Secreted Factors from Staphylococcus aureus Biofilm and Planktonic Cultures Differentially Impact Human Keratinocytes in vitro
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE24370 | GEO | 2011/08/31
SECONDARY ACCESSION(S): PRJNA132965
REPOSITORIES: GEO
Similar Datasets
Project description:Interactions between human keratinocytes and secreted factors from Staphylococcus aureus biofilm and planktonic cultures were investigated using microarray analysis. Relative to planktonic secreted factors, biofilm secreted factors up regulated cytokine and chemokine genes in keratinocytes. Genes associated with DNA damage and oxidative stress were also induced in keratinocytes treated with secreted factors from S. aureus biofilm. Here we show that secreted factors from S. aureus planktonic (PCM) and biofilm (BCM) cultures differentially impact several aspects of wound healing processes.
2011-08-31 | GSE24118 | GEO
Project description:Interactions between human keratinocytes and secreted factors from Staphylococcus aureus biofilm and planktonic cultures were investigated using microarray analysis. Relative to planktonic secreted factors, biofilm secreted factors up regulated cytokine and chemokine genes in keratinocytes. Genes associated with DNA damage and oxidative stress were also induced in keratinocytes treated with secreted factors from S. aureus biofilm. Here we show that secreted factors from S. aureus planktonic (PCM) and biofilm (BCM) cultures differentially impact several aspects of wound healing processes. Secreted factors from S. aureus biofilm and planktonic cultures with equivalent population sizes were placed in contact with human foreskin keratinocytes for 4 hours. Keratinocytes were grown to ~90% confluency between passages 4-10.
2011-08-30 | E-GEOD-24118 | biostudies-arrayexpress
Project description:Interactions between human keratinocytes and secreted factors from Staphylococcus aureus biofilm were investigated using microarray analysis. Relative to control cells, biofilm-secreted factors upregulated cytokine and chemokine genes in keratinocytes. Genes associated with DNA damage and oxidative stress were also induced in keratinocytes treated with secreted factors from S. aureus. Here we show that secreted factors from S. aureus biofilm cultures differentially impact several aspects of wound healing processes. Human keratinocytes were grown in co-culture with mature S. aureus biofilms for 24 hours. Keratinocytes exposed to S. aureus biofilm were analyzed in quadruplicate. Control cells were also analyzed in quadruplicate. Dye-swaps were performed.
2011-08-30 | E-GEOD-24370 | biostudies-arrayexpress
Project description:Staphylococcus aureus produces the cyclic dipeptides tyrvalin and phevalin (aureusimine A and B, respectively). A previous study reported that S. aureus mutants not capable of producing these compounds were less virulent in vivo through the deranged regulation of virulence factor genes. These findings, however, have been questioned as an unknown mutation in an operon that regulates virulence was discovered in the mutant strain. Here, we report that S. aureus biofilms produce greater amounts of phevalin than their planktonic counterparts. When administered to human keratinocytes, phevalin had no substantial effect on gene expression. Phevalin had no obvious impact on the extracellular metabolome of S. aureus. However, conditioned medium from S. aureus spiked with phevalin resulted in significant differences in keratinocyte gene expression compared to conditioned medium alone. A role for phevalin in manipulating host responses is apparent. Additionally, phevalin is a potential biomarker and/or therapeutic target for chronic, biofilm-based infections. Secreted factors from S. aureus biofilm and planktonic cultures with equivalent population sizes were placed in contact with human HaCaT keratinocytes for 4 hours. Keratinocytes were grown to ~90% confluency.
2012-10-01 | E-GEOD-32920 | biostudies-arrayexpress
Project description:Is there a universal genetically programmed defense providing tolerance to antibiotics when bacteria grow as biofilms? A comparison between biofilms of three different bacterial species by transcriptomic and metabolomic approaches uncovered no evidence of one. Single-species biofilms of three bacterial species (Pseudomonas aeruginosa, Staphylococcus aureus, and Acinetobacter baumannii) were grown in vitro for three days then challenged with respective antibiotics (ciprofloxacin, daptomycin, tigecycline) for an additional 24 h. All three microorganisms displayed reduced susceptibility in biofilms compared to planktonic cultures. Global transcriptomic profiling of gene expression comparing biofilm to planktonic and antibiotic-treated biofilm to untreated biofilm was performed. Extracellular metabolites including 18 amino acids, glucose, lactate, acetate, formate, and ethanol were measured to characterize the utilization of carbon sources between biofilms, treated biofilms, and planktonic cells. While all three bacteria exhibited a species-specific signature of stationary phase, no conserved gene, gene set, or common functional pathway could be identified that changed consistently across the three microorganisms. Across the three species, glucose consumption was increased in biofilms compared to planktonic cells and alanine and aspartic acid utilization were decreased in biofilms compared to planktonic cells. The reasons for these changes were not readily apparent in the transcriptomes. No common shift in the utilization pattern of carbon sources was discerned when comparing untreated to antibiotic-exposed biofilms. Overall, our measurements do not support the existence of a common genetic or biochemical basis for biofilm tolerance against antibiotics. Rather, there are likely myriad genes, proteins, and metabolic pathways that influence the physiological state of microorganisms in biofilms contributing to antibiotic tolerance. The Staphylococcus aureus microarray data from the study described above is deposited here.
2021-10-18 | GSE185864 | GEO
Project description:The SaeRS two-component regulatory system of Staphylococcus aureus is known to affect the expression of many genes. The SaeS protein is the histidine kinase responsible for phosphorylation of the response regulator SaeR. In S. aureus Newman, the sae system is constitutively expressed due to a point mutation in saeS, relative to other S. aureus strains, which results in substitution of proline for leucine at amino acid 18. Strain Newman is unable to form a robust biofilm and we report here that the biofilm-deficient phenotype is due to the saeSP allele. Replacement of the Newman saeSP with saeSL, or deletion of saeRS, resulted in a biofilm-proficient phenotype. Newman culture supernatants were observed to inhibit biofilm formation by other S. aureus strains, but did not affect biofilm formation by S. epidermidis. Culture supernatants of Newman saeSL or Newman ΔsaeRS had no significant effect on biofilm formation. The inhibitory factor was inactivated by incubation with proteinase K, but survived heating, indicating that the inhibitory protein is heat-stable. The inhibitory protein was found to affect the attachment step in biofilm formation, but had no effect on preformed biofilms. Replacement of saeSL with saeSP in the biofilm-proficient S. aureus USA300 FPR3757 resulted in the loss of biofilm formation. Culture supernatants of USA300 FPR3757 saeSP, did not inhibit biofilm formation by other staphylococci, suggesting that the inhibitory factor is produced but not secreted in the mutant strain. A number of biochemical methods were utilized to isolate the inhibitory protein. Although a number of candidate proteins were identified, none were found to be the actual inhibitor. In an effort to reduce the number of potential inhibitory genes, RNA-Seq analyses were done with wild-type strain Newman and the saeSL and ΔsaeRS mutants. RNA-Seq results indicated that sae regulates many genes that may affect biofilm formation by Newman.
2015-04-30 | GSE65827 | GEO
Project description:Comparison of biofilm versus planktonic mode of growth in Staphylococcus aureus
2014-01-18 | E-MEXP-3924 | biostudies-arrayexpress
Project description:Staphylococcus aureus (S. aureus) is one of the most important pathogens in humans and animals. The formation of S. aureus biofilm is considered an important mechanism of antimicrobial resistance. Therefore, finding effective drugs against the biofilm produced by S. aureus has been a high priority. Licochalcone A, a natural plant product, was reported to have antibacterial activities and showed good activity against all 21 tested strains of S. aureus biofilm and planktonic cells. To detect the possible molecular mechanism of Licochalcone A against S. aureus biofillm or planktonic cells, Affymetrix GeneChips were used to determine the global comparative transcription of S. aureus biofilm and planktonic cells triggered by treatment with sub-bactericidal and sub-inhibitory concentrations of Licochalcone A, respectively.
2014-07-01 | GSE58938 | GEO
Project description:Methicillin-resistant Staphylococcus aureus (MRSA) strains are important human pathogens and a significant health hazard for hospitals and the food industry. They are resistant to β-lactam antibiotics including methicillin and extremely difficult to treat. In this study, we show that the Staphylococcus aureus COL (MRSA) strain, with a known complete genome, can easily survive and grow under acidic and alkaline conditions (pH 5 and pH9, respectively), both planktonically and as a biofilm. Α microarray-based analysis of both planktonic and biofilm cells was performed under acidic and alkaline conditions showing that several genes are up- or down-regulated under different environmental conditions and growth modes. These genes were coding for transcription regulators, ion transporters, cell wall biosynthetic enzymes, autolytic enzymes, adhesion proteins and antibiotic resistance factors, most of which are associated with biofilm formation. These results will facilitate a better understanding of the physiological adjustments occurring in biofilm-associated S. aureus COL cells growing in acidic or alkaline environments, which will enable the development of new efficient treatment or disinfection strategies. We used microarrays to detail the global programme of gene expression underlying growth of S. aureus COL growing under acidic and alkaline conditions in biofilm or planktonic mode and identified distinct classes of up-regulated genes during this process.
2019-09-27 | GSE138075 | GEO
Project description:In Staphylococcus aureus, the role of the GGDEF domain containing protein GdpS remains poorly understood. Previous studies reported that gdpS mutant strains had decreased biofilm formation due to changes in icaADBC expression that were independent of cyclic-di-GMP levels. We deleted gdpS in three unrelated S. aureus isolates, and analyzed the resultant mutants for alterations in biofilm formation, metabolism and transcription. Dynamic imaging during biofilm development showed that GdpS inhibited early biofilm formation in only two out of the three strains examined, without affecting bacterial survival. However, quantification of biofilm formation using crystal violet staining revealed that inactivation of gdpS affected biofilm formation in all three studied strains. Extraction of metabolites from S. aureus cells confirmed the absence of cyclic-di-GMP, suggesting that biofilm formation in this species differs from that in other Gram-positive organisms. In addition, targeted mutagenesis demonstrated that the GGDEF domain was not required for GdpS activity. Transcriptomic analysis revealed that the vast majority of GGDEF-regulated genes were involved in virulence, metabolism, cell wall biogenesis and eDNA release. Finally, expression of lrgAB or deletion of cidABC in a strain lacking gdpS confirmed the role of GdpS on regulation of eDNA production that occurred without an increase in cell autolysis. In summary, S. aureus GdpS contributes to cell-to-cell interactions during early biofilm formation by influencing expression of lrgAB and cidABC mediated eDNA release. We conclude that GdpS acts as a negative regulator of eDNA release.
2014-06-30 | GSE48656 | GEO