与人类完美共生的微生物
胃肠的粘膜表面具有复杂的微环境，许多无害的微生物寄居于此。然而病原微生物也企图破坏粘膜的表面，打开入侵人体的大门。这些病原微生物要么直接侵入粘膜，要么分泌毒素破坏之。肠表皮的细胞也进化出一套防御机制，如一些非经典免疫细胞表达MHC
I，II参与对病原微生物的免疫识别，还有的细胞在膜上表达Toll-like受体，使之能检测到病菌的存在，且引发免疫反应。
已知这些防御机制怎样分清敌我呢?Science上intimin提出了一个观点，无非致病的沙门氏菌不会引起肠表皮合成炎症因子，他们发现此细菌抑制了IkB的降解，IkB是一个重要转录因子NF－kB的抑制剂，正是此效应诱导了细菌对肠表皮细胞的耐受。
肠道内的微生物与生物体具有良好的共生关系，两者互惠互利。有益微生物与有害微生物的特征区分并不明显，一般来说，病原微生物会有一些附着装置，如(type
, http://www.100md.com
III translocation proteins),致病E.coli结合在人体肠表皮细胞上的intimin蛋白上，intimin的工作是第一例报道有益微生物怎样避免表皮细胞的炎症反应的。
越来越多的证据表明NF－kB是肠炎症免疫反应的重要因子，IkB与NF－kB结合时定位在核外，当IkB被IkBa,b磷酸化后，引起泛素化及降解，然后NF－kB得以入核行使转录因子功能。已知许多病原微生物可以激活NF－kB。
随着研究的深入，我们对在这个充满敌意的世界上与自己完美共生的一些微生物的了解日益加深。
图片说明：
A bug's life. Nonpathogenic Salmonella bacteria
interfere with NF-kB activation in gut epithelial cells. The
, 百拇医药
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
, 百拇医药
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.
相关文章：
Prokaryotic
, 百拇医药
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.
, 百拇医药
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), 百拇医药
I，II参与对病原微生物的免疫识别，还有的细胞在膜上表达Toll-like受体，使之能检测到病菌的存在，且引发免疫反应。
已知这些防御机制怎样分清敌我呢?Science上intimin提出了一个观点，无非致病的沙门氏菌不会引起肠表皮合成炎症因子，他们发现此细菌抑制了IkB的降解，IkB是一个重要转录因子NF－kB的抑制剂，正是此效应诱导了细菌对肠表皮细胞的耐受。
肠道内的微生物与生物体具有良好的共生关系，两者互惠互利。有益微生物与有害微生物的特征区分并不明显，一般来说，病原微生物会有一些附着装置，如(type
, http://www.100md.com
III translocation proteins),致病E.coli结合在人体肠表皮细胞上的intimin蛋白上，intimin的工作是第一例报道有益微生物怎样避免表皮细胞的炎症反应的。
越来越多的证据表明NF－kB是肠炎症免疫反应的重要因子，IkB与NF－kB结合时定位在核外，当IkB被IkBa,b磷酸化后，引起泛素化及降解，然后NF－kB得以入核行使转录因子功能。已知许多病原微生物可以激活NF－kB。
随着研究的深入，我们对在这个充满敌意的世界上与自己完美共生的一些微生物的了解日益加深。
图片说明：
A bug's life. Nonpathogenic Salmonella bacteria
interfere with NF-kB activation in gut epithelial cells. The
, 百拇医药
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
, 百拇医药
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.
相关文章：
Prokaryotic
, 百拇医药
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.
, 百拇医药
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), 百拇医药