Proteomics

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Proteomic characterization of the interplay of Staphylococcus aureus and human alveolar epithelial cells during infection - host cell proteins


ABSTRACT: Since infectious diseases caused by Staphylococcus aureus are still a major threat for human health we aimed to gain a detailed understanding of the molecular interplay of pathogen and host upon internalization by proteome analyses. In the present study we infected human alveolar epithelial A549 cells with S. aureus HG001 pMV158GFP and separated intact bacteria from host cell debris or infected from non-infected A549 cells prior to proteome analysis by cell sorting thus facilitating detailed analyses. During the first 6.5 h in the intracellular milieu S. aureus displayed reduced growth rate, induction of the stringent response, and adaptation to microaerobic conditions as well as cell wall stress. Interestingly, both truly infected host cells and those only potentially exposed to secreted S. aureus proteins but not infected displayed differences in the proteome pattern compared to A549 cells which had never been in contact with S. aureus. However, adaptation reactions were more pronounced in infected compared to non-infected A549 cells. Additional cytokine measurements revealed elaborated levels of pro-inflammatory cytokines in supernatants of the infection setting compared to pure host cell cultures which might mediate communication among the host cells and trigger adaptation even in cells not infected with S. aureus.

INSTRUMENT(S): LTQ Orbitrap Velos

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Epithelial Cell, Cell Culture

SUBMITTER: Kristin Surmann  

LAB HEAD: Uwe Völker

PROVIDER: PXD002388 | Pride | 2015-08-05

REPOSITORIES: Pride

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Publications


Infectious diseases caused by pathogens such as Staphylococcus aureus are still a major threat for human health. Proteome analyses allow detailed monitoring of the molecular interplay between pathogen and host upon internalization. However, the investigation of the responses of both partners is complicated by the large excess of host cell proteins compared to bacterial proteins as well as by the fact that only a fraction of host cells are infected. In the present study we infected human alveolar  ...[more]

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