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MyD88-dependent changes in the pulmonary transcriptome after infection with Chlamydia pneumoniae

ABSTRACT: Chlamydia pneumoniae, an obligate intracellular bacterium, causes pneumonia in humans and mice. Toll-like receptors and the key adaptor molecule MyD88 play a critical role in inducing immunity against this microorganism and are crucial to survive the infection. To explore the influence of MyD88 on induction of immune responses in vivo on a genome wide level, WT or MyD88-/- mice were infected with C. pneumoniae upon anesthesia and the pulmonary transcriptome was analyzed three days later by microarrays. We find that the infection induced the transcription of 360 genes and repressed 18 genes in WT mice. Of these, 221 genes were not or weakly induced in lungs of MyD88-/- mice. This cluster contains primarily genes encoding for chemokines, cytokines and other immune effector molecules. Genes induced by interferons were abundant in a cluster of 102 genes which were only partially MyD88-dependent. Interestingly, a set of 37 genes were induced more strongly in MyD88-/- mice and most of them are involved in the regulation of cellular replication. In summary, ex vivo analysis of the pulmonary transcriptome upon infection with C. pneumoniae demonstrated a major impact of MyD88 on inflammatory responses but not on interferon-type responses, and identified MyD88-independent genes involved in cellular replication Keywords: lung, Chlamydia pneumoniae, mice, myd88, TLR, infection, knock out

ORGANISM(S): Mus musculus

PROVIDER: GSE6688 | GEO | 2007/03/27

SECONDARY ACCESSION(S): PRJNA99067

REPOSITORIES: GEO

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Transcription profiling of lungs from wild type and MyD88 knockout mice infected with Chlamydia pneumoniae to explore the influence of MyD88 on induction of immune responses.

Project description:Chlamydia pneumoniae, an obligate intracellular bacterium, causes pneumonia in humans and mice. Toll-like receptors and the key adaptor molecule MyD88 play a critical role in inducing immunity against this microorganism and are crucial to survive the infection. To explore the influence of MyD88 on induction of immune responses in vivo on a genome wide level, WT or MyD88-/- mice were infected with C. pneumoniae upon anesthesia and the pulmonary transcriptome was analyzed three days later by microarrays. We find that the infection induced the transcription of 360 genes and repressed 18 genes in WT mice. Of these, 221 genes were not or weakly induced in lungs of MyD88-/- mice. This cluster contains primarily genes encoding for chemokines, cytokines and other immune effector molecules. Genes induced by interferons were abundant in a cluster of 102 genes which were only partially MyD88-dependent. Interestingly, a set of 37 genes were induced more strongly in MyD88-/- mice and most of them are involved in the regulation of cellular replication. In summary, ex vivo analysis of the pulmonary transcriptome upon infection with C. pneumoniae demonstrated a major impact of MyD88 on inflammatory responses but not on interferon-type responses, and identified MyD88-independent genes involved in cellular replication Experiment Overall Design: Microarray analysis was performed in biological triplicates with RNA from individual mice derived from three independent infection experiments. Samples were lungs from wt and myd88 knock out mice, three days after Chlamydia pneumoniae or mock infection. Altogther 12 samples were analyzed on Affymetrix MOE430A arrays.

2007-11-15 | E-GEOD-6688 | biostudies-arrayexpress

Mus musculus

Project description:MyD88-dependent changes in the pulmonary transcriptome after infection with Chlamydia pneumoniae

| PRJNA99067 | ENA

Host Immune Response to Clinical Hypervirulent Klebsiella pneumoniae Pulmonary Infections via Transcriptome Analysis

Project description:Klebsiella pneumoniae is an arising threat to human health. However, host immune responses in response to this bacterium remain to be elucidated. The goal of this study was to identify the dominant host immune responses associated with Klebsiella pneumoniae pulmonary infection. Pulmonary mRNA profiles of 6-8-weeks-old BALB/c mice infected with/without Klebsiella pneumoniae were generated by deep sequencing using Illumina Novaseq 6000. qRT–PCR validation was performed using SYBR Green assays. Using KEGG (Kyoto Encyclopedia of Genes and Genomes) analysis, we identified several immune associated pathways, including complement and coagulation cascades, Toll-like receptor signaling pathway, Rap1 signaling pathway, chemokine signaling pathway, TNF signaling pathway, phagosome and NOD-like receptor signaling pathway, were involved in Klebsiella pneumoniae pulmonary infection. Using ICEPOP (Immune CEll POPulation) analysis, we found that several cell types were involved in the host immune response to Klebsiella pneumoniae pulmonary infection, including dendritic cells, macrophages, monocytes, NK (natural killer) cells, stromal cells. Further, IL-17 chemokines were significantly increased during Klebsiella pneumoniae infection. This study provided evidence for further studying the pathogenic mechanism of Klebsiella pneumoniae pneumonia infection.

2021-03-30 | GSE171048 | GEO

ANA-1 macrophages infected with Chlamydia pneumoniae

Project description:This experiment is an additional experiment to GSE6688. Mouse macrophages (ANA-1 cells) were infected in vitro with C. pneumoniae with a M.O.I. of 10. Twenty two genes were significantly upregulated. Examples of the most upregulated genes in mouse macrophages after C. pneumoniae infection are serum amyloid A3 (saa3), a protein that is mainly produced by activated macrophages during tissue injury or inflammation, MIP-2 (cxcl2) and irg1. Expression levels of all genes induced by C. pneumoniae in macrophages in vitro correlated with the results obtained from infected lungs from wild type mice (GSE6688), suggesting that this cell type participates in host defense in vivo against C. pneumoniae. Keywords: Chlamydia pneumoniae, ANA-1 macrophages, in vitro, infection

2007-03-27 | GSE6690 | GEO

Variation in the immune and inflammatory responses during pneumonia, an important role of the host and pathogen genetic background

Project description:Analysis of the pulmonary gene expression in two mouse strains BALB/cOlaHsd (BALB/c) and CBA/CaOlaHsd (CBA/Ca) after infection with various serotypes of Streptococcus pneumoniae. BALB/c mice show high resistance to infection with S. pneumoniae strain D39 (serotype 2), while CBA/Ca mice are highly susceptible. The lung samples of BALB/c and CBA/Ca were collected at 6h post-infection with one of the tested pneumococcal serotypes (2, 3, 6B and 19F) and for control animals (PBS-treated). Additionally lung samples from both mouse strains were collected at 12h and 24h post-infection with pneumococcal strain D39. The lists of differentially expressed genes were created by the comparison of infected versus PBS-treated animals and infected BALB/c versus infected CBA/Ca for each pneumococcal strain. The tested hypotheses were: 1) infection with S. pneumoniae will change the pulmonary transcriptomes of both mouse strains 2) The pulmonary gene expression will be specific for mouse strains and for the pneumococcal serotype and 3) The change in the pulmonary gene expression will associate with future clinical outcome of infection or with the type of observed inflammatory responses. Total RNA obtained from lung tissue from BALB/cOlaHsd and CBA/CaOlaHsd mouse strains (Harlan) post intranasal infection with Streptococcus pneumoniae of various serotypes (2, 3, 6B and 19F) dose 5.0E06 CFU or PBS-treated animals

2015-10-28 | E-GEOD-61459 | biostudies-arrayexpress

Transcription profiling of mouse ANA-1 macrophages infected with Chlamydia pneumoniae

Project description:This experiment is an additional experiment to GSE6688. Mouse macrophages (ANA-1 cells) were infected in vitro with C. pneumoniae with a M.O.I. of 10. Twenty two genes were significantly upregulated. Examples of the most upregulated genes in mouse macrophages after C. pneumoniae infection are serum amyloid A3 (saa3), a protein that is mainly produced by activated macrophages during tissue injury or inflammation, MIP-2 (cxcl2) and irg1. Expression levels of all genes induced by C. pneumoniae in macrophages in vitro correlated with the results obtained from infected lungs from wild type mice (GSE6688), suggesting that this cell type participates in host defense in vivo against C. pneumoniae. Experiment Overall Design: ANA-1 macrophages were infected with Chlamydia pneumoniae or left untreated. After 8h total RNA was extracted. Two biological replicates were performed resulting in 4 arrays in total

2008-06-15 | E-GEOD-6690 | biostudies-arrayexpress

Variation in the immune and inflammatory responses during pneumonia, an important role of the host and pathogen genetic background

2015-10-28 | GSE61459 | GEO

Effect of Batf2 deficiency on gene epxression in murine alveolar macrophages treated ex vivo with IFNg and K. pneumoniae supernatant

Project description:Basic leucine zipper transcription factor ATF-like 2 (BATF2) is a transcription factor that is emerging as an important regulator of the innate immune system. We previously identified BATF2 among the top upregulated genes in human alveolar macrophages treated with LPS, but the signaling pathways that induce BATF2 expression in response to Gram-negative stimuli are incompletely understood. In addition, the role of BATF2 in the host response to pulmonary infection with a Gram-negative pathogen like Klebsiella pneumoniae (Kp) is not known. We show that induction of Batf2 gene expression in macrophages in response to Kp in vitro requires TRIF and type I interferon (IFN) signaling, but not MyD88 signaling. Analysis of the impact of BATF2-deficiency on macrophage effector functions in vitro showed that BATF2 does not directly impact macrophage phagocytic uptake and intracellular killing of Kp. However, BATF2 markedly enhanced macrophage pro-inflammatory gene expression and Kp-induced cytokine responses. In vivo, we observed that Batf2 gene expression was elevated in the lung tissue of wild type (WT) mice 24 h after pulmonary Kp infection, and Kp-infected BATF2-deficient (Batf2-/-) mice displayed a modest but significant increase in bacterial burden in the lung, spleen and liver compared to WT mice. WT and Batf2-/- mice showed similar recruitment of leukocytes following infection, but in line with our in vitro observations, pro-inflammatory cytokine levels in the alveolar space were reduced in Batf2-/- mice. Altogether, these results suggest that BATF2 enhances pro-inflammatory cytokine responses in macrophages in response to Kp, and that as such, BATF2 contributes to the host defense against pulmonary Kp infection.

2023-08-31 | GSE235114 | GEO

Inhibition of Chlamydia pneumoniae Replication in Human Dendritic cells by TNF-alpha-Induced Indoleamine 2,3-Dioxygenase

Project description:Infection with Chlamydia pneumoniae, a human respiratory pathogen, has been associated with various chronic diseases such as asthma, coronary heart disease and importantly atherosclerosis. Possibly because the pathogen can exist in a persistent form. TNF-a has been reported to induce chlamydial persitence in epithelial cell lines, however the mechanism of TNF-a-induced persistence has not been reported. Moreover, C. pneumoniae persistently infect human dendritic cells (DCs) and activate DCs to produce cytokines including TNF-a. Induction of chlamydial persistence by other cytokines such as IFN-g is known to be due to indoleamine 2,3-dioxygenase (IDO) activity. The present study therefore, investigated whether C. pneumoniae infection can induce IDO activity in dendritic cells, and whether the restriction of chlamydial growth in the DCs by TNF-a is IDO-dependent. Our data indicate that infection of DCs with C. pneumoniae resulted in the induction of IDO expression. Reporting on our use of anti-TNF-a antibody adalimumab and varying concentrations of TNF-a, we further demonstrate that IDO induction following infection of DCs with C. pneumoniae is TNF-a-dependent. The anti-chlamydial activity induced by TNF-a and the expression of chlamydial 16S rRNA gene, euo, groEL1, ftsk and tal genes was correlated with the induction of IDO. Addition of excess amounts of tryptophan to the DC cultures resulted in abrogation of the TNF-a-mediated chlamydial growth restriction. These findings suggest that infection of DCs by C. pneumoniae induces production of functional IDO, which subsequently causes depletion of tryptophan. This may represent a potential mechanism for DCs to restrict bacterial growth in chlamydial infections. Keywords: Chlamydia pneumoniae, Dendritic cells, TNF-a, Indoleamine 2,3-dioxygenase

2009-08-21 | GSE12806 | GEO

E-GEOD-6688

Project description:Transcription profiling of lungs from wild type and MyD88 knockout mice infected with Chlamydia pneumoniae to explore the influence of MyD88 on induction of immune responses.

2015-10-13 | E-GEOD-6688 | ExpressionAtlas

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