The Staphylococcus aureus CamS lipoprotein is a repressor of toxin production that shapes host-pathogen interaction
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ABSTRACT:
PROVIDER: PRJNA1000613 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25469867_1.fastq.gz | Fastqsanger.gz | |||
| SRR25469867_2.fastq.gz | Fastqsanger.gz | |||
| SRR25469868_1.fastq.gz | Fastqsanger.gz | |||
| SRR25469868_2.fastq.gz | Fastqsanger.gz | |||
| SRR25469869_1.fastq.gz | Fastqsanger.gz |
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Project description:Lipoproteins of the opportunistic pathogen Staphylococcus aureus play a crucial role in various cellular processes and host interactions. Consisting of a protein and a lipid moiety, they support nutrient acquisition and anchor the protein to the bacterial membrane. Recently, we identified several processed and secreted small linear peptides that derive from the secretion signal sequence of S. aureus lipoproteins. Here, we show for the first time, that the protein moiety of the S. aureus lipoprotein CamS has a biological role that is distinct from its associated linear peptide staph-cAM373. The small peptide was shown to be involved in interspecies horizontal gene transfer, the primary mechanism for the dissemination of antibiotic resistance among bacteria. We provide evidence that the CamS protein moiety is a potent repressor of cytotoxins, such as α-toxin and leukocidins. The CamS-mediated suppression of toxin transcription was reflected by altered disease severity in in vivo infection models involving skin and soft tissue, as well as bloodstream infections. Collectively, we have uncovered the role of the protein moiety of the staphylococcal lipoprotein CamS as a previously uncharacterized repressor of S. aureus toxin production, which consequently regulates virulence and disease outcomes. Notably, the camS gene is conserved in S. aureus, and we also demonstrated the muted transcriptional response of cytotoxins in another S. aureus lineage. Our findings provide the first evidence of distinct biological functions of the protein moiety and its associated linear peptide for a specific lipoprotein. Therefore, lipoproteins in S. aureus consist of three functional components: a lipid moiety, a protein moiety, and a small linear peptide, with putative different biological roles that might not only determine the outcome of host-pathogen interactions but also drive the acquisition of antibiotic resistance determinants.
2023-11-20 | GSE239718 | GEO
Project description: Not available
| S-EPMC10769083 | biostudies-literature
Project description:Perivascular and leptomeningeal macrophages are non-parenchymal macrophages summarized as central nervous system (CNS)-associated macrophages (CAMs) that mediate immune responses at brain boundaries. Both, CAMs and juxtaneuronal microglia are derived from prenatal yolk sac (YS) precursors, long-living and maintain their populations by homeostatic self-renewal without input from the periphery. Whereas microglia have been shown to be repopulated by CNS endogenous remnants of the same lineage following depletion, the renewal biology of CAMs is still poorly understood. Here, by combining multilineage myeloid fate mapping, bulk and single-cell profiling and high resolution confocal imaging, we show that the repopulation is strikingly different between CAMs and microglia. In contrast to microglia, CAMs do not renew exclusively cell-autonomously, but transiently utilize CCR2+Ly-6C+ monocytes after niche induction in an integrin-dependent manner. Remarkably and unlike repopulated microglia, replenished monocyte-derived CAMs remain transcriptionally and functionally distinct from their YS-derived counterparts. Finally, we established a protocol that allows to selectively exchange CAMs modulating disease response without functionally affecting parenchymal microglia. These new insights into the biology of the CNS immune system offer completely new therapeutic avenues for diverse neuroinflammatory and neurodegenerative diseases.
2026-03-01 | GSE294773 | GEO
Project description:Perivascular and leptomeningeal macrophages are non-parenchymal macrophages summarized as central nervous system (CNS)-associated macrophages (CAMs) that mediate immune responses at brain boundaries. Both, CAMs and juxtaneuronal microglia are derived from prenatal yolk sac (YS) precursors, long-living and maintain their populations by homeostatic self-renewal without input from the periphery. Whereas microglia have been shown to be repopulated by CNS endogenous remnants of the same lineage following depletion, the renewal biology of CAMs is still poorly understood. Here, by combining multilineage myeloid fate mapping, bulk and single-cell profiling and high resolution confocal imaging, we show that the repopulation is strikingly different between CAMs and microglia. In contrast to microglia, CAMs do not renew exclusively cell-autonomously, but transiently utilize CCR2+Ly-6C+ monocytes after niche induction in an integrin-dependent manner. Remarkably and unlike repopulated microglia, replenished monocyte-derived CAMs remain transcriptionally and functionally distinct from their YS-derived counterparts. Finally, we established a protocol that allows to selectively exchange CAMs modulating disease response without functionally affecting parenchymal microglia. These new insights into the biology of the CNS immune system offer completely new therapeutic avenues for diverse neuroinflammatory and neurodegenerative diseases.
2026-03-01 | GSE295335 | GEO
Project description:Perivascular and leptomeningeal macrophages are non-parenchymal macrophages summarized as central nervous system (CNS)-associated macrophages (CAMs) that mediate immune responses at brain boundaries. Both, CAMs and juxtaneuronal microglia are derived from prenatal yolk sac (YS) precursors, long-living and maintain their populations by homeostatic self-renewal without input from the periphery. Whereas microglia have been shown to be repopulated by CNS endogenous remnants of the same lineage following depletion, the renewal biology of CAMs is still poorly understood. Here, by combining multilineage myeloid fate mapping, bulk and single-cell profiling and high resolution confocal imaging, we show that the repopulation is strikingly different between CAMs and microglia. In contrast to microglia, CAMs do not renew exclusively cell-autonomously, but transiently utilize CCR2+Ly-6C+ monocytes after niche induction in an integrin-dependent manner. Remarkably and unlike repopulated microglia, replenished monocyte-derived CAMs remain transcriptionally and functionally distinct from their YS-derived counterparts. Finally, we established a protocol that allows to selectively exchange CAMs modulating disease response without functionally affecting parenchymal microglia. These new insights into the biology of the CNS immune system offer completely new therapeutic avenues for diverse neuroinflammatory and neurodegenerative diseases.
2026-03-01 | GSE318071 | GEO
Project description:Perivascular and leptomeningeal macrophages are non-parenchymal macrophages summarized as central nervous system (CNS)-associated macrophages (CAMs) that mediate immune responses at brain boundaries. Both, CAMs and juxtaneuronal microglia are derived from prenatal yolk sac (YS) precursors, long-living and maintain their populations by homeostatic self-renewal without input from the periphery. Whereas microglia have been shown to be repopulated by CNS endogenous remnants of the same lineage following depletion, the renewal biology of CAMs is still poorly understood. Here, by combining multilineage myeloid fate mapping, bulk and single-cell profiling and high resolution confocal imaging, we show that the repopulation is strikingly different between CAMs and microglia. In contrast to microglia, CAMs do not renew exclusively cell-autonomously, but transiently utilize CCR2+Ly-6C+ monocytes after niche induction in an integrin-dependent manner. Remarkably and unlike repopulated microglia, replenished monocyte-derived CAMs remain transcriptionally and functionally distinct from their YS-derived counterparts. Finally, we established a protocol that allows to selectively exchange CAMs modulating disease response without functionally affecting parenchymal microglia. These new insights into the biology of the CNS immune system offer completely new therapeutic avenues for diverse neuroinflammatory and neurodegenerative diseases.
2026-03-01 | GSE318386 | GEO
Project description:Perivascular and leptomeningeal macrophages are non-parenchymal macrophages summarized as central nervous system (CNS)-associated macrophages (CAMs) that mediate immune responses at brain boundaries. Both, CAMs and juxtaneuronal microglia are derived from prenatal yolk sac (YS) precursors, long-living and maintain their populations by homeostatic self-renewal without input from the periphery. Whereas microglia have been shown to be repopulated by CNS endogenous remnants of the same lineage following depletion, the renewal biology of CAMs is still poorly understood. Here, by combining multilineage myeloid fate mapping, bulk and single-cell profiling and high resolution confocal imaging, we show that the repopulation is strikingly different between CAMs and microglia. In contrast to microglia, CAMs do not renew exclusively cell-autonomously, but transiently utilize CCR2+Ly-6C+ monocytes after niche induction in an integrin-dependent manner. Remarkably and unlike repopulated microglia, replenished monocyte-derived CAMs remain transcriptionally and functionally distinct from their YS-derived counterparts. Finally, we established a protocol that allows to selectively exchange CAMs modulating disease response without functionally affecting parenchymal microglia. These new insights into the biology of the CNS immune system offer completely new therapeutic avenues for diverse neuroinflammatory and neurodegenerative diseases.
2026-03-01 | GSE294912 | GEO
Project description:Perivascular and leptomeningeal macrophages are non-parenchymal macrophages summarized as central nervous system (CNS)-associated macrophages (CAMs) that mediate immune responses at brain boundaries. Both, CAMs and juxtaneuronal microglia are derived from prenatal yolk sac (YS) precursors, long-living and maintain their populations by homeostatic self-renewal without input from the periphery. Whereas microglia have been shown to be repopulated by CNS endogenous remnants of the same lineage following depletion, the renewal biology of CAMs is still poorly understood. Here, by combining multilineage myeloid fate mapping, bulk and single-cell profiling and high resolution confocal imaging, we show that the repopulation is strikingly different between CAMs and microglia. In contrast to microglia, CAMs do not renew exclusively cell-autonomously, but transiently utilize CCR2+Ly-6C+ monocytes after niche induction in an integrin-dependent manner. Remarkably and unlike repopulated microglia, replenished monocyte-derived CAMs remain transcriptionally and functionally distinct from their YS-derived counterparts. Finally, we established a protocol that allows to selectively exchange CAMs modulating disease response without functionally affecting parenchymal microglia. These new insights into the biology of the CNS immune system offer completely new therapeutic avenues for diverse neuroinflammatory and neurodegenerative diseases.
2026-03-01 | GSE295334 | GEO
Project description:Perivascular and leptomeningeal macrophages are non-parenchymal macrophages summarized as central nervous system (CNS)-associated macrophages (CAMs) that mediate immune responses at brain boundaries. Both, CAMs and juxtaneuronal microglia are derived from prenatal yolk sac (YS) precursors, long-living and maintain their populations by homeostatic self-renewal without input from the periphery. Whereas microglia have been shown to be repopulated by CNS endogenous remnants of the same lineage following depletion, the renewal biology of CAMs is still poorly understood. Here, by combining multilineage myeloid fate mapping, bulk and single-cell profiling and high resolution confocal imaging, we show that the repopulation is strikingly different between CAMs and microglia. In contrast to microglia, CAMs do not renew exclusively cell-autonomously, but transiently utilize CCR2+Ly-6C+ monocytes after niche induction in an integrin-dependent manner. Remarkably and unlike repopulated microglia, replenished monocyte-derived CAMs remain transcriptionally and functionally distinct from their YS-derived counterparts. Finally, we established a protocol that allows to selectively exchange CAMs modulating disease response without functionally affecting parenchymal microglia. These new insights into the biology of the CNS immune system offer completely new therapeutic avenues for diverse neuroinflammatory and neurodegenerative diseases.
2026-03-01 | GSE318159 | GEO
Project description:The central nervous system (CNS) includes anatomically distinct macrophage populations including parenchyma microglia and CNS-associated macrophages (CAMs). The stepwise development and specification of macrophage populations in the CNS rely on several key transcription factors, such as IRF8 and MAFB. In order to better understand the roles of IRF8 and MAFB for phenotypic determination of homeostatic microglia and CAMs, we performed quantitative bulk RNA sequencing of microglia and CAMs isolated from mouse models with myeloid cell-specific deletion of IRF8 or MAFB transcription factors. We found the distinct transcriptional machinery, mediated by IRF8 and MAFB, which underlies the diversity of macrophages in the CNS.
2024-07-09 | GSE269745 | GEO