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本文引用的文献

1
Salmonella enterica Typhimurium SipA induces CXC-chemokine expression through p38MAPK and JUN pathways.鼠伤寒沙门氏菌SipA通过p38丝裂原活化蛋白激酶和JUN途径诱导CXC趋化因子表达。
Microbes Infect. 2009 Feb;11(2):302-10. doi: 10.1016/j.micinf.2008.12.005. Epub 2008 Dec 16.
2
Multidrug resistance-associated transporter 2 regulates mucosal inflammation by facilitating the synthesis of hepoxilin A3.多药耐药相关转运蛋白2通过促进肝氧素A3的合成来调节黏膜炎症。
J Immunol. 2008 Dec 1;181(11):8044-52. doi: 10.4049/jimmunol.181.11.8044.
3
Shigella flexneri type III secretion system effectors OspB and OspF target the nucleus to downregulate the host inflammatory response via interactions with retinoblastoma protein.福氏志贺菌Ⅲ型分泌系统效应蛋白OspB和OspF通过与视网膜母细胞瘤蛋白相互作用靶向细胞核,从而下调宿主炎症反应。
Mol Microbiol. 2009 Jan;71(2):350-68. doi: 10.1111/j.1365-2958.2008.06524.x. Epub 2008 Nov 14.
4
Study of Helicobacter pullorum proinflammatory properties on human epithelial cells in vitro.鸡源幽门螺杆菌对人上皮细胞促炎特性的体外研究。
Gut. 2009 May;58(5):629-35. doi: 10.1136/gut.2007.144501. Epub 2008 Jun 25.
5
Distinct isoforms of phospholipase A2 mediate the ability of Salmonella enterica serotype typhimurium and Shigella flexneri to induce the transepithelial migration of neutrophils.磷脂酶A2的不同亚型介导了鼠伤寒沙门氏菌和福氏志贺氏菌诱导中性粒细胞跨上皮迁移的能力。
Infect Immun. 2008 Aug;76(8):3614-27. doi: 10.1128/IAI.00407-08. Epub 2008 May 27.
6
Adhesion molecules involved in hepoxilin A3-mediated neutrophil transepithelial migration.参与hepoxilin A3介导的中性粒细胞跨上皮迁移的黏附分子。
Clin Exp Immunol. 2008 Feb;151(2):297-305. doi: 10.1111/j.1365-2249.2007.03551.x. Epub 2007 Nov 15.
7
The NleE/OspZ family of effector proteins is required for polymorphonuclear transepithelial migration, a characteristic shared by enteropathogenic Escherichia coli and Shigella flexneri infections.效应蛋白的NleE/OspZ家族是多形核白细胞跨上皮迁移所必需的,这是肠道致病性大肠杆菌和福氏志贺菌感染所共有的特征。
Infect Immun. 2008 Jan;76(1):369-79. doi: 10.1128/IAI.00684-07. Epub 2007 Nov 5.
8
The proinflammatory CXC-chemokines GRO-alpha/CXCL1 and MIG/CXCL9 are concomitantly expressed in ulcerative colitis and decrease during treatment with topical corticosteroids.促炎CXC趋化因子GRO-α/CXCL1和MIG/CXCL9在溃疡性结肠炎中同时表达,并在局部使用皮质类固醇治疗期间减少。
Int J Colorectal Dis. 2007 Dec;22(12):1421-7. doi: 10.1007/s00384-007-0370-3. Epub 2007 Aug 17.
9
Beneficial suicide: why neutrophils die to make NETs.有益的自杀:中性粒细胞为何通过死亡来形成中性粒细胞胞外陷阱。
Nat Rev Microbiol. 2007 Aug;5(8):577-82. doi: 10.1038/nrmicro1710.
10
Shigella's ways of manipulating the host intestinal innate and adaptive immune system: a tool box for survival?志贺氏菌操纵宿主肠道先天性和适应性免疫系统的方式:生存的工具箱?
Immunol Cell Biol. 2007 Feb-Mar;85(2):119-29. doi: 10.1038/sj.icb7100025. Epub 2007 Jan 9.

中性粒细胞在肠道炎症中的作用。

The role of neutrophils in the event of intestinal inflammation.

机构信息

The Department of Molecular Genetics and Microbiology, University of Massachusetts Medical School, Worcester, MA, USA.

出版信息

Curr Opin Pharmacol. 2009 Dec;9(6):697-701. doi: 10.1016/j.coph.2009.10.004. Epub 2009 Oct 24.

DOI:10.1016/j.coph.2009.10.004
PMID:19854677
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2798135/
Abstract

The transmigration of polymorphonuclear leukocytes (PMNs; neutrophils) into the intestinal lumen is a classical phenomenon associated with a wide variety of disease states, including those of both pathogenic and autoimmune/idiopathic origin. While PMNs are highly effective at killing invading pathogens by releasing microbiocidal products, excessive or unnecessary release of these substances can cause substantial damage to the intestinal epithelium. Therefore, it is necessary to understand the underlying mechanisms that lure neutrophils into the lumen allowing them to perform their desired functions, so that researchers may begin to identify which processes may be potential targets for inhibiting the transmigration of PMNs during noninfectious states.

摘要

多形核白细胞(PMN;中性粒细胞)向肠腔的迁移是一种与多种疾病状态相关的经典现象,包括病原性和自身免疫/特发性疾病。虽然 PMN 通过释放杀菌产物在杀死入侵病原体方面非常有效,但这些物质的过度或不必要释放会对肠上皮造成实质性损伤。因此,有必要了解吸引中性粒细胞进入肠腔使其发挥预期功能的潜在机制,以便研究人员能够开始确定哪些过程可能是在非感染状态下抑制 PMN 迁移的潜在靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86ec/2798135/ceeb8c666cd1/nihms-162030-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86ec/2798135/ceeb8c666cd1/nihms-162030-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86ec/2798135/ceeb8c666cd1/nihms-162030-f0001.jpg