2005
DOI: 10.1128/iai.73.3.1452-1465.2005
|View full text |Cite
|
Sign up to set email alerts
|

Escherichia coliNissle 1917 Distinctively Modulates T-Cell Cycling and Expansion via Toll-Like Receptor 2 Signaling

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1
1
1

Citation Types

6
105
0
1

Year Published

2007
2007
2022
2022

Publication Types

Select...
8
1
1

Relationship

0
10

Authors

Journals

citations
Cited by 127 publications
(112 citation statements)
references
References 82 publications
6
105
0
1
Order By: Relevance
“…In addition, it has been shown that probiotic lactobacilli upregulate TLR2 expression (54,55). The observation that Nissle 1917 increased TLR4 and TLR5 expression may in part explain the ability of Nissle 1917 to induce a chemokine response following exposure to the basolateral surfaces of polarized epithelial cells (19) and the finding that Nissle 1917 ameliorates experimental colitis via activation of the TLR4 and TLR2 signaling pathways (14,47). The increase in signaling will also lead to induction of antimicrobial peptides that are induced following treatment with Nissle 1917 and will help to combat pathogenic bacteria (44).…”
Section: Discussionmentioning
confidence: 99%
“…In addition, it has been shown that probiotic lactobacilli upregulate TLR2 expression (54,55). The observation that Nissle 1917 increased TLR4 and TLR5 expression may in part explain the ability of Nissle 1917 to induce a chemokine response following exposure to the basolateral surfaces of polarized epithelial cells (19) and the finding that Nissle 1917 ameliorates experimental colitis via activation of the TLR4 and TLR2 signaling pathways (14,47). The increase in signaling will also lead to induction of antimicrobial peptides that are induced following treatment with Nissle 1917 and will help to combat pathogenic bacteria (44).…”
Section: Discussionmentioning
confidence: 99%
“…Recent in vitro data have demonstrated that E. coli Nissle 1917 induces intestinal epithelial cells to block adherence and inhibit invasion of various pathogenic strains (1,5). These observations proposed a soluble factor responsible for the inhibition of the pathogen itself or engagement of an epithelial defense mechanism (1) apart from anti-inflammatory influences on T-cell proliferation and function (38). We have recently provided a possible explanation for the probiotic effect of E. coli Nissle 1917 as it induces human ␤-defensin 2 (hBD-2) expression in cell culture in a time-and dose-dependent manner (41).…”
mentioning
confidence: 99%
“…В конце периода наблюдения в группе, получавшей Bifidobacterium lactis BВ12, индекс SCORAD [первоначально равный 16 (7-25)] составил 0 (0-3,8), тогда как в группе, получавшей Lactobacillus GG, эта вели-чина равнялась 1 (0,1-8,7). Среди детей, получавших смесь без введения пробиотиков, индекс SCORAD соста-вил 13,4 (4,(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)2). Таким образом, в данном исследо-вании показана не только эффективность пробиотиков для профилактики аллергии, но и более выраженное действие штамма Bifidobacterium lactis BВ12.…”
Section: обзор литературыunclassified