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Genome-wide gene expression analysis of 16HBE14 human bronchial epithelial cells in response to Neisseria

ABSTRACT: We looked at host gene expression signatures common and specfic to occasionally pathogenic N. meningitidis and commensal N. lactamica. We hypothesise that similar host cell responses during early interactions with N. meningitidis and N. lactamica could inform common mechanisms of colonisation of commensals while differential host cell responses could be capable of altering the outcome of the colonisation process. Total RNA obtained from 16HBE14 cells infected with the different strains of Neisseria from 0 to 7 hours are compared to mock-infected controls at the respective timepoints. 192 samples are analysed. There are 4 to 8 biological replicates per condition.

ORGANISM(S): Homo sapiens

SUBMITTER: ling ling

PROVIDER: E-GEOD-27557 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Genome-wide gene expression analysis of 16HBE14 human bronchial epithelial cells in response to Neisseria

Project description:We looked at host gene expression signatures common and specfic to occasionally pathogenic N. meningitidis and commensal N. lactamica. We hypothesise that similar host cell responses during early interactions with N. meningitidis and N. lactamica could inform common mechanisms of colonisation of commensals while differential host cell responses could be capable of altering the outcome of the colonisation process.

2012-06-01 | GSE27557 | GEO

Transcriptional profiling of NMB0419 mutant of Neisseria meningitidis MC58

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A master virulence regulator of S. aureus inactivated during carriage in man

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The phosphoproteome of choroid plexus epithelial cells following infection with Neisseria meningitidis

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2016-12-30 | GSE81756 | GEO

Host gene expression response to Toxoplasma gondii infection is not different between RH?ku80 and RH?ku80?rop5 parasites.

Project description:The normally virulent type-I RH parasite is rendered avirulent when lacking ROP5. The avirulent phenotype is a consequence of interaction with the host innate immune system. We sought to understand if ROP5 alters host gene expression in order to escape host defenses. We saw no gene expression differences between host cells infected with wt (RH?ku80) or RH?ku80?rop5 parasites. We have included uninfected HFF samples that were harvested in parallel with the infected samples. Host gene expression in response to infection with Toxoplasma gondii. Two independent samples per sample type. Three sample types: HFF infected with RH?ku80, HFF infected with RH?ku80?rop5, and uninfected HFF.

2012-09-13 | E-GEOD-32104 | biostudies-arrayexpress

Signaling of Neisseria meningitidis MC58 mutants to primary human umbilical vein endothelial cells (HUVEC)

Project description:We examined the adherence-mediated signaling of meningococci to human cells by comparing gene expression profiles of primary human umbilical vein endothelial cells (HUVEC) infected by piliated and adherent wild-type (WT), frpC/frpA-deficient mutant, or the non-adherent (ΔpilD) N. meningitidis MC58 bacteria defective in production of the type IV pilus, respectively. Surprisingly, no significant difference was found between the transcriptomes of HUVECs infected by bacteria producing, or not the RTX FrpC and FrpA proteins, thus failing to provide any hints on their biological activity. In contrast, pili-mediated adhesion of meningococci resulted in alterations of expression levels of human genes known to regulate apoptosis, cell proliferation, inflammatory response or adhesion. In particular, genes for signaling pathway proteins involved in early embryonic development, such as transforming growth factor-β (TGF-β)/Smad, Wnt/β-catenin, and Notch/Jagged were found to be upregulated upon adhesion of N. meningitidis together with genes for a number of transcription factors. This reveals that adhering piliated meningocci manipulate signaling pathways controlling human cell proliferation, survival and defense mechanisms, while establishing a commensal relationship with the host. Keywords: time course, infection response, genetic modification

2006-09-01 | GSE4646 | GEO

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