过Toll样受体诱导破骨细胞分化因子的基因表达”J.
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Noguchi T. et al.: "Gene expression of osteoclast differentiation factor is induced by lipopolysaccharide in mouse osteoblasts via toll-like receptors"J.Immunol. 166(5). 3574-3579 (2001)
Noguchi T.等人:“小鼠成骨细胞中脂多糖通过Toll样受体诱导破骨细胞分化因子的基因表达”J.Immunol。
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共 6 条
Metagenomic Analysis of Oral Microbiota from Normal Subjects and Patients with Periodontal Disease
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批准号:20249082
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项目类别:Grant-in-Aid for Scientific Research (A)
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资助金额:$30.95万
-
财政年份:2008
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负责人:NOGUCHI Toshihide
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依托单位:
The working mechanism of bone resorption inhibitory protein induced by osteoclasts
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Cell-surface components Actinobacillus actinomycetemcomitans promote osteoclast formation in vitro
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财政年份:1996
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负责人:NOGUCHI Toshihide
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依托单位:
Immunological properties of a heat schock protein from Actinobacillus actinomycetemcomitans.
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批准号:05454524
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项目类别:Grant-in-Aid for General Scientific Research (B)
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资助金额:$3.97万
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财政年份:1993
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负责人:NOGUCHI Toshihide
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依托单位:
The role of collagenase and TIMP in Periodontal disease.
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批准号:02454443
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项目类别:Grant-in-Aid for General Scientific Research (B)
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资助金额:$2.37万
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财政年份:1990
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负责人:NOGUCHI Toshihide
-
依托单位:
Research for Clarifying Aetiologic Factors of Periodontal Disease -the Role of Neutrophil-
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批准号:63870115
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项目类别:Grant-in-Aid for Developmental Scientific Research (B).
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资助金额:$1.6万
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财政年份:1988
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负责人:NOGUCHI Toshihide
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依托单位:
Basic Research for Aetiology and Pathology of Periodontal Disease
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批准号:61480396
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项目类别:Grant-in-Aid for General Scientific Research (B)
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资助金额:$2.75万
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财政年份:1986
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负责人:NOGUCHI Toshihide
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依托单位:
New Method for Local Drug Delivery using Resorbable Base Material in Periodontal Therapy
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批准号:60870069
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项目类别:Grant-in-Aid for Developmental Scientific Research
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资助金额:$1.98万
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财政年份:1985
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负责人:NOGUCHI Toshihide
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依托单位:
国内基金
海外基金
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