Toll-like Receptor (TLR) 2 and TLR5, but Not TLR4, Are Required for Helicobacter pylori-induced NF-κB Activation and Chemokine Expression by Epithelial Cells

Smith, F; Mitchell, Anastasia; Li, Guolian; Ding, Song; Fitzmaurice, Ann Marie; Ryan, Kevin; Crowe, Sheila E.; Goldberg, Joanna B.

doi:10.1074/jbc.m305536200

Cited by 389 publications

(400 citation statements)

References 35 publications

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“…HCT116 cells do not express detectable amounts of TLR2 and TLR4. HEK293T cells also do not express detectable amounts of TLR4 and TLR2, consistent with previous reports (11,30). In contrast, HCT116 express both Nod1 and Nod2 mRNA.…”

Section: Methodssupporting

confidence: 79%

Differential Modulation of Nods Signaling Pathways by Fatty Acids in Human Colonic Epithelial HCT116 Cells

Zhao

Kwon

Huang

et al. 2007

Journal of Biological Chemistry

105

101

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Section: Methodssupporting

confidence: 79%

Differential Modulation of Nods Signaling Pathways by Fatty Acids in Human Colonic Epithelial HCT116 Cells

Zhao

Kwon

Huang

et al. 2007

Journal of Biological Chemistry

105

101

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“…5B). It has been reported that intestinal epithelial cells do not respond to LPS due to their lack of expression of the TLR4 coreceptor MD4 (1,2,54). Consistent with these reports, incubation of T84 cells with 10 g/ml of purified E. coli LPS increased the IL-8 secretion level only slightly.…”

Section: Campylobacter Increases Il-8 Secretion In Polarized Human Insupporting

confidence: 80%

Campylobacter-Induced Interleukin-8 Secretion in Polarized Human Intestinal Epithelial Cells RequiresCampylobacter-Secreted Cytolethal Distending Toxin- and Toll-Like Receptor-Mediated Activation of NF-κB

Zheng¹,

Meng²,

Zhao

et al. 2008

Infect Immun

113

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“…It may also be an evolutionarily acquired adaptive attribute of the mammary gland to help it fight infections since it is constantly under attack by invading pathogens. Furthermore, TLR2 has been shown to recognize LPS preparations from sources like Leptospira interrogans, Porphyromonas gingivalis, and Helicobacter pyroli, all non-enterobacteria [21,36,43]. Another study demonstrated TLR2/CD14 complex as the exogenous mediators of Trypanosoma cruzi induced inflammation [8].…”

Section: Discussionmentioning

confidence: 99%

Bacterial lipopolysaccharide induces increased expression of toll-like receptor (TLR) 4 and downstream TLR signaling molecules in bovine mammary epithelial cells

et al. 2007

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-Bovine mammary epithelial cells contribute to the innate immune response to intramammary infections by recognizing pathogens through specialized pattern recognition receptors. Toll-like receptor 4 (TLR4) is one such receptor that binds and is activated by lipopolysaccharide (LPS), a component of the outer envelope of Gram-negative bacteria. In this study, MAC-T cells (a bovine mammary epithelial cell line) were incubated in the presence or absence of increasing concentrations of LPS for 24 h. Expression of TLR2 and TLR4 were analyzed at both mRNA and protein levels by quantitative real-time PCR (qPCR) and flow cytometry, respectively. The mRNA of both receptors were up-regulated by all concentrations of LPS used (P < 0.01). Similarly, flow cytometry with specific antibodies against TLR2 and TLR4 detected increased surface expression of these proteins. Furthermore, expression of downstream TLR4 signaling molecules was examined by qPCR following varying exposure times to 1 μg/mL of LPS. Results demonstrate that the required adaptor molecules and transcription factors were up-regulated in a time-dependent manner. Both the MyD88 dependent and independent pathways in TLR4 signaling were activated in MAC-T cells. Expression of TOLLIP increased in response to LPS as did the pro-apoptotic protease, CASP8. These results suggest that the bovine mammary epithelium possesses the necessary immune repertoires required to achieve a robust defense against E. coli. The current findings, coupled with previous findings that S. aureus ligands induce up-regulation of TLR4, may indicate a positive adaptation by mammary epithelial cells to effectively respond to different types of mastitis pathogens.lipopolysaccharide / TLR4 and TLR2 / signal transduction / bovine mammary epithelial cells / mastitis

show abstract

Toll-like Receptor (TLR) 2 and TLR5, but Not TLR4, Are Required for Helicobacter pylori-induced NF-κB Activation and Chemokine Expression by Epithelial Cells

Abstract: Infection with

Cited by 389 publications

References 35 publications

Differential Modulation of Nods Signaling Pathways by Fatty Acids in Human Colonic Epithelial HCT116 Cells

Differential Modulation of Nods Signaling Pathways by Fatty Acids in Human Colonic Epithelial HCT116 Cells

Campylobacter-Induced Interleukin-8 Secretion in Polarized Human Intestinal Epithelial Cells RequiresCampylobacter-Secreted Cytolethal Distending Toxin- and Toll-Like Receptor-Mediated Activation of NF-κB

Bacterial lipopolysaccharide induces increased expression of toll-like receptor (TLR) 4 and downstream TLR signaling molecules in bovine mammary epithelial cells

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