Transcriptional responses of murine macrophages to infection with Yersinia enterocolitica

Hoffmann, Reinhard; Erp, Katrin van; Trülzsch, Konrad; Heesemann, Jürgen

doi:10.1111/j.1462-5822.2004.00365.x

Cited by 49 publications

(58 citation statements)

References 45 publications

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“…The Gramnegative lung pathogen P. aeruginosa also induced KLF2 expression in airway epithelial cells (22), suggesting that KLF2 induction is not restricted to pneumococci or Gram-positive bacteria. Moreover, global gene-expression analysis showed increased KLF2 mRNA expression in Yersinia enterocolitica-infected cells (32,33). These data strengthen the hypothesis that KLF2 is involved in the regulation of the host response to bacterial infections.…”

Section: Discussionsupporting

confidence: 72%

TLR2- and Nucleotide-Binding Oligomerization Domain 2-Dependent Krüppel-Like Factor 2 Expression Downregulates NF-κB–Related Gene Expression

Zahlten

Steinicke

Opitz

et al. 2010

The Journal of Immunology

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The release of potent proinflammatory mediators is not only central for mounting an efficient host response, but also bears the risk for deleterious excessive tissue-damaging inflammation. This is highlighted in severe pneumococcal pneumonia, in which the delicate balance between a robust inflammatory response to kill pneumococci and loss of organ function determines the outcome of disease. In this study, we tested the hypothesis that Krüppel-like factor (KLF)2 counterregulates pneumococci- and pattern recognition receptor-related human lung cell activation. Pneumococci induced KLF2 expression in vitro and in a murine pneumonia model. Activation of TLR2- and nucleotide-binding oligomerization domain protein 2-related signaling induced KLF2 expression in a PI3K-dependent manner. Overexpression of KLF2 downregulated pneumococci-, TLR2-, and nucleotide-binding oligomerization domain protein 2-related NF-κB–dependent gene expression and IL-8 release, whereas small interfering RNA-based silencing of KLF2 provoked an enhanced inflammatory response. KLF2-dependent downregulation of NF-κB activity is partly reversible by overexpression of the histone acetylase p300/CREB-binding protein-associated factor. In conclusion, KLF2 may act as a counterregulatory transcription factor in pneumococci- and pattern recognition receptor-related proinflammatory activation of lung cells, thereby preventing lung hyperinflammation and subsequent organ failure.

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Section: Discussionsupporting

confidence: 72%

TLR2- and Nucleotide-Binding Oligomerization Domain 2-Dependent Krüppel-Like Factor 2 Expression Downregulates NF-κB–Related Gene Expression

Zahlten

Steinicke

Opitz

et al. 2010

The Journal of Immunology

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“…KLF6 binding has been shown to alter the transcription of a number of genes with roles in cell proliferation, development, and tissue repair (28,29,63). Increased expression of KLF2 following infection of murine macrophages with Yersinia enterocolitica has been reported (1,19,54). Additionally, induction of both KLF2 and KLF6 has been documented following infection of tracheal epithelial cells with Staphylococcus aureus (40).…”

Section: Discussionmentioning

confidence: 99%

“…These genes were also chosen because they showed altered transcription in response to PAO1, but not the rsmA mutant, compared to that in uninfected cells. In addition, KLF2 and KLF6 expression has been shown to be induced by both gram-positive (40) and gram-negative (1,19,22,54) bacteria. However, the mechanism(s) behind the induction of these genes has not yet been elucidated.…”

Section: Vol 74 2006mentioning

confidence: 99%

Pseudomonas aeruginosaInfection of Airway Epithelial Cells Modulates Expression of Kruppel-Like Factors 2 and 6 via RsmA-Mediated Regulation of Type III Exoenzymes S and Y

et al. 2006

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Pseudomonas aeruginosa is an important opportunistic pathogen which is capable of causing both acute and chronic infections in immunocompromised patients. Successful adaptation of the bacterium to its host environment relies on the ability of the organism to tightly regulate gene expression. RsmA, a small RNA-binding protein, controls the expression of a large number of virulence-related genes in P. aeruginosa, including those encoding the type III secretion system and associated effector proteins, with important consequences for epithelial cell morphology and cytotoxicity. In order to examine the influence of RsmA-regulated functions in the pathogen on gene expression in the host, we compared global expression profiles of airway epithelial cells in response to infection with P. aeruginosa PAO1 and an rsmA mutant. The RsmA-dependent response of host cells was characterized by significant changes in the global transcriptional pattern, including the increased expression of two Kruppel-like factors, KLF2 and KLF6. This increased expression was mediated by specific type III effector proteins. ExoS was required for the enhanced expression of KLF2, whereas both ExoS and ExoY were required for the enhanced expression of KLF6. Neither ExoT nor ExoU influenced the expression of the transcription factors. Additionally, the increased gene expression of KLF2 and KLF6 was associated with ExoS-mediated cytotoxicity. Therefore, this study identifies for the first time the human transcription factors KLF2 and KLF6 as targets of the P. aeruginosa type III exoenzymes S and Y, with potential importance in host cell death.

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“…There have been many studies using microarray data to compare immune gene expression programs under different conditions [29][30][31] .…”

Section: Applications To Cross-species Gene Regulatory Network Discoverymentioning

confidence: 99%

Temporal Graphical Models for Cross-Species Gene Regulatory Network Discovery

Liu

Niculescu-Mizil²,

Lozano³

et al. 2011

J. Bioinform. Comput. Biol.

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Many genes and biological processes function in similar ways across different species. Cross-species gene expression analysis, as a powerful tool to characterize the dynamical properties of the cell, has found a number of applications, such as identifying a conserved core set of cell cycle genes. However, to the best of our knowledge, there is limited effort on developing appropriate techniques to capture the causal relations between genes from time-series microarray data across species. In this paper, we present hidden Markov random field regression with L 1 penalty to jointly uncover the regulatory networks for multiple species. The algorithm provides a framework for sharing information across species via hidden component graphs and can conveniently incorporate domain knowledge over evolution relationship between species. We demonstrate the effectiveness of our method on two synthetic datasets and one innate immune response microarray dataset.

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Transcriptional responses of murine macrophages to infection with Yersinia enterocolitica

Cited by 49 publications

References 45 publications

TLR2- and Nucleotide-Binding Oligomerization Domain 2-Dependent Krüppel-Like Factor 2 Expression Downregulates NF-κB–Related Gene Expression

TLR2- and Nucleotide-Binding Oligomerization Domain 2-Dependent Krüppel-Like Factor 2 Expression Downregulates NF-κB–Related Gene Expression

Pseudomonas aeruginosaInfection of Airway Epithelial Cells Modulates Expression of Kruppel-Like Factors 2 and 6 via RsmA-Mediated Regulation of Type III Exoenzymes S and Y

Temporal Graphical Models for Cross-Species Gene Regulatory Network Discovery

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