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Mol. Cells 2009; 27(2): 257-261

Published online February 20, 2009

https://doi.org/10.1007/s10059-009-0031-1

© The Korean Society for Molecular and Cellular Biology

Chemokines Gene Expression of RAW 264.7 Cellsby Actinobacillus actinomycetemcomitans Lipopolysaccharide Using Microarray and RT-PCR Analysis

Jin Chung, Mun Jeoung Choi, So Yeon Jeong, Jong Suk Oh, Hyung Keun Kim

Received: July 29, 2008; Revised: November 7, 2008; Accepted: November 28, 2009

Abstract

Actinobacillus actinomycetemcomitans (A. actinomycetemcomitans) is an important pathogen casuing aggressive periodontitis. The present study was designed to investigate the chemokines expression regulated by A. actinomycetemcomitans lipopolysaccharide (LPS). Chemokines genes expression profiling was performed in Raw 264.7 cells by analyses of microarray and reverse transcription-polymerase chain reaction (RT-PCR). Microarray results showed that the induction of monocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-1? (MIP-1?), MIP-1?, MIP-1?, regulated upon activation, normal T-cell expressed and secreted (RANTES), macrophage inflammatory protein-2 (MIP-2), and interferon-? inducible protein 10 (IP 10) by A. actinomycetemcomitans LPS was increased to 12.5, 1.53, 9.09, 17.3, 2.82, 16.1, and 18.1 folds at 18 h, respectively. To check these chemo- kines expression by A. actinomycetemcomitans LPS, we examined gene expressions by RT-PCR, and found that the expression of MIP-1?, MIP-1?, RANTES, MIP-2, and IP 10 was increased 107.1, 93.6, 106.8, 86.5, and 162.0 folds at 18 h, respectively. These results indicate that A. actinomy-cetemcomitans LPS stimulates the several chemokines expressions (MIP-1?, MIP-1?, MIP-1?, RANTES, MIP-2, and IP 10) in Raw 264.7 cells.

Keywords A. actinomycetemcomitans LPS, IP 10, MCP-1, MIP-1, MIP-2, RANTES

Article

Communication

Mol. Cells 2009; 27(2): 257-261

Published online February 28, 2009 https://doi.org/10.1007/s10059-009-0031-1

Copyright © The Korean Society for Molecular and Cellular Biology.

Chemokines Gene Expression of RAW 264.7 Cellsby Actinobacillus actinomycetemcomitans Lipopolysaccharide Using Microarray and RT-PCR Analysis

Jin Chung, Mun Jeoung Choi, So Yeon Jeong, Jong Suk Oh, Hyung Keun Kim

Received: July 29, 2008; Revised: November 7, 2008; Accepted: November 28, 2009

Abstract

Actinobacillus actinomycetemcomitans (A. actinomycetemcomitans) is an important pathogen casuing aggressive periodontitis. The present study was designed to investigate the chemokines expression regulated by A. actinomycetemcomitans lipopolysaccharide (LPS). Chemokines genes expression profiling was performed in Raw 264.7 cells by analyses of microarray and reverse transcription-polymerase chain reaction (RT-PCR). Microarray results showed that the induction of monocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-1? (MIP-1?), MIP-1?, MIP-1?, regulated upon activation, normal T-cell expressed and secreted (RANTES), macrophage inflammatory protein-2 (MIP-2), and interferon-? inducible protein 10 (IP 10) by A. actinomycetemcomitans LPS was increased to 12.5, 1.53, 9.09, 17.3, 2.82, 16.1, and 18.1 folds at 18 h, respectively. To check these chemo- kines expression by A. actinomycetemcomitans LPS, we examined gene expressions by RT-PCR, and found that the expression of MIP-1?, MIP-1?, RANTES, MIP-2, and IP 10 was increased 107.1, 93.6, 106.8, 86.5, and 162.0 folds at 18 h, respectively. These results indicate that A. actinomy-cetemcomitans LPS stimulates the several chemokines expressions (MIP-1?, MIP-1?, MIP-1?, RANTES, MIP-2, and IP 10) in Raw 264.7 cells.

Keywords: A. actinomycetemcomitans LPS, IP 10, MCP-1, MIP-1, MIP-2, RANTES

Mol. Cells
Nov 30, 2023 Vol.46 No.11, pp. 655~725
COVER PICTURE
Kim et al. (pp. 710-724) demonstrated that a pathogen-derived Ralstonia pseudosolanacearum type III effector RipL delays flowering time and enhances susceptibility to bacterial infection in Arabidopsis thaliana. Shown is the RipL-expressing Arabidopsis plant, which displays general dampening of the transcriptional program during pathogen infection, grown in long-day conditions.

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