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本文引用的文献

1
Regulation of tissue homeostasis by NF-kappaB signalling: implications for inflammatory diseases.NF-κB信号通路对组织稳态的调控:对炎症性疾病的影响
Nat Rev Immunol. 2009 Nov;9(11):778-88. doi: 10.1038/nri2655.
2
Secretory IgA-mediated neutralization of Shigella flexneri prevents intestinal tissue destruction by down-regulating inflammatory circuits.分泌型IgA介导的福氏志贺菌中和作用通过下调炎症信号通路预防肠道组织破坏。
J Immunol. 2009 Nov 1;183(9):5879-85. doi: 10.4049/jimmunol.0901838. Epub 2009 Oct 14.
3
Crystal structure of a mucus-binding protein repeat reveals an unexpected functional immunoglobulin binding activity.一种黏液结合蛋白重复序列的晶体结构揭示了意想不到的功能性免疫球蛋白结合活性。
J Biol Chem. 2009 Nov 20;284(47):32444-53. doi: 10.1074/jbc.M109.040907. Epub 2009 Sep 16.
4
TSLP regulates intestinal immunity and inflammation in mouse models of helminth infection and colitis.在蠕虫感染和结肠炎的小鼠模型中,胸腺基质淋巴细胞生成素(TSLP)调节肠道免疫和炎症。
J Exp Med. 2009 Mar 16;206(3):655-67. doi: 10.1084/jem.20081499. Epub 2009 Mar 9.
5
Conditioned polarized Caco-2 cell monolayers allow to discriminate for the ability of gut-derived microorganisms to modulate permeability and antigen-induced basophil degranulation.条件极化的Caco-2细胞单层可用于区分肠道来源微生物调节通透性和抗原诱导嗜碱性粒细胞脱颗粒的能力。
Clin Exp Allergy. 2009 Apr;39(4):527-36. doi: 10.1111/j.1365-2222.2008.03185.x. Epub 2009 Jan 22.
6
IKK/NF-kappaB signaling in intestinal epithelial cells controls immune homeostasis in the gut.肠道上皮细胞中的IKK/NF-κB信号传导控制肠道内的免疫稳态。
Mucosal Immunol. 2008 Nov;1 Suppl 1:S54-7. doi: 10.1038/mi.2008.53.
7
The biology of intestinal immunoglobulin A responses.肠道免疫球蛋白A反应的生物学
Immunity. 2008 Jun;28(6):740-50. doi: 10.1016/j.immuni.2008.05.001.
8
Secretory IgA mediates retrotranscytosis of intact gliadin peptides via the transferrin receptor in celiac disease.在乳糜泻中,分泌型免疫球蛋白A通过转铁蛋白受体介导完整麦醇溶蛋白肽的逆向转运。
J Exp Med. 2008 Jan 21;205(1):143-54. doi: 10.1084/jem.20071204. Epub 2007 Dec 31.
9
Secretory IgA mediates bacterial translocation to dendritic cells in mouse Peyer's patches with restriction to mucosal compartment.分泌型免疫球蛋白A介导细菌向小鼠派尔集合淋巴结中的树突状细胞转移,并局限于黏膜区室。
J Immunol. 2007 Dec 1;179(11):7751-7. doi: 10.4049/jimmunol.179.11.7751.
10
IgA response to symbiotic bacteria as a mediator of gut homeostasis.对共生细菌的IgA反应作为肠道稳态的介质。
Cell Host Microbe. 2007 Nov 15;2(5):328-39. doi: 10.1016/j.chom.2007.09.013.

增强与分泌型免疫球蛋白 A 结合的益生菌对极化肠 Caco-2 细胞反应性。

Potentiation of polarized intestinal Caco-2 cell responsiveness to probiotics complexed with secretory IgA.

机构信息

R&D Laboratory of the Division of Immunology and Allergy, Centre Hospitalier Universitaire Vaudois, Rue du Bugnon, 1011 Lausanne, Switzerland.

出版信息

J Biol Chem. 2010 Oct 29;285(44):33906-13. doi: 10.1074/jbc.M110.135111. Epub 2010 Aug 20.

DOI:10.1074/jbc.M110.135111
PMID:20729211
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2962490/
Abstract

The precise mechanisms underlying the interaction between intestinal bacteria and the host epithelium lead to multiple consequences that remain poorly understood at the molecular level. Deciphering such events can provide valuable information as to the mode of action of commensal and probiotic microorganisms in the gastrointestinal environment. Potential roles of such microorganisms along the privileged target represented by the mucosal immune system include maturation prior, during and after weaning, and the reduction of inflammatory reactions in pathogenic conditions. Using human intestinal epithelial Caco-2 cell grown as polarized monolayers, we found that association of a Lactobacillus or a Bifidobacterium with nonspecific secretory IgA (SIgA) enhanced probiotic adhesion by a factor of 3.4-fold or more. Bacteria alone or in complex with SIgA reinforced transepithelial electrical resistance, a phenomenon coupled with increased phosphorylation of tight junction proteins zonula occludens-1 and occludin. In contrast, association with SIgA resulted in both enhanced level of nuclear translocation of NF-κB and production of epithelial polymeric Ig receptor as compared with bacteria alone. Moreover, thymic stromal lymphopoietin production was increased upon exposure to bacteria and further enhanced with SIgA-based complexes, whereas the level of pro-inflammatory epithelial cell mediators remained unaffected. Interestingly, SIgA-mediated potentiation of the Caco-2 cell responsiveness to the two probiotics tested involved Fab-independent interaction with the bacteria. These findings add to the multiple functions of SIgA and underscore a novel role of the antibody in interaction with intestinal bacteria.

摘要

肠道细菌与宿主上皮细胞相互作用的确切机制导致了多种后果,这些后果在分子水平上仍知之甚少。破译这些事件可以提供有价值的信息,了解共生菌和益生菌微生物在胃肠道环境中的作用模式。这些微生物在黏膜免疫系统这一重要靶点上的潜在作用包括在断奶前、期间和之后的成熟,以及减少在致病条件下的炎症反应。我们用人肠上皮细胞 Caco-2 进行培养,使其成为极化单层细胞,发现乳酸杆菌或双歧杆菌与非特异性分泌型免疫球蛋白 A(SIgA)的结合使益生菌的黏附增强了 3.4 倍或更多。细菌本身或与 SIgA 结合增强了跨上皮电阻,这一现象与紧密连接蛋白闭合蛋白-1 和闭合蛋白的磷酸化增加有关。相比之下,与 SIgA 结合导致核内 NF-κB 的易位水平和上皮多聚免疫球蛋白受体的产生都比单独的细菌增强。此外,暴露于细菌后胸腺基质淋巴细胞生成素的产生增加,并且与基于 SIgA 的复合物进一步增强,而上皮细胞促炎介质的水平保持不变。有趣的是,SIgA 介导的对两种益生菌的 Caco-2 细胞反应性的增强涉及与细菌的 Fab 非依赖性相互作用。这些发现增加了 SIgA 的多种功能,并强调了抗体在与肠道细菌相互作用中的新作用。