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Expression data from uninfected and pneumococcus-infected wt and PGLYPR4-KO primary alveolar epithelial cells

ABSTRACT: Streptococcus pneumoniae is the most frequent cause of community-acquired pneumonia. Endogenous antimicrobial proteins such as PGLYRP4 might participate to the course of the disease. PGLYRP4 is expressed in different cell types but is downregulated in alveolar epithelial after stimulation with Streptococcus pneumoniae. Interestingly, mice lacking PGLYRP4 displayed an enhanced bacterial clearance in the lungs and less mice develop a bacteremia. This may depend on a higher proinflammatory cytokine response in PGLYRP4KO compared to wt cells, which contribute to the recruitment of more immune cells to the side of infection and an enhanced bacterial clearance by additionally stronger activation of the phagocytes. We implemented microarray analysis of infected primary epithelial cells to identify possible regulated genes by PGLYPR4-deficency, which contribute to the seen phenotype.

ORGANISM(S): Mus musculus

PROVIDER: GSE108358 | GEO | 2019/08/27

REPOSITORIES: GEO

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Expression data from uninfected and pneumococcus-infected wt and PGLYPR4-KO primary alveolar macrophages

Project description:Streptococcus pneumoniae is the most frequent cause of community-acquired pneumonia. Endogenous antimicrobial proteins such as PGLYRP4 might participate to the course of the disease. PGLYRP4 is expressed in different cell types but is downregulated in alveolar epithelial after stimulation with Streptococcus pneumoniae. Interestingly, mice lacking PGLYRP4 displayed an enhanced bacterial clearance in the lungs and less mice develop a bacteremia. We investigated the gene expression in alveolar macrphages and found most top 50 up- and down-regulated genes to be not annotated. Genes which could be annotated seem unlikely to play a major role in the phenotype of PGLYRP4-KO mice. We implemented microarray analysis of infected primary alveolar macrophage cells to identify possible regulated genes by PGLYPR4-deficency, which contribute to the seen phenotype.

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Project description:Epithelial cells are the first point of contact for bacteria entering the respiratory tract. Streptococcus pneumoniae is an obligatory human pathobiont of the nasal mucosa, carried asymptomatically but also the cause of severe pneumoniae. The role of the epithelium in maintaining homeostatic interactions or mounting an inflammatory response to invasive S. pneumoniae is currently poorly understood. However, studies have shown that chromatin modifications, at the histone level, induced by bacterial pathogens interfere with the host transcriptional program and promote infection. In this study, we demonstrate that S. pneumoniae actively induces di-methylation of histone H3 on lysine 4 (H3K4me2), which persists for at least 9 days upon clearance of bacteria with antibiotics. We show that infection establishes a unique epigenetic program affecting the transcriptional response of epithelial cells, rendering them more permissive upon secondary infection. Our results establish H3K4me2 as a unique modification induced by infection, distinct from H3K4me3, which localizes to enhancer regions genome-wide. Therefore, this study reveals evidence that bacterial infection leaves a memory in epithelial cells after bacterial clearance, in an epigenomic mark, thereby altering cellular responses for subsequent infections.

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Epithelial cells maintain memory of prior infection with Streptococcus pneumoniae through di-methylation of histone H3 [Affymetrix]

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Transcription profiling by array of pneumococcal virulence factors expressed during meningitis in mice

Project description:Streptococcus pneumoniae is the most common cause of severe bacterial meningitis in children, the elderly, and immunocompromised individuals. To identify virulence factors preferentially expressed during meningitis, we conducted niche-specific genome-wide in vivo transcriptomic analysis after intranasal infection of mice with serotype 4 or 6A pneumococci. The expression of 34 bacterial genes was substantially altered in brain tissue of mice infected with either of the 2 strains. Ten upregulated genes were common to both strains, 7 of which were evaluated for their role in the development of meningitis. One previously uncharacterized protein, alpha-glycerophosphate oxidase (GlpO), was cytotoxic for human brain microvascular endothelial cells (HBMECs) via generation of H2O2. A glpO deletion mutant was defective in adherence to HBMECs in vitro as well as in progression from the blood to the brain in vivo. Mutant bacteria also induced markedly reduced meningeal inflammation and brain pathology compared with WT, despite similar levels of bacteremia. Immunization of mice with GlpO protected against invasive pneumococcal disease and provided additive protection when formulated with pneumolysin toxoid. Our results provide the basis of a strategy that can be adapted to identify genes that contribute to the development of meningitis caused by other pathogens. [Data is also available from http://bugs.sgul.ac.uk/E-BUGS-130]

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