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Toll-like receptor 2-mediated gene expression in epithelial cells during Helicobacter pylori infection.
Helicobacter. 2005 Jun; 10(3):193-204.H

Abstract

BACKGROUND

Helicobacter pylori is the major pathogen causing chronic gastritis and peptic ulcer disease and is closely linked to gastric malignancy. We have previously shown that H. pylori-induced NF-(kappa)B activation and interleukin (IL)-8 secretion are mediated by Toll-like receptor (TLR) 2 in epithelial cells. However, the TLR2-mediated global gene expression profile of the epithelial cell during H. pylori infection is still unknown. The goal of this study was to identify TLR2-regulated genes in epithelial cells induced by H. pylori.

MATERIALS AND METHODS

The HEK293 and HEK-TLR2 cells were cocultured with H. pylori 26695 for 6 hours. Total RNA was extracted and hybridized to the Affymetrix human U133A microarray chipset, which contains 22,283 total probe sets including 14,285 genes. Data analyses were performed using affymetrix suite 5 software. The expression of selected genes in gastric epithelial cells AGS and MKN45 was monitored by quantitative reverse transcriptase-polymerase chain reaction (RT-PCR).

RESULTS

Forty-six genes, contained in 57 probe sets, were induced > 2-fold and three genes (five probe sets) decreased > 2-fold by H. pylori infection of HEK293 cells. Fifty-four genes, contained in 69 probe sets, were induced > 2-fold, whereas only 1 gene was repressed > 2-fold in H. pylori-infected HEK-TLR2 cells. Comparisons of genes induced in HEK293 or HEK-TLR2 cells identified 28 genes whose expression was dependent on the presence of TLR2. Seventeen genes were selected and their expression was assessed using the quantitative RT-PCR in gastric epithelial cells during H. pylori infection. Eight of the 17 genes showed distinct expression patterns in AGS and MKN45 cells after H. pylori stimulation.

CONCLUSIONS

The current study investigated the TLR2-mediated global gene changes after H. pylori stimulation in the epithelial cell system. This approach will be helpful in identifying genes whose expression is mediated by specific TLRs and in determining the cellular responses that are responsible for diverse signal pathways during H. pylori infection.

Authors+Show Affiliations

Department of Microbiology, The University of Virginia Health Sciences Center, Charlottesville, VA 22908, USA.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

15904477

Citation

Ding, Song-Ze, et al. "Toll-like Receptor 2-mediated Gene Expression in Epithelial Cells During Helicobacter Pylori Infection." Helicobacter, vol. 10, no. 3, 2005, pp. 193-204.
Ding SZ, Torok AM, Smith MF, et al. Toll-like receptor 2-mediated gene expression in epithelial cells during Helicobacter pylori infection. Helicobacter. 2005;10(3):193-204.
Ding, S. Z., Torok, A. M., Smith, M. F., & Goldberg, J. B. (2005). Toll-like receptor 2-mediated gene expression in epithelial cells during Helicobacter pylori infection. Helicobacter, 10(3), 193-204.
Ding SZ, et al. Toll-like Receptor 2-mediated Gene Expression in Epithelial Cells During Helicobacter Pylori Infection. Helicobacter. 2005;10(3):193-204. PubMed PMID: 15904477.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Toll-like receptor 2-mediated gene expression in epithelial cells during Helicobacter pylori infection. AU - Ding,Song-Ze, AU - Torok,Anastasia M, AU - Smith,Michael F,Jr AU - Goldberg,Joanna B, PY - 2005/5/21/pubmed PY - 2005/7/8/medline PY - 2005/5/21/entrez SP - 193 EP - 204 JF - Helicobacter JO - Helicobacter VL - 10 IS - 3 N2 - BACKGROUND: Helicobacter pylori is the major pathogen causing chronic gastritis and peptic ulcer disease and is closely linked to gastric malignancy. We have previously shown that H. pylori-induced NF-(kappa)B activation and interleukin (IL)-8 secretion are mediated by Toll-like receptor (TLR) 2 in epithelial cells. However, the TLR2-mediated global gene expression profile of the epithelial cell during H. pylori infection is still unknown. The goal of this study was to identify TLR2-regulated genes in epithelial cells induced by H. pylori. MATERIALS AND METHODS: The HEK293 and HEK-TLR2 cells were cocultured with H. pylori 26695 for 6 hours. Total RNA was extracted and hybridized to the Affymetrix human U133A microarray chipset, which contains 22,283 total probe sets including 14,285 genes. Data analyses were performed using affymetrix suite 5 software. The expression of selected genes in gastric epithelial cells AGS and MKN45 was monitored by quantitative reverse transcriptase-polymerase chain reaction (RT-PCR). RESULTS: Forty-six genes, contained in 57 probe sets, were induced > 2-fold and three genes (five probe sets) decreased > 2-fold by H. pylori infection of HEK293 cells. Fifty-four genes, contained in 69 probe sets, were induced > 2-fold, whereas only 1 gene was repressed > 2-fold in H. pylori-infected HEK-TLR2 cells. Comparisons of genes induced in HEK293 or HEK-TLR2 cells identified 28 genes whose expression was dependent on the presence of TLR2. Seventeen genes were selected and their expression was assessed using the quantitative RT-PCR in gastric epithelial cells during H. pylori infection. Eight of the 17 genes showed distinct expression patterns in AGS and MKN45 cells after H. pylori stimulation. CONCLUSIONS: The current study investigated the TLR2-mediated global gene changes after H. pylori stimulation in the epithelial cell system. This approach will be helpful in identifying genes whose expression is mediated by specific TLRs and in determining the cellular responses that are responsible for diverse signal pathways during H. pylori infection. SN - 1083-4389 UR - https://www.unboundmedicine.com/medline/citation/15904477/Toll_like_receptor_2_mediated_gene_expression_in_epithelial_cells_during_Helicobacter_pylori_infection_ L2 - https://doi.org/10.1111/j.1523-5378.2005.00311.x DB - PRIME DP - Unbound Medicine ER -