Ontology highlight
ABSTRACT:
PROVIDER: PRJNA488339 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7764501.fastq.gz | Fastqsanger.gz | |||
| SRR7764502.fastq.gz | Fastqsanger.gz | |||
| SRR7764503.fastq.gz | Fastqsanger.gz | |||
| SRR7764504.fastq.gz | Fastqsanger.gz | |||
| SRR7764505.fastq.gz | Fastqsanger.gz |
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Project description:Trained immunity is a phenomenon where innate immune cells develop and long-lasting pro-inflammatory reprogramming mediated by epigenetic and metabolic reprogramming. Trained immunity can be peropheral (circulating monocytes) or central (bone marrow) and it can be caused by exposure to β-glucan, BCG and Western Type Diet vial IL-1β signaling.
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Project description:The main purpose of our study is to investigate if muscle damage in mdx mice alters the phenotype of macropahges at precursor level in the bone marrow. Here we show major remodeling of the epigenetic, metabolic and functional inflammatory profiles of monocyte-derived macrophages from the bone marrow of mdx mice is TLR4-dependent. This altered phenotype of mdx BMDM demonstrates the hallmark features of trained immunity, including being transmissible and long-lasting after bone marrow transplantation to non-dystrophic mice.
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Project description:Systemic inflammation (SI) is a prevalent condition with a high mortality rate1. Survivors of hyperinflammatory state of SI frequently enter a long-lasting immunosuppressive state2 deteriorating their life quality3,4. Due to the extensive heterogeneity in SI etiology, the underlying mechanisms are not well understood. Here, we characterized the short and long-term effects of lipopolysaccharide (LPS)-induced SI (LPS-SI, also called endotoxemia5) on blood monocytes and bone marrow (BM) cells. Similar to clinical features of SI, we observed a profound but transient acute LPS response, followed by a long-term immunosuppressed state. Single-cell transcriptomic analysis of LPS-SI acute phase unveiled the loss of BM monocytes and the appearance of an inflammatory monocyte-like (i-Mono’s) population, expressing gene programs similar to a cell state identified in early-stage sepsis patients6. We observed impairment of myelopoiesis one week after LPS-SI manifested by a significant loss of intermediate and non-classical monocytes which is associated with reduced expression of interferon type I (IFN-I) genes. We confirm that this compromised myelopoiesis also happens in late-stage sepsis patients. Importantly, IFNb treatment reverted the LPS-induced immunosuppression in monocytes. Our results deepened the knowledge about SI and its long-lasting effects on myelopoiesis, substantiating the importance of IFN-I in the pathophysiology of SI-induced immunosuppression.
2025-03-15 | GSE212092 | GEO
Project description:Systemic inflammation (SI) is a prevalent condition with a high mortality rate1. Survivors of hyperinflammatory state of SI frequently enter a long-lasting immunosuppressive state2 deteriorating their life quality3,4. Due to the extensive heterogeneity in SI etiology, the underlying mechanisms are not well understood. Here, we characterized the short and long-term effects of lipopolysaccharide (LPS)-induced SI (LPS-SI, also called endotoxemia5) on blood monocytes and bone marrow (BM) cells. Similar to clinical features of SI, we observed a profound but transient acute LPS response, followed by a long-term immunosuppressed state. Single-cell transcriptomic analysis of LPS-SI acute phase unveiled the loss of BM monocytes and the appearance of an inflammatory monocyte-like (i-Mono’s) population, expressing gene programs similar to a cell state identified in early-stage sepsis patients6. We observed impairment of myelopoiesis one week after LPS-SI manifested by a significant loss of intermediate and non-classical monocytes which is associated with reduced expression of interferon type I (IFN-I) genes. We confirm that this compromised myelopoiesis also happens in late-stage sepsis patients. Importantly, IFNb treatment reverted the LPS-induced immunosuppression in monocytes. Our results deepened the knowledge about SI and its long-lasting effects on myelopoiesis, substantiating the importance of IFN-I in the pathophysiology of SI-induced immunosuppression.
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Project description:Impairment of the intestinal barrier allows the systemic translocation of commensal bacteria, inducing a pro-inflammatory state in the host. To explore this link, we investigated innate immune responses following increased gut permeability upon administration of dextran sulfate sodium (DSS) in mice. We found that microbiota translocation induced trained immunity (TI) in mouse myeloid bone marrow progenitors (BMPs). Enterococcus faecalis was isolated from bone marrow following DSS treatment and induced trained immunity hallmarks in bone marrow-derived mouse macrophages and human monocytes. Notably, DSS treatment or heat-killed E. faecalis reprogrammed BMPs, resulting in enhanced inflammatory responses in vitro and in vivo, and protection against pathogen infections. The C-type lectin receptor Mincle (Clec4e) was essential for E. faecalis-induced TI in BMPs. Clec4e-/- mice showed impaired TI upon E. faecalis and reduced pathology following DSS treatment. Thus, Mincle sensing of E. faecalis induces TI that may contribute to pathologies associated with increased gut permeability. This SuperSeries is composed of the SubSeries listed below.
2025-01-22 | GSE281377 | GEO
Project description:Trained immunity is the phenomenon whereby innate immune cells such as monocytes or macrophages, and their progenitors in the bone-marrow, undergo functional reprogramming after exposure to certain microbial and danger signals, altering their responses to future exposures. In this study, we performed a non-lethal Plasmodium yoelii 17XNL (Py) infection in wild-type C57/BL6J mice to investigate the underlying mechanism of Py-induced myelopoiesis and performed transcriptomic analysis on HSPCs, GMPs, and monocytes 6 weeks following exposure. Next cecal ligation and puncture (CLP) was used to model sepsis in vivo as a secondary exposure, and the transcriptomes of PBS and Py-exposed monocytes were generated.
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Project description:Innate immune memory is a new important area of research. However, innate immune memory at the major mucosal sites remains poorly understood. Here we show that respiratory viral infection induces long-lasting memory alveolar macrophages (AM). Memory AM are programed to express high MHC II, carry a defense-ready gene signature, and produce, upon re-stimulation, neutrophil chemokines. Using a multitude of approaches, we reveal that the priming, but not maintenance, of memory AM requires the help from effector CD8 T cells. T cells jump-start this process in AM via IFN-γ production. We further find that formation/maintenance of memory AM are independent of monocytes or bone marrow progenitors. Finally, we demonstrate that memory AM are poised for robust trained immunity against bacterial infection in the lung via rapid induction of chemokines and neutrophilia. Our study thus establishes a new paradigm of immunological memory formation whereby adaptive T-lymphocytes render innate memory of mucosal-associated macrophages.
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Project description:Phloroglucinol is a key byproduct of gut microbial metabolism that has been widely used as a treatment for irritable bowel syndrome. Here, we demonstrate that phloroglucinol tempers macrophage responses to pro-inflammatory pathogens and stimuli. In vivo, phloroglucinol administration decreases gut and extraintestinal inflammation in murine models of inflammatory bowel disease and systemic infection. The metabolite induces modest modifications in the microbiota. However, the presence of an active microbiota is required to preserve its anti-inflammatory activity. Remarkably, the protective effect of phloroglucinol lasts partially at least 6 months. Single-cell transcriptomic analysis of bone marrow progenitors demonstrates the capacity of the metabolite to induce long-lasting innate immune training in hematopoietic lineages, at least partially through the participation of the receptor and transcription factor, aryl hydrocarbon receptor (AhR). Phloroglucinol induces alterations in metabolic and epigenetic pathways that are most prevalent in upstream progenitors as hallmarks of central trained immunity. These data identify phloroglucinol as a dietary-derived compound capable of inducing central trained immunity and modulating the response of the host to inflammatory insults.
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Project description:MV130 is an inactivated polybacterial mucosal vaccine that confers protection to patients against recurrent respiratory infections, including those of viral etiology. We showed that MV130 induces long term heterologous protection against viral respiratory infections in mice by a mechanism associated with the induction of trained immunity. Moreover, we found that MV130 induces reprogramming of in vitro human monocytes promoting metabolic changes and enhanced cytokine production. To assess the role of epigenetic changes in MV130-mediated trained immunity induction in human monocytes we measured the chromatin accessibility landscape using ATAC-seq.
2021-11-10 | GSE183485 | GEO
Project description:Sepsis is a leading cause of death worldwide, with most patient mortality stemming from lingering immunosuppression in sepsis survivors. This is due in part to immune dysfunction stemming from monocyte exhaustion, a phenotype of reduced antigen presentation, altered CD14/CD16 inflammatory subtypes, and disrupted cytokine production. Whereas previous research demonstrated improved sepsis survival in Ticam2-/- mice, the contribution of TICAM2 signaling to long-term exhaustion memory was unknown. Using a cecal slurry injection sepsis model, we monitored the establishment and recovery of monocyte exhaustion in Ticam2-/- mice. Like wild-type controls, Ticam2-/- monocytes develop an exhaustion phenotype defined by CD38high; CX3CR1low; MHCIIlow cell surface expression 48 hours after sepsis onset. Time course analysis of sepsis patient blood samples revealed a similar effect in human monocytes, which steadily transition into a CD38high; CX3CR1low; HLA-DRlow state within four days of hospital admittance. To determine the impact of TICAM2 ablation on innate epigenetic memory in sepsis, we measured genome-wide DNA methylation in bone marrow monocytes and found that Ticam2-/- cells exhibit a unique profile of altered methylation at CEBPE binding sites and regulatory features for key immune genes such as Dmkn and Btg1. Finally, after one week of sepsis recovery, we profiled bone marrow and splenic reservoir monocytes in Ticam2-/- mice and found that, in contrast to the persistent exhaustion observed in wild-type monocytes, Ticam2-/- monocytes largely resembled healthy controls. Thus, in addition to improving survival during the inflammatory phase of sepsis progression, TICAM2 ablation facilitates the resolution of monocyte exhaustion in sepsis survivors.
2025-01-21 | GSE271939 | GEO