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

ABSTRACT: 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

ORGANISM(S): Homo sapiens

PROVIDER: GSE4646 | GEO | 2006/09/01

SECONDARY ACCESSION(S): PRJNA95283

REPOSITORIES: GEO

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Project description:In vertebrates, all cells except circulating blood cells must adhere to support their normal growth and functions. The adherence to extracellular matrix and/or other cells is critical and adherent cells placed in non-adherent conditions either die or form multicellular spheroids. Placing cells in non-adherent conditions has been used to induce differentiation in teratocarcinoma cells and more recently to form organoids . Because of such important consequences induced by cell adhesion on cell growth and function, the transition between adherent and non-adherent states is rather rare. There are however physiological situations, such as blood cells diapedesis, during which cells that circulate into the blood stream must adhere to the endothelial cells and cross the endothelial barrier to reach target tissues. Another example of transition, from an adherent to a non-adherent state, is observed in the metastasic process, where cells detach from the tumor mass and circulate in the blood and lymphatic vasculature prior to reattaching and extravasating to colonize distant organs. The comparative analysis of the only effects of adherence on cellular functions is complicated by the fact that in many study models the acquisition or loss of adherence induces major alterations in cell physiology that would obscure the effects of the adherence itself. For example, P19 teratocarcinoma cells differentiate in suspension spheroids while they do not in adhering conditions. In this context, the comparison between spheroids and adherent cells would not be a comparison between adherent and non-adherent cells, but between differentiated cells adhering between them and undifferentiated cells adhering on plastic. Mouse macrophage cell lines represent one of the rare experimental models that may be suitable to compare the adherent and non-adherent states. Indeed, they grow equally well under adherent and non-adherent conditions and keep their differentiated functions under both conditions. We therefore decided to use this model to analyze the changes between the adherent and the non-adherent state using a broad approach, based on proteomics.

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

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