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Lung macrophages mediate helminth resistance through differential activation of recruited monocyte-derived alveolar macrophages and arginine depletion

ABSTRACT: Lung macrophages mediate helminth resistance through differential activation of recruited monocyte-derived alveolar macrophages and arginine depletion

PROVIDER: PRJNA784120 | ENA |

REPOSITORIES: ENA

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Lung macrophages mediate helminth resistance through differential activation of recruited monocyte-derived alveolar macrophages and arginine depletion

Project description:Lung macrophages mediate helminth resistance through differential activation of recruited monocyte-derived alveolar macrophages and arginine depletion

2022-01-13 | GSE189674 | GEO

microarray analysis of bone marrow derived macrophages stimulated with helminth larvae and immune serum

Project description:Mouse bone marrow derived macrophages were stimulated with L3 larvae of the helminth Heligmosomoides polygyrus (Hp) (500 L3 /1 mio cells) in the presence or absence of immune serum (1:50 v:v) from challenge-Hp-infected mice.

2013-12-31 | E-MEXP-3920 | biostudies-arrayexpress

ArgR1 and AhrC Mediate Arginine-Dependent Regulation of Arginine Acquisition- and Virulence Genes in the Human Pathogen Streptococcus pneumoniae

Project description:This SuperSeries is composed of the following subset Series: GSE33033: ahrC mutant compared to D39 wild-type in Streptococcus pneumoniae in CDM + 10 mM arginine GSE33034: argR1 mutant compared to D39 wild-type in Streptococcus pneumoniae in CDM + 10 mM arginine GSE33035: argR1-ahrC mutant compared to D39 wild-type in Streptococcus pneumoniae in CDM + 10 mM arginine GSE33036: Streptococcus pneumoniae D39 wild-type grown in CDM+10 mM arginine compared to D39 wild type grown in CDM + 0.05 mM arginine Refer to individual Series

2011-11-02 | E-GEOD-33043 | biostudies-arrayexpress

Cell origin dictates programming of resident versus recruited macrophages during acute lung injury

Project description:The primary objective of this study was to compare global differences in transcriptional programming of resident and recruited alveolar macrophages in a time-limited murine model of lung inflammation. We first performed RNA sequencing of the resident and recruited alveolar macrophages from initiation through resolution of LPS-induced lung inflammation in the mouse. Our results indicate that despite existing in a shared environment, cell origin is the major determinant of programming of resident and recruited AMs during an acute inflammatory response. Major areas of difference include cell proliferation, inflammatory cytokine production and metabolism.

2017-09-19 | GSE94749 | GEO

Differential plasticity and fate of brain-resident and recruited macrophages during the onset and resolution of neuroinflammation

Project description:Microglia and border-associated macrophages (BAMs) are brain-resident self-renewing cells with important homeostatic functions. However, their fate during and after severe episodes of brain inflammation and their relation to recruited monocyte-derived cells remain poorly understood. Here, we show that Trypanosoma brucei parasites invade the brain via its border regions, triggering a disruption of brain barriers and the recruitment of large numbers of monocytes. Fate-mapping combined with single-cell sequencing revealed the remarkable dynamics of resident macrophages, including microglia accumulation around the ventricular ependyma and an expansion of epiplexus cells. Resident macrophages were important for attracting peripheral immune cells and driving a pro-inflammatory response. However, recruited monocyte-derived macrophages reached higher cell densities and exhibited more transcriptional plasticity, adopting anti-microbial gene expression profiles not observed resident macrophages. Remarkably, recruited macrophages were short-lived and rapidly removed upon disease resolution, while activated resident macrophages progressively reverted towards a homeostatic state. Long-term transcriptional alterations were limited for microglia but more pronounced in BAMs. Together our results reveal the diverging responses and dynamics of resident and recruited macrophages upon Trypanosome invasion of the brain.

2022-08-26 | GSE212078 | GEO

Resident and recruited macrophages differentially contribute to cardiac healing after myocardial ischemia [scRNA-seq]

Project description:Cardiac macrophages are heterogenous in phenotype and functions, which has been associated with differences in their ontogeny. Despite extensive research, our understanding of the precise role of different subsets of macrophages in ischemia/reperfusion injury remains incomplete. We here investigated macrophage lineages and ablated tissue macrophages in homeostasis and after I/R injury in a CSF1R-dependent manner. Genomic deletion of a fms-intronic regulatory element (FIRE) in the Csf1r locus resulted in specific absence of resident homeostatic and antigen-presenting macrophages, without affecting the recruitment of monocyte-derived macrophages to the infarcted heart. Specific absence of homeostatic, monocyte-independent macrophages altered the immune cell crosstalk in response to injury and induced proinflammatory neutrophil polarization, resulting in impaired cardiac remodelling without influencing infarct size. In contrast, continuous CSF1R inhibition led to depletion of both resident and recruited macrophage populations. This augmented adverse remodelling after I/R and led to an increased infarct size and deterioration of cardiac function. In summary, resident macrophages orchestrate inflammatory responses improving cardiac remodelling, while recruited macrophages determine infarct size after I/R injury. These findings attribute distinct beneficial effects to different macrophage populations in the context of myocardial infarction.

2024-04-14 | GSE263545 | GEO

The JMJD3-IRF4 axis regulates M2 macrophage polarization and host responses against helminth infection

Project description:Polarization of macrophages to M1 or M2 cells is important for mounting responses against bacterial and helminth infection respectively. Jumonji domain containing 3 (JMJD3), a histone 3 K27 demethylase, has been implicated in the activation of macrophages. Here we show that JMJD3 is essential for M2 macrophage polarization to helminth infection and chitin, though JMJD3 is dispensable for M1 responses. Furthermore, Jmjd3 is critical for proper bone marrow macrophage differentiation in a demethylase activity-dependent manner. Jmjd3 deficiency affected trimethylation of H3K27 in only a limited numbers of genes. Among them, we identified Irf4 as the target transcription factor critical for controlling M2 macrophage polarization. Collectively, these results show that JMJD3-mediated H3K27 demethylation is critical for regulating M2 macrophage development leading to anti-helminth host responses. This SuperSeries is composed of the SubSeries listed below.

2010-08-22 | GSE23306 | GEO

Resident and recruited macrophages differentially contribute to cardiac healing after myocardial ischemia [bulk RNA-seq]

2024-04-14 | GSE263544 | GEO

Comparison of F4/80 high and low peritoneal macrophages in H.polygyrus - Salmonella Typhimurium co-infected mice

Project description:Macrophages are involved in many different biological processes (e.g. tissue homeostasis, embryonic development, immune defence against invading pathogens). To be able to deal with these different tasks macrophages adopt distinct activation phenotypes tailored to the situation. However, macrophages show a remarkable degree of plasticity and can change their activation phenotype in response to new environmental triggers. Macrophages recruited to the site of infection can be derived from two main sources, blood monocytes and tissue resident macrophages. Of note, different types of pathogens lead to the accumulation of different types of macrophages. Thus, we have asked here whether helminth expanded, tissue resident derived macrophages will change their activation phenotype in vivo in response to consecutive bacterial co-infection.types of macrophages.

2017-02-14 | GSE85805 | GEO

Arginine methyltransferase regulates monocyte extravasation and function

Project description:Arginine methyltransferase regulates monocyte extravasation and function

| PRJNA767361 | ENA