Drosophila and Commensal Bacteria Synergistically Compete with Opportunistic Pathogens at Bulk and Single-Cell Resolutions
Ontology highlight
ABSTRACT:
ORGANISM(S): Lactiplantibacillus plantarum Serratia marcescens
PROVIDER: GSE251783 | GEO | 2024/10/01
REPOSITORIES: GEO
Similar Datasets
Project description:A challenging task to reveal health and disease-associated microbiome signatures is to disentangle regulatory networks of microbes among themselves and with their host. Using the integrated Drosophila-commensal-pathogen model system, we here reported that Drosophila and commensal bacterium L. plantarum cooperated to compete with the opportunistic pathogen S. marcescens. At first, we found that Drosophila larvae and L. plantarum efficiently antagonized S. marcescens in the coexisting niche by suppressing population size and altering metabolism. Drosophila and L. plantarum synergistically enforced the transcriptional reprogramming of S. marcescens, including lipopolysaccharide synthesis, peptidoglycan synthesis, and cationic antimicrobial peptide (CAMP) resistance. More importantly, bacterial single-cell RNA sequencing reveals that larvae and L. plantarum modulated carbon utilization and resistance heterogeneity of S. marcescens. On the other hand, L. plantarum adjusted the transcriptional reprogramming in adaption to the alliance with larvae for colonization resistance to S. marcescen. Altogether, our findings provide amenable insight into the host–microbe–microbe interplays at both bulk and single-cell resolutions, advancing fundamental concepts of interactome and precise manipulation of bacterial communities.
2024-10-01 | GSE251782 | GEO
Project description:A challenging task to reveal health and disease-associated microbiome signatures is to disentangle regulatory networks of microbes among themselves and with their host. Using the integrated Drosophila-commensal-pathogen model system, we here reported that Drosophila and commensal bacterium L. plantarum cooperated to compete with the opportunistic pathogen S. marcescens. At first, we found that Drosophila larvae and L. plantarum efficiently antagonized S. marcescens in the coexisting niche by suppressing population size and altering metabolism. Drosophila and L. plantarum synergistically enforced the transcriptional reprogramming of S. marcescens, including lipopolysaccharide synthesis, peptidoglycan synthesis, and cationic antimicrobial peptide (CAMP) resistance. More importantly, bacterial single-cell RNA sequencing reveals that larvae and L. plantarum modulated carbon utilization and resistance heterogeneity of S. marcescens. On the other hand, L. plantarum adjusted the transcriptional reprogramming in adaption to the alliance with larvae for colonization resistance to S. marcescen. Altogether, our findings provide amenable insight into the host–microbe–microbe interplays at both bulk and single-cell resolutions, advancing fundamental concepts of interactome and precise manipulation of bacterial communities.
2024-10-01 | GSE251781 | GEO
Project description:Drosophila and Commensal Bacteria Synergistically Compete with Opportunistic Pathogens at Bulk and Single-Cell Resolutions
| PRJNA1055462 | ENA
Project description:Drosophila and Commensal Bacteria Synergistically Compete with Opportunistic Pathogens at Bulk and Single-Cell Resolutions [bulkRNA-seq]
| PRJNA1055700 | ENA
Project description:Drosophila and Commensal Bacteria Synergistically Compete with Opportunistic Pathogens at Bulk and Single-Cell Resolutions [scRNA-seq]
| PRJNA1055701 | ENA
Project description:Staphylococcus hominis is frequently isolated from human skin and we hypothesize that it may protect the cutaneous barrier from opportunistic pathogens. We determined that S. hominis makes six unique auto inducing peptide (AIP) signals that inhibit the major virulence factor accessory gene regulator (agr) quorum sensing system of Staphylococcus aureus. We solved and confirmed the structures of three novel AIP signals in conditioned media by mass spectrometry, then validated synthetic AIP activity against all S. aureus agr classes. Synthetic AIPs also inhibited the conserved agr system in a related species, Staphylococcus epidermidis. We determined the distribution of S. hominis agr types on healthy human skin and found S. hominis agr-I and agr-II were highly represented across subjects. Further, synthetic AIP-II was protective in vivo against S. aureus-associated dermonecrotic or epicutaneous injury. Together, these findings demonstrate that a ubiquitous colonizer of human skin has a fundamentally protective role against opportunistic damage.
2022-04-04 | GSE199818 | GEO
Project description:Staphylococcus hominis is frequently isolated from human skin, and we hypothesize that it may protect the cutaneous barrier from opportunistic pathogens. We determined that S. hominis makes six unique autoinducing peptide (AIP) signals that inhibit the major virulence factor accessory gene regulator (agr) quorum sensing system of Staphylococcus aureus. We solved and confirmed the structures of three novel AIP signals in conditioned medium by mass spectrometry and then validated synthetic AIP activity against all S. aureus agr classes. Synthetic AIPs also inhibited the conserved agr system in a related species, Staphylococcus epidermidis. We determined the distribution of S. hominis agr types on healthy human skin and found S. hominis agr-I and agr-II were highly represented across subjects. Further, synthetic AIP-II was protective in vivo against S. aureus-associated dermonecrotic or epicutaneous injury. Together, these findings demonstrate that a ubiquitous colonizer of human skin has a fundamentally protective role against opportunistic damage. IMPORTANCE Human skin is home to a variety of commensal bacteria, including many species of coagulase-negative staphylococci (CoNS). While it is well established that the microbiota as a whole maintains skin homeostasis and excludes pathogens (i.e., colonization resistance), relatively little is known about the unique contributions of individual CoNS species to these interactions. Staphylococcus hominis is the second most frequently isolated CoNS from healthy skin, and there is emerging evidence to suggest that it may play an important role in excluding pathogens, including Staphylococcus aureus, from colonizing or infecting the skin. Here, we identified that S. hominis makes 6 unique peptide inhibitors of the S. aureus global virulence factor regulation system (agr). Additionally, we found that one of these peptides can prevent topical or necrotic S. aureus skin injury in a mouse model. Our results demonstrate a specific and broadly protective role for this ubiquitous, yet underappreciated skin commensal.
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