ArticleInfection and immunity1999
Bacterial invasion is not required for activation of NF-kappaB in enterocytes.
Article in Infection and immunity, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
15 citing papers in PubMed, 61 citations in OpenAlex.
- Pathogenesis of human enterovirulent bacteria: lessons from cultured, fully differentiated human colon cancer cell lines.Microbiology and molecular biology reviews : MMBR · 2013Review
- Comparative secretome analysis of four isogenic Bacillus clausii probiotic strains.Proteome science · 2013Article
- Interplay between the QseC and QseE bacterial adrenergic sensor kinases in Salmonella enterica serovar Typhimurium pathogenesis.Infection and immunity · 2012Article
- Activation of NF-kappaB-dependent gene expression by Salmonella flagellins FliC and FljB.Biochemical and biophysical research communications · 2007Article
- Role of Toll-like receptors in health and diseases of gastrointestinal tract.World journal of gastroenterology · 2006Review
- Induction of interleukin-8 production via nuclear factor-kappaB activation in human intestinal epithelial cells infected with Vibrio vulnificus.Immunology · 2005Article
- Flagellin acting via TLR5 is the major activator of key signaling pathways leading to NF-kappa B and proinflammatory gene program activation in intestinal epithelial cells.BMC microbiology · 2004Article
- Pseudomonas aeruginosa slime glycolipoprotein is a potent stimulant of tumor necrosis factor alpha gene expression and activation of transcription activators nuclear factor kappa B and activator protein 1 in human monocytes.Infection and immunity · 2003Article
- Salmonella infection induces a hypersecretory phenotype in human intestinal xenografts by inducing cyclooxygenase 2.Infection and immunity · 2003Article
- Review
- Endotoxin, but not platelet-activating factor, activates nuclear factor-kappaB and increases IkappaBalpha and IkappaBbeta turnover in enterocytes.Immunology · 2002Article
- Salmonella typhimurium translocates flagellin across intestinal epithelia, inducing a proinflammatory response.The Journal of clinical investigation · 2001Article
- Salmonella enterica serovar typhimurium-dependent regulation of inducible nitric oxide synthase expression in macrophages by invasins SipB, SipC, and SipD and effector SopE2.Infection and immunity · 2000Article
- Salmonella typhimurium induces epithelial IL-8 expression via Ca(2+)-mediated activation of the NF-kappaB pathway.The Journal of clinical investigation · 2000Article
- Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Pathogenic enteric microorganisms induce the NF-kappaB-dependent expression of proinflammatory genes in intestinal epithelial cells. The purpose of the present study was to clarify the contribution of microbial invasion to the degradation of the regulatory protein Ikappa Balpha and the subsequent activation of NF-kappaB in cultured intestinal epithelial cells. Caco-2BBe cells were incubated with Salmonella dublin, Salmonella typhimurium, or a weakly invasive strain of E. coli. S. dublin and S. typhimurium (10(7) organisms/ml) induced equivalent concentration-dependent gel mobility shifts of an NF-kappaB consensus sequence that was preceded by Ikappa Balpha degradation. E. coli (10(7) organisms/ml) did not induce Ikappa Balpha degradation or NF-kappaB translocation. Pretreatment with cytochalasin D blocked invasion of all three strains but had no effect on Ikappa Balpha degradation or NF-kappaB activation. S. dublin and S. typhimurium adhered to Caco-2BBe cells 3- to 10-fold more than E. coli. NF-kappaB activation was prevented by physical separation of S. dublin from Caco-2BBe cells by a 0. 4-micrometers-pore-size filter. Our results imply that bacterial adhesion, rather than invasion or release of a secreted factor, is sufficient to induce IkappaBalpha degradation and NF-kappaB activation in intestinal epithelial cells. Our data suggest that strategies to reduce enteric inflammation should be directed to the reduction of bacterial enterocyte adhesion.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.