Biofilm metagenome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA260418 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1571153.fastq.gz | Fastqsanger.gz | |||
| SRR1571158.fastq.gz | Fastqsanger.gz | |||
| SRR1571139.fastq.gz | Fastqsanger.gz |
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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.
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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 Acinetobacter baumannii microarray data from the study described above is deposited here.
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Project description:The transcriptome of Actinobacillus pleuropneumoniae biofilms was compared to the transcriptome of planktonic bacteria
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Project description:The transcriptome of Actinobacillus pleuropneumoniae biofilms was compared to the transcriptome of planktonic bacteria
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Project description:Non-typeable Haemophilus influenzae (NTHi) is a common acute otitis media pathogen, with an incidence that is increased by previous antibiotic treatment. NTHi is also an emerging causative agent of other chronic infections in humans, some linked to morbidity, and all of which impose substantial treatment costs. In this study we explore the possibility that antibiotic exposure may stimulate biofilm formation by NTHi bacteria. We discovered that sub-inhibitory concentrations of beta-lactam antibiotic (i.e., amounts that partially inhibit bacterial growth) stimulated the biofilm-forming ability of NTHi strains, an effect that was strain and antibiotic dependent. When exposed to sub-inhibitory concentrations of beta-lactam antibiotics NTHi strains produced tightly packed biofilms with decreased numbers of culturable bacteria but increased biomass. The ratio of protein per unit weight of biofilm decreased as a result of antibiotic exposure. Antibiotic-stimulated biofilms had altered ultrastructure, and genes involved in glycogen production and transporter function were up regulated in response to antibiotic exposure. Down-regulated genes were linked to multiple metabolic processes but not those involved in stress response. Antibiotic-stimulated biofilm bacteria were more resistant to a lethal dose (10µg/mL) of cefuroxime. Our results suggest that beta-lactam antibiotic exposure may act as a signaling molecule that promotes transformation into the biofilm phenotype. Loss of viable bacteria, increase in biofilm biomass and decreased protein production coupled with a concomitant up-regulation of genes involved with glycogen production might result in a biofilm of sessile, metabolically inactive bacteria sustained by stored glycogen. These biofilms may protect surviving bacteria from subsequent antibiotic challenges, and act as a reservoir of viable bacteria once antibiotic exposure has ended.
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Project description:Biofilms are a communal of one or several kinds of microorganisms that growing on of both non-living and biotic surfaces by the production of multi-layers high-abundance extracellular matrix (ECM) to survive in the harsh environments (1-4). Biofilms consist of 85% (by volume) of matrix materials and 15% microbial cells (5). Biofilm ECM, consists of proteins, polysaccharides and/or extracellular DNAs, is important for biofilm integrity that increases environmental adaptability and induces antimicrobial resistance (6-7). Surface-adherent (sessile) bacteria in biofilms are more difficult to eradicate as minimum inhibitory concentrations (MICs) of antibiotics against bacterial biofilms is 100-1000 folds higher than the free living (planktonic) form that resulting in recurrent infections (8). Biofilms also possibly form nidus at the surface for the attachment of other pathogens lead to biofilms of multiple bacteria or multi-organisms (9ref). The communication, among organisms within biofilm, controls density of cell population refers to as “quorum sensing” (10) and different combinations of organisms in biofilms with either multiple bacteria or multi-species might induce different biofilm properties. While catheter-related colonization of Gram-positive bacteria from skin microbiota such as Streptococcus spp. and Staphylococcus spp. is common, biofilms in the inner lumen of catheter consist of both Gram-positive and Gram-negative bacteria. Because i) translocation of gut microbiota (eg. Enterococcus spp., Gram-negative bacteria and Candida albicans) into blood circulation during sepsis is one of the common causes of severe sepsis , ii) mixed systemic infection between bacteria and Candida spp. is even more severe than the infection by each organism in separation and iii) biofilms could be formed during bacteremia and fungemia, the biofilms from mixed species between bacteria and Candida spp. during sepsis is possible. In addition, central venous catheter-related candidiasis is common in intensive care units (ICU) patients refer to as “Candida catheter-related bloodstream infection (CRCBSI)”. Moreover, synergistic interaction between Candida albicans and several Gram-negative bacteria such as Escherichia coli (in peritonitis), Pseudomonas aeruginosa (in cystic fibrosis and ventilation associated pneumonia) and Acinetobacter baumannii (in ventilation associated pneumonia) has been mentioned. Hence, the collaboration between bacteria and Candida spp. might affect biofilm production as C. albicans in coexistence with the sessile microbes possibly enhance biofilms production that is detectable by crystal violet color (16,7). It is interesting to note that C. albicans are normal microbiota in human intestine and gut-translocation from intestine into blood circulation during severe sepsis (gut leakage) is demonstrated. Furthermore, both Gram-negative bacteria and C. albicans are the most and the second most predominant intestinal human microbiota, respectively, in which the natural interactions between these organisms is possible. Accordingly, catheter-related bacteremia is common among patients in ICU. Gut translocation of Candida spp. during sepsis, due to gut leakage, might induce the collaboration between bacteria and fungi results in persistent infection (20-21Chen L, 2011, 66//Wu H, 2015, 1, IJOS). Although the understanding in the interaction between organisms in biofilms should be beneficial for eradication strategies, the data of biofilms from the combination between gut-derived bacteria and fungi is still limited. As such, production of exo-polymers for biofilm-forming is a pathogenic virulent factor because biofilms is one of the important defend-mechanisms against host immune responses and antibiotics. Because i) antibiotic resistance caused by biofilm is a current serious medical problem , ii) the eradication of both bacterial and fungal biofilms is difficult and iii) antimicrobial treatment without biofilms-removal resulting in recurrent or persistent infection (23ref), biofilm prevention agent is needed (2410). Here, we explored i) the interaction between Gram-negative bacteria and C. albicans, in vitro, ii) macrophage responses against biofilm components, iii) biofilms in catheter-insertion mouse model and an evaluation on an interesting anti-biofilm.
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