Study of the mucosal immunomoduLation by intestinal commensal bacteria
肠道共生菌对粘膜免疫调节的研究
基本信息
- 批准号:18380084
- 负责人:
- 金额:$ 10.42万
- 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:2006
- 资助国家:日本
- 起止时间:2006 至 2007
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
Intestinal commensal bacteria play important roles in the regulation of intestinal immune responses such as anti-allergic reaction and anti-infection. It has been shown that intestinal commensal bacteria greatly affect the development of gut-associated lymphoid tissues and mucosal immune responses, such as IgA production, in the gut. Given the large numbers of intestinal microbiota, particularly in the large intestine, it is believed that immunocytes in the large intestine are modulated by microbacteria. While IgA production by immunocytes in the small intestine has been previously studied, IgA production in the large intestine is, however, poorly understood. In this study, we show that IgA production by lymphocytes is induced by microbacteria present in the large intestine.Lamina propria lymphocytes from the large intestine (L-LP) were isolated from germ-free (GF) and conventional (CV) mice. Flow cytometric analysis of L-LP lymphocytes was used to assess the frequency of IgM+B220+ cel … More ls, IgA+B220+ cells, and IgA+Syndecan-l+B220- cells. In addition, to determine whether stimulation by commensal bacteria influences differentiation of IgM+ cells into IgA-plasma cells, IgM+ cells separated from L-LP lymphocytes of GF mice were co-cultured with Bacteroides acidofaciens isolated from intestinal commensal bacteria of CV mice.The frequency of IgA+Syndecan-1+B220- cells and IgA+B220+ cells in L-LP of GF were all lower than that of CV mice, but there was no difference in the frequency of IgM+13220+ cells in L-LP between GF and CV mice. IgA production by IgM+ cells stimulated by B. acidofaciens was higher than in those without bacterial stimulation.These results indicate that direct stimulation by B. acidofaciens induces differentiation of IgM+ cells into IgA-producing plasma cells from the large intestine. These also suggest that IgA production in the large intestine might be induced by intestinal commensal bacteria, thus intestinal microbacteria promote the class switching from IgM to IgA in the large intestine. Less
肠道细菌在调节肠道免疫反应(例如抗过敏反应和抗感染)中起着重要作用。已经表明,肠道细菌极大地影响了肠道中与肠道相关的淋巴组织和粘膜免疫反应(例如IgA产生)的发展。考虑到大量肠道菌群,尤其是在大肠中,据信大肠中的免疫细胞受微细菌调节。虽然先前已经研究了小肠中免疫细胞的IgA产生,但大肠中的IgA产生知之甚少。在这项研究中,我们表明淋巴细胞的IgA产生是由大肠中存在的微单细菌诱导的。从无菌(GF)和常规(CV)小鼠中分离出来自大肠(L-LP)的层次淋巴细胞(L-LP)。 L-LP淋巴细胞的流式细胞仪分析用于评估IgM+B220+Cel的频率…更多LS,IgA+B220+细胞和IgA+Syndecan-L+B220-细胞。另外,为了确定相当细菌的刺激是否影响IgM+细胞分化为IgA-铂 - - 铂型细胞,将与GF小鼠的L-LP淋巴细胞分离的IgM+细胞与与CV MITE的肠道+b220+iga+syndeca+syndedededeca+syndededecaNdeDecain+syndededecain+syndedededecaimefaciens共培养的IgM+细胞。 GF的L-LP中的细胞均低于CV小鼠的细胞,但是GF和CV小鼠之间L-LP中IgM+ 13220+细胞的频率没有差异。由酸性芽孢杆菌刺激的IgM+细胞产生的IgA高于没有细菌刺激的IgA。这些结果表明,酸性芽孢杆菌的直接刺激会影响IgM+细胞的分化为来自大肠的产生IgA产生的浆细胞。这些还表明,大肠中的IgA产生可能是由肠道菌群引起的,因此肠道微细菌促进了大肠中从IgM转换为IgA的类别。较少的
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Modulation of cytokine and immunoglobulin A release bybeta-(1,3-1,6)-glucan from Aureobasidium ullulans strain IA 1
Aureobasidium ullulans 菌株 IA 1 中 β-(1,3-1,6)-葡聚糖对细胞因子和免疫球蛋白 A 释放的调节
- DOI:
- 发表时间:2006
- 期刊:
- 影响因子:0
- 作者:Suzuki T;Hosono A;Hachimura S;Suzuki T;Kaminogawa S
- 通讯作者:Kaminogawa S
Increase in terminal fragments of 16S rRNA genes derived from Bacteroidetes after administratin of short-chain fructooligosaccharides.
给予短链低聚果糖后,来自拟杆菌门的 16S rRNA 基因末端片段增加。
- DOI:
- 发表时间:2006
- 期刊:
- 影响因子:0
- 作者:Nakanishi Y;Murashima K;Ohara H;Suzuki T;Hayashi H;Sakamoto M;Fukusawa T;Kubota H;Hosono A;Kono T;Kaminogawa S;Benno Y
- 通讯作者:Benno Y
The role of CD4^+T cells in IgA production in murine Peyer's patches followin oral feeding of Bifidobacterium components
口服双歧杆菌成分后 CD4^ T 细胞在小鼠派尔氏集结中 IgA 产生中的作用
- DOI:
- 发表时间:2006
- 期刊:
- 影响因子:0
- 作者:Nakanishi Y;Hosono A;Kimura T;Kaminogawa S
- 通讯作者:Kaminogawa S
The role of CD4^+ T cells in IgA production in murine Peyer's patches following oral feeding of Bifidobacterium components.
口服双歧杆菌成分后,CD4^T 细胞在小鼠派尔氏集结中 IgA 产生中的作用。
- DOI:
- 发表时间:2006
- 期刊:
- 影响因子:0
- 作者:Nakanishi Y;Hosono A;Kimura T;Kaminogawa S
- 通讯作者:Kaminogawa S
調製法の異なるBifidobacterium菌体成分が修飾する免疫応答の特
不同制备方法双歧杆菌细胞成分修饰免疫反应的特点
- DOI:
- 发表时间:2007
- 期刊:
- 影响因子:0
- 作者:平松 靖浩;細野 朗;高橋 恭子;上野川 修一
- 通讯作者:上野川 修一
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KAMINOGAWA Shuichi其他文献
“えん下困難者用食品”の基準中のテクスチャー試験法(TPA)に関する考察
《吞咽困难者食品》标准中关于质构测试方法(TPA)的思考
- DOI:
- 发表时间:
2014 - 期刊:
- 影响因子:0
- 作者:
KURIHARA Kenta;TAKAHASHI Kyoko;SUGI Yutaka;HOSONO Akira;KAMINOGAWA Shuichi;秋間彩香,谷米(長谷川)温子,熊谷日登美,熊谷仁 - 通讯作者:
秋間彩香,谷米(長谷川)温子,熊谷日登美,熊谷仁
病原性の異なるマツノザイセンチュウを接種したマツ切枝における通水阻害
接种不同致病性松树线虫对松枝断枝水流的抑制作用
- DOI:
- 发表时间:
2008 - 期刊:
- 影响因子:0
- 作者:
MURAKAMI Hitoshi;HACHIMURA Satoshi;TANABE Kosuke;ADACHI(NAKAJIMA)Haruyo;TSUDA Masato;WAKATSUKI Yoshio;SATO Ryuichiro;TAKAHASHI Kyoko;HOSONO Akira;KAMINOGAWA Shuichi;外岡遼・梅林利弘・福田健二 - 通讯作者:
外岡遼・梅林利弘・福田健二
48年周期で一斉開花するタケ:インド・ミゾラム州におけるMelocanna bacc i foraの開花周期記録
48年一次开花的竹子:印度米佐拉姆邦Melocanna bacc i fora开花周期的记录
- DOI:
- 发表时间:
2009 - 期刊:
- 影响因子:0
- 作者:
TAKAHASHI Kyoko;SUGI Yutaka;NAKANO Ko;TSUDA Masato;HOSONO Akira;KAMINOGAWA Shuichi;陶山佳久・齋藤智之・西脇亜也・蒔田明史・長谷川尚史・柴田昌三 - 通讯作者:
陶山佳久・齋藤智之・西脇亜也・蒔田明史・長谷川尚史・柴田昌三
天然生針広混交林における枯死木の腐朽に及ぼす立地・樹種の影響
位置和树种对自然生长混交林死树腐烂的影响
- DOI:
- 发表时间:
2012 - 期刊:
- 影响因子:0
- 作者:
TAKAHASHI Kyoko;SUGI Yutaka;KURIHARA Kenta;HOSONO Akira;KAMINOGAWA Shuichi;井上太樹・南雲未智・吉田俊也 - 通讯作者:
井上太樹・南雲未智・吉田俊也
Role of commensal bacteria in regulation of host gene expression in intestinal epithelial cells.
共生细菌在调节肠上皮细胞宿主基因表达中的作用。
- DOI:
- 发表时间:
2012 - 期刊:
- 影响因子:0
- 作者:
TAKAHASHI Kyoko;SUGI Yutaka;KURIHARA Kenta;HOSONO Akira;KAMINOGAWA Shuichi - 通讯作者:
KAMINOGAWA Shuichi
KAMINOGAWA Shuichi的其他文献
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{{ truncateString('KAMINOGAWA Shuichi', 18)}}的其他基金
Immunoregulation by the gut commensal bacteria or probiotics
肠道共生细菌或益生菌的免疫调节
- 批准号:
20380079 - 财政年份:2008
- 资助金额:
$ 10.42万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
Study of the regulatory function for immune and allergic responses by the intestinal microbacteria and probiotic bacteria
肠道微生物和益生菌对免疫和过敏反应调节功能的研究
- 批准号:
16380093 - 财政年份:2004
- 资助金额:
$ 10.42万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
INDUCTION AND REGULATION OF IMMUNE AND ALLERGIC RESPONSES BY FOOD-DERIVED IMMUNE FUNCTIONAL MOLECULES
食物来源的免疫功能分子对免疫和过敏反应的诱导和调节
- 批准号:
13306010 - 财政年份:2001
- 资助金额:
$ 10.42万 - 项目类别:
Grant-in-Aid for Scientific Research (A)
ESTABLISHMENT OF NOVEL EXPERIMENTAL SYSTEM(S) FOR EVALUATION OF THE IMMUNE FUNCTION OF FOOD COMPONENTS USING CELLS FROM THE INTESTINAL IMMUNE SYSTEM
建立利用肠道免疫系统细胞评估食品成分免疫功能的新型实验系统
- 批准号:
11556023 - 财政年份:1999
- 资助金额:
$ 10.42万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
THE MOLECULAR MECHANISMS OF IMMUNE RESPONSE AND INTERACTION OF THE IMMUNE AND NERVOUS SYSTEMS IN FOOD ALLERGY
食物过敏中免疫反应的分子机制以及免疫和神经系统的相互作用
- 批准号:
10306008 - 财政年份:1998
- 资助金额:
$ 10.42万 - 项目类别:
Grant-in-Aid for Scientific Research (A).
Screening of factors triggering food allergy and research on development of hypoallergic food products.
食物过敏诱发因素筛选及低过敏食品开发研究。
- 批准号:
08556020 - 财政年份:1996
- 资助金额:
$ 10.42万 - 项目类别:
Grant-in-Aid for Scientific Research (A)
Inhibition of allergic and autoimmune responses by means of food proteins and peptides.
通过食物蛋白质和肽抑制过敏和自身免疫反应。
- 批准号:
07406006 - 财政年份:1995
- 资助金额:
$ 10.42万 - 项目类别:
Grant-in-Aid for Scientific Research (A)
Gene analysis of antibodies specific for allergen and antigenrelating to autoimmunity
过敏原和自身免疫相关抗原特异性抗体的基因分析
- 批准号:
04454070 - 财政年份:1992
- 资助金额:
$ 10.42万 - 项目类别:
Grant-in-Aid for General Scientific Research (B)
Purification, identification and functional analysis of immune suppressive factol
免疫抑制因子的纯化、鉴定及功能分析
- 批准号:
02454065 - 财政年份:1990
- 资助金额:
$ 10.42万 - 项目类别:
Grant-in-Aid for General Scientific Research (B)
The analysis of the epitope structures of food allergens by using the synthetic peptides.
利用合成肽分析食物过敏原的表位结构。
- 批准号:
62560115 - 财政年份:1987
- 资助金额:
$ 10.42万 - 项目类别:
Grant-in-Aid for General Scientific Research (C)
相似海外基金
Study of the regulatory function for immune and allergic responses by the intestinal microbacteria and probiotic bacteria
肠道微生物和益生菌对免疫和过敏反应调节功能的研究
- 批准号:
16380093 - 财政年份:2004
- 资助金额:
$ 10.42万 - 项目类别:
Grant-in-Aid for Scientific Research (B)