Lactobacillus plantarum Enhanced IL-22 Production in Natural Killer (NK) Cells That Protect the Integrity of Intestinal Epithelial Cell Barrier Damaged by Enterotoxigenic Escherichia coli.
Lactobacillus plantarum Enhanced IL-22 Production in Natural Killer (NK) Cells That Protect the Integrity of Intestinal Epithelial Cell Barrier Damaged by Enterotoxigenic Escherichia coli.
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植物乳杆菌增强自然杀伤 (NK) 细胞中 IL-22 的产生，从而保护被产肠毒素大肠杆菌破坏的肠上皮细胞屏障的完整性
DOI：
10.3390/ijms18112409
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发表时间：
2017-11-13
影响因子：
5.6
通讯作者：
Yang X
中科院分区：
文献类型：
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作者：
Qiu Y;Jiang Z;Hu S;Wang L;Ma X;Yang X
产生白细胞介素 (IL)-22 的自然杀伤 (NK) 细胞可保护肠道上皮细胞屏障免受病原体侵害。我们实验室之前发现一株益生菌植物乳杆菌（L. plantarum，LP）可以显着改善猪的粘膜屏障完整性和小肠功能。然而，尚不清楚 LP 是否通过与肠道 NK 细胞的相互作用而使肠粘膜屏障受益。因此，本研究的重点是LP刺激的NK细胞对减轻产肠毒素大肠杆菌（ETEC）引起的上皮细胞屏障完整性损伤的治疗作用。结果表明，LP能有效提高NK细胞中天然细胞毒性受体（NCR）家族的蛋白水平，以及IL-22 mRNA和蛋白的表达水平。 LP 刺激的 NK 细胞转移可在 NCM460 细胞中提供针对 ETEC K88 诱导的肠上皮屏障损伤的保护。我们发现LP刺激的NK细胞可以部分抵消ETEC K88引起的NCM460细胞单层跨上皮电阻（TEER）的降低，并增加ETEC K88感染的NCM460细胞中ZO-1和occludin mRNA和蛋白的表达。此外，将LP刺激的NK细胞添加到ETEC K88感染的NCM460细胞中，NCM460细胞的IL-22R1、p-Stat3和p-Tyk2表达增加。机制实验表明，当使用多克隆抗IL-22抗体阻断IL-22产生时，LP刺激的NK细胞失去了维持ETEC K88攻击的NCM460细胞TEER的功能。总的来说，我们的结果表明，LP 刺激 NK 可以增强 IL-22 的产生，这可能能够防御 ETEC 引起的肠上皮屏障完整性损伤。
Interleukin (IL)-22-producing Natural Killer (NK) cells protect the gut epithelial cell barrier from pathogens. A strain of probiotics, Lactobacillus plantarum (L. plantarum, LP), was previously found by our laboratory to significantly improve the mucosal barrier integrity and function of the small intestine in pigs. However, it was unclear whether LP benefited the intestinal mucosal barrier via interactions with the intestinal NK cells. The present study, therefore, was focused on the therapeutic effect of NK cells that were stimulated by LP on attenuating enterotoxigenic Escherichia coli (ETEC)-induced the damage to the integrity of the epithelial cell barrier. The results showed that LP can efficiently increase protein levels of the natural cytotoxicity receptor (NCR) family, and the expression levels of IL-22 mRNA and protein in NK cells. Transfer of NK cells stimulated by LP conferred protection against ETEC K88-induced intestinal epithelial barrier damage in NCM460 cells. We found that NK cells stimulated by LP could partially offset the reduction in NCM460 cell monolayers transepithelial electrical resistance (TEER) caused by ETEC K88, and increase ZO-1 and occludin mRNA and protein expressions by ETEC K88-infected NCM460 cells. Furthermore, adding NK cells that were stimulated by LP to ETEC K88-infected NCM460cells, IL-22R1, p-Stat3, and p-Tyk2 expression by NCM460 cells was increased. Mechanistic experiment showed that NK cells stimulated by LP lost the function of maintaining TEER of NCM460 cells challenged with ETEC K88, when polyclonal anti-IL-22 antibody was used to block IL-22 production. Collectively, our results suggested that LP stimulation of NK could enhance IL-22 production, which might be able to provide defense against ETEC-induced damage to the integrity of intestinal epithelial barrier.
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影响因子：
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作者：
Rizzello V;Bonaccorsi I;Dongarrà ML;Fink LN;Ferlazzo G
通讯作者：
Ferlazzo G
DOI：
10.1084/jem.20082683
发表时间：
2009-07-06
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Pickert G;Neufert C;Leppkes M;Zheng Y;Wittkopf N;Warntjen M;Lehr HA;Hirth S;Weigmann B;Wirtz S;Ouyang W;Neurath MF;Becker C
通讯作者：
Becker C
影响因子：
30.3
作者：
Tsai PY;Zhang B;He WQ;Zha JM;Odenwald MA;Singh G;Tamura A;Shen L;Sailer A;Yeruva S;Kuo WT;Fu YX;Tsukita S;Turner JR
通讯作者：
Turner JR
影响因子：
30.3
作者：
Pham TA;Clare S;Goulding D;Arasteh JM;Stares MD;Browne HP;Keane JA;Page AJ;Kumasaka N;Kane L;Mottram L;Harcourt K;Hale C;Arends MJ;Gaffney DJ;Sanger Mouse Genetics Project;Dougan G;Lawley TD
通讯作者：
Lawley TD
影响因子：
8
作者：
通讯作者：
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