Probiotic bacteria Bifidobacterium animalis MB5 and Lactobacillus rhamnosus GG protect intestinal Caco-2 cells from the inflammation-associated response induced by enterotoxigenic Escherichia coli K88
Probiotic bacteria Bifidobacterium animalis MB5 and Lactobacillus rhamnosus GG protect intestinal Caco-2 cells from the inflammation-associated response induced by enterotoxigenic Escherichia coli K88
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DOI：
10.1079/bjn20051681
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发表时间：
2006-06-01
影响因子：
3.6
通讯作者：
Mengheri, Elena
中科院分区：
文献类型：
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作者：
Roselli, Marianna;Finamore, Alberto;Mengheri, Elena
益生菌可能对病原体引起的肠道损伤提供保护，但其潜在机制仍在很大程度上未知。我们研究了动物双歧杆菌MB5和鼠李糖乳杆菌GG （LGG）是否通过抑制病原体附着细胞（ETEC致病性的第一步）和调节中性粒细胞募集（炎症的关键组成部分）来保护肠道Caco-2细胞免受肠产毒素大肠杆菌（ETEC） K88诱导的炎症相关反应。益生菌及其未消化或被蛋白酶消化的培养上清液部分降低了ETEC的粘附。ETEC活力不受B. animalis、LGG或其上清组分存在的影响，表明缺乏益生菌杀菌活性。益生菌及其上清组分，无论是未消化的还是被蛋白酶消化的，都能强烈抑制ETEC引起的中性粒细胞迁移。B. animalis和LGG均能抑制病原体诱导的IL-8、生长相关癌基因α和上皮中性粒细胞激活肽-78基因表达上调，这些基因是中性粒细胞迁移所必需的趋化因子。此外，益生菌可以抑制ec诱导的IL-1 β和tnf - α表达升高和转化生长因子α表达降低，这两种因子是趋化因子表达的调节因子。这些结果表明，B. animalis MB5和LGG可能通过调节趋化因子和细胞因子的表达，部分减少病原体粘附和抑制中性粒细胞迁移，从而保护肠细胞免受ETEC K88引起的炎症相关反应。
Probiotic bacteria may provide protection against intestinal damage induced by pathogens, but the underlying mechanisms are still largely unknown. We investigated whether Bifidobacterium animalis MB5 and Lactobacillus rhamnosus GG (LGG) protected intestinal Caco-2 cells from the inflammation-associated response induced by enterotoxigenic Escherichia coli (ETEC) K88, by inhibiting pathogen attachment to the cells, which is the first step of ETEC pathogenicity, and regulating neutrophil recruitment, a crucial component of inflammation. A partial reduction of ETEC adhesion was exerted by probiotics and their culture supernatant fractions either undigested or digested with proteases. ETEC viability was unaffected by the presence of B. animalis, LGG or their supernatant fractions in the culture medium, indicating an absence of probiotic bactericidal activity. Probiotics and their supernatant fractions, either undigested or digested with proteases, strongly inhibited the neutrophil transmigration caused by ETEC. Both B. animalis and LGG counteracted the pathogen-induced up regulation of IL-8, growth-related oncogene-alpha and epithelial neutrophil-activating peptide-78 gene expression, which are chemokines essential for neutrophil migration. Moreover, the probiotics prevented the ETEC-induced increased expression of IL-1 beta and TNF-alpha and decrease of transforming growth factor-alpha, which are regulators of chemokine expression. These results indicate that B. animalis MB5 and LGG protect intestinal cells from the inflammation-associated response caused by ETEC K88 by partly reducing pathogen adhesion and by counteracting neutrophil migration, probably through the regulation of chemokine and cytokine expression.