與人類完美共生的微生物
胃腸的粘膜表面具有復(fù)雜的微環(huán)境，許多無害的微生物寄居于此。然而病原微生物也企圖破壞粘膜的表面，打開入侵人體的大門。這些病原微生物要么直接侵入粘膜，要么分泌毒素破壞之。腸表皮的細(xì)胞也進(jìn)化出一套防御機(jī)制，如一些非經(jīng)典免疫細(xì)胞表達(dá)MHC
I，II參與對(duì)病原微生物的免疫識(shí)別，還有的細(xì)胞在膜上表達(dá)Toll-like受體，使之能檢測(cè)到病菌的存在，且引發(fā)免疫反應(yīng)。
已知這些防御機(jī)制怎樣分清敵我呢?Science上intimin提出了一個(gè)觀點(diǎn)，無非致病的沙門氏菌不會(huì)引起腸表皮合成炎癥因子，他們發(fā)現(xiàn)此細(xì)菌抑制了IkB的降解，IkB是一個(gè)重要轉(zhuǎn)錄因子NF－kB的抑制劑，正是此效應(yīng)誘導(dǎo)了細(xì)菌對(duì)腸表皮細(xì)胞的耐受。
腸道內(nèi)的微生物與生物體具有良好的共生關(guān)系，兩者互惠互利。有益微生物與有害微生物的特征區(qū)分并不明顯，一般來說，病原微生物會(huì)有一些附著裝置，如(type
, http://www.www.srpcoatings.com
III translocation proteins),致病E.coli結(jié)合在人體腸表皮細(xì)胞上的intimin蛋白上，intimin的工作是第一例報(bào)道有益微生物怎樣避免表皮細(xì)胞的炎癥反應(yīng)的。
越來越多的證據(jù)表明NF－kB是腸炎癥免疫反應(yīng)的重要因子，IkB與NF－kB結(jié)合時(shí)定位在核外，當(dāng)IkB被IkBa,b磷酸化后，引起泛素化及降解，然后NF－kB得以入核行使轉(zhuǎn)錄因子功能。已知許多病原微生物可以激活NF－kB。
隨著研究的深入，我們對(duì)在這個(gè)充滿敵意的世界上與自己完美共生的一些微生物的了解日益加深。
圖片說明：
A bug's life. Nonpathogenic Salmonella bacteria
interfere with NF-kB activation in gut epithelial cells. The
, 百拇醫(yī)藥
transcription factor NF-kB is activated by binding of bacterial
products such as lipopolysaccharide to the surface of gut epithelial Cells. Commensal bacteria that normally inhabit the gut such as Nonpathogenic Salmonella have devised schemes to interfere with NF-kB activation and hence with the expression of genes involved in the
inflammatory response. Nonpathogenic Salmonella block ubiquitination (UBQ) and degradation of IkB, an inhibitor that binds to and sequesters NF-kB
, 百拇醫(yī)藥
in the cytoplasm. When IkB is degraded, NF-kB is released and moves to
the nucleus where it switches on target genes involved in
inflammation. This strategy may explain the virtual absence of inflammation in the gut mucosa despite its constant exposure to a
variety of indigenous bacteria.
相關(guān)文章：
Prokaryotic
, 百拇醫(yī)藥
Regulation of Epithelial Responses by Inhibition of IB- Ubiquitination. andrew
S. Neish, Andrew T. Gewirtz, Hui Zeng, Andrew N. Young, Michael E.
Hobert, Vinit Karmali, Anjali S. Rao, and James L. Madara
Science
2000 289: 1560-1563. (in Reports) R.
Medzhitov, P. Preston-Hurlburt, C. A. Janeway Jr., Nature 388, 394 (1997)[Medline]. E.
, 百拇醫(yī)藥
Cario et al., J. Immunol. 164, 966 (2000)[Medline]. A.
S. Neish et al., Science 289, 1560 (2000).
L.
Bry, P. G. Falk, T. Midtvedt, J. I. Gordon, Science 273, 1380 (1996).
L. M. Higgins et al., Science 285, 588 (1999). M.
Karin and Y. Ben-Neriah, Annu. Rev. Immunol. 18, 621 (2000)[Medline]. K.
Orth et al., Science 285, 1920 (1999).
B. J. Rembacken et al., Lancet 354, 635 (1999)[Medline].
P.
Gionchetti et al., Gastroenterology 119, 305 (2000), 百拇醫(yī)藥
I，II參與對(duì)病原微生物的免疫識(shí)別，還有的細(xì)胞在膜上表達(dá)Toll-like受體，使之能檢測(cè)到病菌的存在，且引發(fā)免疫反應(yīng)。
已知這些防御機(jī)制怎樣分清敵我呢?Science上intimin提出了一個(gè)觀點(diǎn)，無非致病的沙門氏菌不會(huì)引起腸表皮合成炎癥因子，他們發(fā)現(xiàn)此細(xì)菌抑制了IkB的降解，IkB是一個(gè)重要轉(zhuǎn)錄因子NF－kB的抑制劑，正是此效應(yīng)誘導(dǎo)了細(xì)菌對(duì)腸表皮細(xì)胞的耐受。
腸道內(nèi)的微生物與生物體具有良好的共生關(guān)系，兩者互惠互利。有益微生物與有害微生物的特征區(qū)分并不明顯，一般來說，病原微生物會(huì)有一些附著裝置，如(type
, http://www.www.srpcoatings.com
III translocation proteins),致病E.coli結(jié)合在人體腸表皮細(xì)胞上的intimin蛋白上，intimin的工作是第一例報(bào)道有益微生物怎樣避免表皮細(xì)胞的炎癥反應(yīng)的。
越來越多的證據(jù)表明NF－kB是腸炎癥免疫反應(yīng)的重要因子，IkB與NF－kB結(jié)合時(shí)定位在核外，當(dāng)IkB被IkBa,b磷酸化后，引起泛素化及降解，然后NF－kB得以入核行使轉(zhuǎn)錄因子功能。已知許多病原微生物可以激活NF－kB。
隨著研究的深入，我們對(duì)在這個(gè)充滿敵意的世界上與自己完美共生的一些微生物的了解日益加深。
圖片說明：
A bug's life. Nonpathogenic Salmonella bacteria
interfere with NF-kB activation in gut epithelial cells. The
, 百拇醫(yī)藥
transcription factor NF-kB is activated by binding of bacterial
products such as lipopolysaccharide to the surface of gut epithelial Cells. Commensal bacteria that normally inhabit the gut such as Nonpathogenic Salmonella have devised schemes to interfere with NF-kB activation and hence with the expression of genes involved in the
inflammatory response. Nonpathogenic Salmonella block ubiquitination (UBQ) and degradation of IkB, an inhibitor that binds to and sequesters NF-kB
, 百拇醫(yī)藥
in the cytoplasm. When IkB is degraded, NF-kB is released and moves to
the nucleus where it switches on target genes involved in
inflammation. This strategy may explain the virtual absence of inflammation in the gut mucosa despite its constant exposure to a
variety of indigenous bacteria.
相關(guān)文章：
Prokaryotic
, 百拇醫(yī)藥
Regulation of Epithelial Responses by Inhibition of IB- Ubiquitination. andrew
S. Neish, Andrew T. Gewirtz, Hui Zeng, Andrew N. Young, Michael E.
Hobert, Vinit Karmali, Anjali S. Rao, and James L. Madara
Science
2000 289: 1560-1563. (in Reports) R.
Medzhitov, P. Preston-Hurlburt, C. A. Janeway Jr., Nature 388, 394 (1997)[Medline]. E.
, 百拇醫(yī)藥
Cario et al., J. Immunol. 164, 966 (2000)[Medline]. A.
S. Neish et al., Science 289, 1560 (2000).
L.
Bry, P. G. Falk, T. Midtvedt, J. I. Gordon, Science 273, 1380 (1996).
L. M. Higgins et al., Science 285, 588 (1999). M.
Karin and Y. Ben-Neriah, Annu. Rev. Immunol. 18, 621 (2000)[Medline]. K.
Orth et al., Science 285, 1920 (1999).
B. J. Rembacken et al., Lancet 354, 635 (1999)[Medline].
P.
Gionchetti et al., Gastroenterology 119, 305 (2000), 百拇醫(yī)藥
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