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双歧杆菌 HN019 对肠道上皮细胞 INT-407 的黏附和免疫调节作用。

Adhesion and immunomodulatory effects of Bifidobacterium lactis HN019 on intestinal epithelial cells INT-407.

机构信息

Department of Medical Microbiology and Parasitology, Institutes of Medical Sciences, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.

出版信息

World J Gastroenterol. 2010 May 14;16(18):2283-90. doi: 10.3748/wjg.v16.i18.2283.

DOI:10.3748/wjg.v16.i18.2283
PMID:20458767
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2868223/
Abstract

AIM

To elucidate the adherence and immunomodulatory properties of a probiotic strain Bifidobacterium lactis (B. lactis) HN019.

METHODS

Adhesion assays of B. lactis HN019 and Salmonella typhimurium (S. typhimurium) ATCC 14028 to INT-407 cells were carried out by detecting copies of species-specific genes with real-time polymerase chain reaction. Morphological study was further conducted by transmission electron microscopy. Interleukin-1beta (IL-1beta), interleukin-8, and tumor necrosis factor-alpha (TNF-alpha) gene expression were assessed while enzyme linked immunosorbent assay was used to detect IL-8 protein secretion.

RESULTS

The attachment of S. typhimurium ATCC 14028 to INT407 intestinal epithelial cells was inhibited significantly by B. lactis HN019. B. lactis HN019 could be internalized into the INT-407 cells and attenuated IL-8 mRNA level at both baseline and S. typhimurium-induced pro-inflammatory responses. IL-8 secretion was reduced while IL-1beta and TNF-alpha mRNA expression level remained unchanged at baseline after treated with B. lactis HN019.

CONCLUSION

B. lactis HN019 does not up-regulate the intestinal epithelium expressed pro-inflammatory cytokine, it showed the potential to protect enterocytes from an acute inflammatory response induced by enteropathogen.

摘要

目的

阐明益生菌双歧杆菌(B. lactis)HN019 的黏附和免疫调节特性。

方法

通过实时聚合酶链反应检测种特异性基因的拷贝数,对 B. lactis HN019 和鼠伤寒沙门氏菌(S. typhimurium)ATCC 14028 与 INT-407 细胞的黏附进行检测。通过透射电子显微镜进一步进行形态学研究。采用酶联免疫吸附试验检测白细胞介素-1β(IL-1β)、白细胞介素-8(IL-8)和肿瘤坏死因子-α(TNF-α)基因的表达。

结果

S. typhimurium ATCC 14028 与 INT407 肠道上皮细胞的黏附被 B. lactis HN019 显著抑制。B. lactis HN019 可以被内化到 INT-407 细胞中,并在基线和鼠伤寒沙门氏菌诱导的促炎反应中减弱 IL-8 mRNA 水平。B. lactis HN019 处理后,IL-8 分泌减少,而 IL-1β和 TNF-αmRNA 表达水平在基线时保持不变。

结论

B. lactis HN019 不会上调肠道上皮细胞表达的促炎细胞因子,它具有保护肠细胞免受肠道病原体引起的急性炎症反应的潜力。

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