Membrane-Anchored CD14 Is Important for Induction of Interleukin-8 by Lipopolysaccharide and Peptidoglycan in Uroepithelial Cells

Shimizu, Toshiaki; Yokota, Shinichi; Takahashi, Satoshi; Kunishima, Yasuharu; Takeyama, Koh; Masumori, Naoya; Takahashi, Atsushi; Matsukawa, Masanori; Itoh, Naoki; Tsukamoto, Taiji; Fujii, Nobuhiro

doi:10.1128/cdli.11.5.969-976.2004

Cited by 32 publications

(28 citation statements)

References 35 publications

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“…The quantitative nature of the PCR was validated by the linearity of the determination curve at various concentrations of RNA. In accordance with previous papers, the primer sets used were as follows: cystatin A (37), cystatin C (40); TLRs 1,5,6,7,8,9, and 10 (13); TLR2, TLR4, and glyceraldehyde-3=-phosphate dehydrogenase (GAPDH) (33); and TLR3 (28). Primer sets for adenosine receptors A 1 , A 2A , A 2B , and A 3 were as described by Schön et al (31), except for the reverse primer of A 2A (5=-CTGCTTCAGCTGTCGTCGC G-3=).…”

Section: Methodsmentioning

confidence: 99%

Imiquimod Suppresses Propagation of Herpes Simplex Virus 1 by Upregulation of Cystatin A via the Adenosine Receptor A₁Pathway

Kan

Okabayashi

Yokota

et al. 2012

J Virol

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Imiquimod is recognized as an agonist for Toll-like receptor 7 (TLR7) in immunocompetent cells. TLR7, as well as TLR3 and TLR8, triggers the immune responses, such as the production of type I interferons (IFNs) and proinflammatory cytokines via recognition of viral nucleic acids in the infected cells. In this study, we proposed that imiquimod has an IFN-independent antiviral effect in nonimmune cells. Imiquimod, but not resiquimod, suppressed replication of human herpes simplex virus 1 (HSV-1) in FL cells. We analyzed alternation of gene expression by treatment with imiquimod using microarray analysis. Neither type I IFNs, nor TLRs, nor IFN-inducible antiviral genes were induced in imiquimod-treated FL cells. Cystatin A, a host cysteine protease inhibitor, was strongly upregulated by imiquimod and took a major part in the anti-HSV-1 activity deduced by the suppression experiment using its small interfering RNA. Upregulation of cystatin A was suggested to be mediated by antagonizing adenosine receptor A 1 and activating the protein kinase A pathway. Imiquimod, but not resiquimod, was shown to interact with adenosine receptor A 1 . Imiquimod-induced anti-HSV-1 activity was observed in other cells, such as HeLa, SiHa, and CaSki cells, in a manner consistent with the cystatin A induction by imiquimod. These results indicated that imiquimod acted as an antagonist for adenosine receptor A 1 and induced a host antiviral protein, cystatin A. The process occurred independently of TLR7 and type I IFNs.

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Section: Methodsmentioning

confidence: 99%

Imiquimod Suppresses Propagation of Herpes Simplex Virus 1 by Upregulation of Cystatin A via the Adenosine Receptor A₁Pathway

Kan

Okabayashi

Yokota

et al. 2012

J Virol

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“…Reverse transcription-PCR (RT-PCR) was performed by using the OneStep RT-PCR kit (Qiagen). mRNA levels of TLR2, TLR4, and glyceraldehyde-3-phosphate dehydrogenase (GAPDH), used as a control, were determined as previously described (27). The quantitative nature of the RT-PCR was validated by the linearity of the determination curve at various concentrations of RNA.…”

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confidence: 99%

“…Flow cytometry was performed by using a FACSCalibur (Becton Dickinson, San Jose, CA) as previously described (27,37). Phycoerythrin-labeled mouse monoclonal antibodies against TLR2 (clone TL2.1), TLR4 (HTA125), and CD14 (61D3), and their isotype controls, phycoerythrinlabeled mouse monoclonal immunoglobulin G1 (IgG1) and IgG2a, were purchased from eBioscience (San Diego, CA).…”

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confidence: 99%

Helicobacter pylori Lipopolysaccharides Upregulate Toll-Like Receptor 4 Expression and Proliferation of Gastric Epithelial Cells via the MEK1/2-ERK1/2 Mitogen-Activated Protein Kinase Pathway

et al. 2010

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Helicobacter pylori is recognized as an etiological agent of gastroduodenal diseases. H. pylori produces various toxic substances, including lipopolysaccharide (LPS). However, H. pylori LPS exhibits extremely weakly endotoxic activity compared to the typical LPS, such as that produced by Escherichia coli, which acts through Toll-like receptor 4 (TLR4) to induce inflammatory molecules. The gastric epithelial cell lines MKN28 and MKN45 express TLR4 at very low levels, so they show very weak interleukin-8 (IL-8) production in response to E. coli LPS, but pretreatment with H. pylori LPS markedly enhanced IL-8 production induced by E. coli LPS by upregulating TLR4 via TLR2 and the MEK1/2-ERK1/2 pathway. The transcription factor NF-Y was activated by this signal and promoted transcription of the tlr4 gene. These MEK1/2-ERK1/2 signal-mediated activities were more potently activated by LPS carrying a weakly antigenic epitope, which is frequently found in gastric cancers, than by LPS carrying a highly antigenic epitope, which is associated with chronic gastritis. H. pylori LPS also augmented the proliferation rate of gastric epithelial cells via the MEK1/2-ERK1/2 pathway. H. pylori LPS may be a pathogenic factor causing gastric tumors by enhancing cell proliferation and inflammation via the MEK1/2-ERK1/2 mitogenactivated protein kinase cascade in gastric epithelial cells.

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“…The different response to sCD14 observed by us and by Asai et al (2003a) could be due to a difference in the contamination degree and molecules in the peptidoglycan used by the two groups. Shimizu et al (2004) showed that cells expressing mCD14 did not need exogenous sCD14 for TLR2-mediated peptidiglycan signalling. This result is consistent with our observation that peptidoglycan stimulated cells in an sCD14-independent manner.…”

Section: Discussionmentioning

confidence: 99%

Phenol/water extract of Treponema socranskii subsp. socranskii as an antagonist of Toll-like receptor 4 signalling

et al. 2006

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Treponema socranskii is one of the most frequently found oral spirochaetes in periodontitis and endodontic infections. LPS or glycolipids from bacteria are potent stimulators of innate immune and inflammatory systems. In this study the bioactivity of a phenol/water extract from T. socranskii subsp. socranskii (TSS-P) was analysed. TSS-P showed minimal endotoxicity and no inducing potential for proinflammatory cytokines (TNF-α and IL-8) or for intercellular adhesion molecule-1 (ICAM-1) in human monocyte cell line THP-1 cells and primary cultured human gingival fibroblasts. Rather, it inhibited ICAM-1 expression and IL-8 secretion from cells stimulated by the LPS of Escherichia coli and Actinobacillus actinomycetemcomitans, which are known to be Toll-like receptor 4 (TLR4) agonists. However, this antagonistic activity was not shown in cells stimulated by peptidoglycan or IL-1β. As its antagonistic mechanism, TSS-P blocked the binding of E. coli LPS to LPS-binding protein (LBP) and CD14, which are molecules involved in the recruitment of LPS to the cell membrane receptor complex TLR4–MD-2 for the intracellular signalling of LPS. TSS-P itself did not bind to MD-2 or THP-1 cells, but inhibited the binding of E. coli LPS to MD-2 or to the cells in the presence of serum (which could be replaced by recombinant human LBP and recombinant human CD14). The results suggest that TSS-P acts as an antagonist of TLR4 signalling by interfering with the functioning of LBP/CD14.

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Membrane-Anchored CD14 Is Important for Induction of Interleukin-8 by Lipopolysaccharide and Peptidoglycan in Uroepithelial Cells

Abstract: We investigated the induction of interleukin-8 (IL-8

Cited by 32 publications

References 35 publications

Imiquimod Suppresses Propagation of Herpes Simplex Virus 1 by Upregulation of Cystatin A via the Adenosine Receptor A₁Pathway

Imiquimod Suppresses Propagation of Herpes Simplex Virus 1 by Upregulation of Cystatin A via the Adenosine Receptor A₁Pathway

Helicobacter pylori Lipopolysaccharides Upregulate Toll-Like Receptor 4 Expression and Proliferation of Gastric Epithelial Cells via the MEK1/2-ERK1/2 Mitogen-Activated Protein Kinase Pathway

Phenol/water extract of Treponema socranskii subsp. socranskii as an antagonist of Toll-like receptor 4 signalling

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Membrane-Anchored CD14 Is Important for Induction of Interleukin-8 by Lipopolysaccharide and Peptidoglycan in Uroepithelial Cells

Abstract: We investigated the induction of interleukin-8 (IL-8

Cited by 32 publications

References 35 publications

Imiquimod Suppresses Propagation of Herpes Simplex Virus 1 by Upregulation of Cystatin A via the Adenosine Receptor A1Pathway

Imiquimod Suppresses Propagation of Herpes Simplex Virus 1 by Upregulation of Cystatin A via the Adenosine Receptor A1Pathway

Helicobacter pylori Lipopolysaccharides Upregulate Toll-Like Receptor 4 Expression and Proliferation of Gastric Epithelial Cells via the MEK1/2-ERK1/2 Mitogen-Activated Protein Kinase Pathway

Phenol/water extract of Treponema socranskii subsp. socranskii as an antagonist of Toll-like receptor 4 signalling

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Imiquimod Suppresses Propagation of Herpes Simplex Virus 1 by Upregulation of Cystatin A via the Adenosine Receptor A₁Pathway

Imiquimod Suppresses Propagation of Herpes Simplex Virus 1 by Upregulation of Cystatin A via the Adenosine Receptor A₁Pathway