Interaction between enteric epithelial cells and Peyer's patch lymphocytes in response to Shigella lipopolysaccharide: Effect on nitric oxide and IL-6 release

瞄准：在氮的氧化物的版本上调查在伤寒上皮细胞和 Peyer 的补丁的淋巴细胞之间的相互作用的效果(没有) 并且响应志贺氏菌属脂肪的多糖(LPS ) 的 IL-6。方法：人的结肠的上皮细胞(Caco-2 ) 是有 Peyer 的补丁从的淋巴细胞的混合 cocultured 野类型(C57 老鼠) 并且可诱导没有 synthase 大美人老鼠，并且与志贺氏菌属 F2a-12 LPS 质问了。版本没有并且 mIL-6 被 Griess 比色测定和连接酶的免疫吸着剂试金(ELISA ) 分别地测量。结果：当 LPS 挑战不在时，不在 Caco-2 上皮细胞的培养基然而并非在 Peyer 的补丁的淋巴细胞被检测，并且 NO 版本在有从也的淋巴细胞的两 cocultures 是进一步起来调整的野类型或 i NOS 大美人老鼠，与一显著地，高水平与 i NOS 猛烈淋巴细胞在 coculture 观察了。在为 24-h 的志贺氏菌属 F2a-12 LPS 挑战以后，没有生产显著地从野类型的老鼠然而并非从 i NOS 猛烈老鼠与 Peyer 的补丁的淋巴细胞在独自一个的 Caco-2 和 coculture 被增加。LPS 被发现从淋巴细胞刺激 mIL-6 的版本，它被 coculture 与 Caco-2 上皮细胞压制。在从 i NOS 猛烈老鼠的淋巴细胞的导致 LPS 的 mIL-6 生产从野类型的老鼠比那显著地大。结论：Peyer 的补丁的淋巴细胞从伤寒维持没有生产的组成的基础水平上皮的房间 Caco-2。从 Peyer 的补丁的淋巴细胞的导致 LPS 的 mIL-6 版本被 cocultured 上皮细胞压制。当没有变化在在淋巴细胞从的没有生产是可检测的时野类型并且在 LPS 前后的 i NOS 猛烈老鼠质问，不从淋巴细胞看起来起一个禁止的作用在上皮响应 LPS 的没有版本和他们的自己的 mIL-6 版本。

AIM： TO investigate the effect of interaction between enteric epithelial cells and lymphocytes of Peyer＇s patch on the release of nitric oxide （NO） and IL-6 in response to Shigella lipopolysaccharide （LPS）. METHODS： Human colonic epithelial cells （Caco-2） were mixed cocultured with lymphocytes of Peyer＇s patch from wild-type （C57 mice） and inducible NO synthase knockout mice, and challenged with Shigella F2a-12 LPS. Release of NO and raiL-6 was measured by Griess colorimetric assay and enzyme-linked immunosorbent assay （ELISA）, respectively. RESULTS： In the absence of LPS challenge, NO was detected in the culture medium of Caco-2 epithelial cells but not in lymphocytes of Peyer＇s patch, and the NO release was further up-regulated in both cocultures with lymphocytes from either the wild-type or iNOS knockout mice, with a significantly higher level observed in the coculture with iNOS knockout lymphocytes. After Shigella F2a-12 LPS challenge for 24-h, NO production was significantly increased in both Caco-2 alone and the coculture with lymphocytes of Peyer＇s patch from the wild-type mice but not from iNOS knockout mice. LPS was found to stimulate the release of mIL-6 from lymphocytes, which was suppressed by coculture with Caco-2 epithelial cells. The LPS-induced mIL-6 production in lymphocytes from iNOS knockout mice was significantly greater than that from the wild-type mice. CONCLUSION： Lymphocytes of Peyer＇s patch maintain a constitutive basal level of NO production from the enteric epithelial cell Caco-2. LPS-induced mIL-6 release from lymphocytes of Peyer＇s patch is suppressed by the cocultured epithelial cells. While no changes are detectable in NO production in lymphocytes from both wild-type and iNOS knockout mice before and after LPS challenge, NO from lymphocytes appears to play an inhibitory role in epithelial NO release and their own mIL-6 release in response to LPS.