Molecular Modulation of Intestinal Epithelial Barrier: Contribution of Microbiota

被引:150
作者
Sharma, Renu [2 ]
Young, Christopher [1 ]
Neu, Josef [1 ]
机构
[1] Univ Florida, Gainesville, FL 32610 USA
[2] Univ Florida, Div Neonatol, Jacksonville, FL 32209 USA
来源
JOURNAL OF BIOMEDICINE AND BIOTECHNOLOGY | 2010年
基金
美国国家卫生研究院;
关键词
SEGMENTED FILAMENTOUS BACTERIA; INFLAMMATORY-BOWEL-DISEASE; PROTEIN-COUPLED RECEPTORS; TOLL-LIKE-RECEPTORS; IMMUNE-RESPONSES; GUT MICROBIOTA; INTRAEPITHELIAL LYMPHOCYTES; TIGHT JUNCTIONS; PANETH CELLS; GERM-FREE;
D O I
10.1155/2010/305879
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
The daunting task required of the gut-barrier to prevent luminal pathogens and harmful substances from entering into the internal milieu and yet promoting digestion and absorption of nutrients requires an exquisite degree of coordination between the different architectural units of this barrier. The complex integration and execution of these functions are superbly carried out by the intestinal mucosal (IM) surface. Exposed to trillions of luminal microbes, the IM averts threats by signaling to the innate immune system, through pattern recognition receptors (PRR), to respond to the commensal bacteria by developing tolerance (hyporesponsiveness) towards them. This system also acts by protecting against pathogens by elaborating and releasing protective peptides, cytokines, chemokines, and phagocytic cells. The IM is constantly sampling luminal contents and making molecular adjustments at its frontier. This article describes the topography of the IM and the mechanisms of molecular adjustments that protect the internal milieu, and also describes the role of the microbiota in achieving this goal.
引用
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页数:15
相关论文
共 94 条
[1]  
ABRAMS GD, 1963, LAB INVEST, V12, P355
[2]   TLR signaling in the gut in health and disease [J].
Abreu, MT ;
Fukata, M ;
Arditi, M .
JOURNAL OF IMMUNOLOGY, 2005, 174 (08) :4453-4460
[3]  
Adlerberth I, 2008, NESTLE NUTR WORKS SE, V62, P13, DOI 10.1159/000146245
[4]   Pathogen recognition by innate immunity and its signaling [J].
Akira, Shizuo .
PROCEEDINGS OF THE JAPAN ACADEMY SERIES B-PHYSICAL AND BIOLOGICAL SCIENCES, 2009, 85 (04) :143-156
[5]   The re-emerging role of the intestinal microflora in critical illness and inflammation: why the gut hypothesis of sepsis syndrome will not go away [J].
Alverdy, John C. ;
Chang, Eugene B. .
JOURNAL OF LEUKOCYTE BIOLOGY, 2008, 83 (03) :461-466
[6]   Mucosal cytokine network in inflammatory bowel disease [J].
Andoh, Akira ;
Yagi, Yuhki ;
Shioya, Makoto ;
Nishida, Atsushi ;
Tsujikawa, Tomoyuki ;
Fujiyama, Yoshihide .
WORLD JOURNAL OF GASTROENTEROLOGY, 2008, 14 (33) :5154-5161
[7]   RELMβ/FIZZ2 is a goblet cell-specific immune-effector molecule in the gastrointestinal tract [J].
Artis, D ;
Mei, LW ;
Keilbaugh, SA ;
He, WM ;
Brenes, M ;
Swain, GP ;
Knight, PA ;
Donaldson, DD ;
Lazar, MA ;
Miller, HRP ;
Schad, GA ;
Scott, P ;
Wu, GD .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2004, 101 (37) :13596-13600
[8]   Formyl peptide receptor-1 activation enhances intestinal epithelial cell restitution through phosphatidylinositol 3-kinase-dependent activation of Rac1 and Cdc42 [J].
Babbin, Brian A. ;
Jesaitis, Algirdas J. ;
Ivanov, Andrei I. ;
Kelly, Daina ;
Laukoetter, Mike ;
Nava, Porfirio ;
Parkos, Charles A. ;
Nusrat, Asma .
JOURNAL OF IMMUNOLOGY, 2007, 179 (12) :8112-8121
[9]  
BIOL MC, 1992, NUTRITION, V8, P368
[10]   Lymphoid tissue genesis induced by commensals through NOD1 regulates intestinal homeostasis [J].
Bouskra, Djahida ;
Brezillon, Christophe ;
Berard, Marion ;
Werts, Catherine ;
Varona, Rosa ;
Boneca, Ivo Gomperts ;
Eberl, Gerard .
NATURE, 2008, 456 (7221) :507-U34