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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

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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

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

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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.

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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

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2022-10-28 | GSE205186 | GEO

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

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2013-07-01 | GSE41295 | GEO

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