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Postnatal monocyte maturation requires age-dependent initiation of regulatory gene programs when losing birth-associated stress tolerance

ABSTRACT: We disprove that the impaired Myd88-dependent proinflammatory response of neonatal monocytes is a correlate for immaturity and confirm it as display of transient alarmin-mediated stress tolerization. We find a strong inducibility of TRIF-dependent genes in neonatal monocytes by LPS but a barely detectable expression at baseline.

ORGANISM(S): Homo sapiens

PROVIDER: GSE78697 | GEO | 2017/05/01

SECONDARY ACCESSION(S): PRJNA313229

REPOSITORIES: GEO

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Postnatal monocyte maturation requires age-dependent initiation of regulatory gene programs when losing birth-associated stress tolerance

Project description:We disprove that the impaired Myd88-dependent proinflammatory response of neonatal monocytes is a correlate for immaturity and confirm it as display of transient alarmin-mediated stress tolerization. We find a strong inducibility of TRIF-dependent genes in neonatal monocytes by LPS but a barely detectable expression at baseline. Isolated adult blood (AB) and cord blood (CB) monocytes were stimulated for 4h with lipopolysaccharide (LPS).

2017-05-01 | E-GEOD-78697 | biostudies-arrayexpress

Transcription profiling of mouse Myd88-/-Trif-/- and Myd88-/-Rip2-/- macrophages after infection with wild type or dotA mutant L. pneumophila

Project description:Microarray analysis of Myd88-/-Trif-/- and Myd88-/-Rip2-/- macrophage responses to WT or dotA mutant L. pneumophila. Experiment Overall Design: Bone marrow-derived macrophages from Myd88-/-Trif-/- and Myd88-/-Rip2-/- mice were infected with WT L. pneumophila (Lp02) or dotA mutant L. pneumophila (Lp03) for 4 hours. The RNA was extracted, processed, and hybridized onto Affymetrix 430 2.0 microarrays

2008-11-22 | E-GEOD-13147 | biostudies-arrayexpress

Transcription profiling of mouse LPS-stimulated macrophages from wild-type, MyD88-/- and TRIF-/- animals

Project description:Lipopolysaccharide (LPS), a Toll-like receptor (TLR) 4 ligand, activates intracellular signaling via adaptors, MyD88 and TRIF, leading to the expression of various genes including proinflammatory cytokines. We used microarrays to examine influence of MyD88 or TRIF deficiency in LPS-inducible gene expression. Experiment Overall Design: Peritoneal macrophages from wild-type, MyD88-/- and TRIF-/- mice were stimulated with LPS for 0, 1 and 4 hours, followed by RNA extraction. Then hybridization on affymetrix microarrays was performed.

2009-03-01 | E-GEOD-14890 | biostudies-arrayexpress

Myd88, Trif, and Rip2-independent macrophage responses to Legionella pneumophila

Project description:Microarray analysis of Myd88-/-Trif-/- and Myd88-/-Rip2-/- macrophage responses to WT or dotA mutant L. pneumophila. Keywords: Expression profiling by microarray

2008-11-15 | GSE13147 | GEO

Oxidative phosphorylation is a key ontogenetic feature of monocyte immunometabolism promoting myeloid differentiation after birth

Project description:Neonates primarily rely on innate immunity, yet their inflammatory responses to microbes, particularly those of monocytes, are usually restricted compared to adults. This is controversially interpreted as immaturity increasing the risk of sepsis or essential programming allowing immune adaptation after birth. Which changes the cellular immunometabolism undergoes after birth and its role in these concepts are poorly defined. Here, we applied transcriptomic, metabolic, and immunological approaches and found that monocytes exhibit an inverse ontogenetic balance of immunometabolism. Our data show that glycolysis in monocytes increases within the first year of life and fuels their inflammatory responsiveness. In contrast, oxidative phosphorylation (OXPHOS) is high in neonatal monocytes supporting myeloid differentiation but declines only gradually during the first five years of life. Treatment of neonatal monocytes with lipopolysaccharide induces an adult-like immunometabolic phenotype. Ketogenic diet restricts glycolysis in adult monocytes, but cannot reactivate OXPHOS and revive a neonatal-like immunometabolic phenotype, suggesting that neonatal metabolism is hardwired and cannot be restored by simple dietary changes. Transcriptional network and population-wide human variation analyses identified E2F1, MYB, STAT1 and FLI1 as important regulators of age-dependent cell functions and related energy demands in human monocytes. Collectively, our findings show that restricted glycolysis and increased OXPHOS are a physiological programming in neonatal monocytes. Premature switching to an adult-like metabolism could untimely enhance inflammatory responses and disrupt important myeloid differentiation, whereas microbial challenges accumulating during childhood seem to induce an essential gradual metabolic switch.

| EGAS00001007555 | EGA

Expression data of LPS-stimulated macrophages from wild-type, MyD88-/- and TRIF-/- mice.

2009-02-19 | GSE14890 | GEO

Cross-linking mass spectrometry identifies interacting regions between VACV A46 and human MAL or MyD88

Project description:Vaccinia virus immunomodulator A46 is a member of the poxviral Bcl-2-like protein family that inhibits the cellular innate immune response at the level of the TIR domain-containing TLR adaptor proteins MAL, MyD88, TRAM and TRIF. The mechanism of interaction of A46 with its targets has remained unclear. We used BS3 and EDC + sulfo-NHS to cross-link A46 to the TIR domains of MAL and MyD88 to help identify interacting residues and regions.

2020-10-02 | PXD018786 | Pride

In vitro responses of PBMC and fibroblasts from patients with TRIF deficiency after TRIF dependent and independent stimuli

Project description:We report here unrelated HSE patients with autosomal recessive (AR) or autosomal dominant (AD) TRIF deficiency. The AR form of the disease is due to a homozygous nonsense mutation, resulting in a complete absence of the TRIF protein. Both the TLR3 and the TRIF-dependent TLR4 signaling pathways are abolished. The AD form of TRIF deficiency is due to a heterozygous missense mutation resulting in a dysfunctional protein. The TLR3 signaling pathway is impaired, whereas the TRIF-dependent TLR4 pathway is unaffected. Both patients however showed reduced capacity to respond to cytosolic double stranded RNA, consistent with recent reports of TRIF’s involvement in the DExD/H-box helicases pathway. Skin fibroblast cell lines were derived from healthy controls (n=3), patient with deficiencies for TRIF (n=1), MYD88 (n=1), and TLR3 (n=1) and cultured for 4 hours in the presence of IL1B (20ng/ml) or poly I:C (25ng/ml) or left unstimulated for the same length of time. PBMCs (previously frozen) collected from a healthy control (n=1) and patients with deficiencies for TRIF (n=1), and MYD88 (n=1) were cultured together with LPS (10ng/ml) or R848 (3ug/ml) for 2hrs or left unstimulated for the same length of time.

2011-10-19 | E-GEOD-32390 | biostudies-arrayexpress

The effect of Monophosphoryl Lipid A (MPLA) on gene expression of wild type, MyD88 KO, and TRIF KO bone marrow-derived macrophages

Project description:We aimed to determine the relative contributions of MyD88- and TRIF-dependent signaling in Toll-like receptor-induced trained immunity in macrophages.

2022-10-28 | GSE205186 | GEO

Expression data from monocyte-derived macrophages after stimulation with mock, LPS, PolyI:C and P3C.

Project description:Pre-stimulation of MDMs with LPS (signals via MyD88 and TRIF dependent pathways) and PolyI:C (signals via a TRIF dependent pathway) leads to a reduced viral infection. In contrast, pre-stimulation with P3C (signals via MyD88 dependent pathway) does not lead to a reduced viral infection. This microarray was performed to find genes that are specifically upregulated in LPS and PolyI:C stimulated MDMs but not P3C stimulated MDMs. So to give us leads into the mechanism involved in the reduction of viral infection.

2013-07-01 | GSE41295 | GEO

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