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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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			Action	DRS
	SRR17053162_1.fastq.gz	Fastqsanger.gz
	SRR17053162_2.fastq.gz	Fastqsanger.gz
	SRR17053163_1.fastq.gz	Fastqsanger.gz
	SRR17053163_2.fastq.gz	Fastqsanger.gz
	SRR17053164_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

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

Helminth resistance is mediated by differential activation of recruited monocyte-derived alveolar macrophages and arginine depletion.

Project description:Macrophages are known to mediate anti-helminth responses, but it remains uncertain which subsets are involved or how macrophages actually kill helminths. Here, we show rapid monocyte recruitment to the lung after infection with the nematode parasite Nippostrongylus brasiliensis. In this inflamed tissue microenvironment, these monocytes differentiate into an alveolar macrophage (AM)-like phenotype, expressing both SiglecF and CD11c, surround invading parasitic larvae, and preferentially kill parasites in vitro. Monocyte-derived AMs (Mo-AMs) express type 2-associated markers and show a distinct remodeling of the chromatin landscape relative to tissue-derived AMs (TD-AMs). In particular, they express high amounts of arginase-1 (Arg1), which we demonstrate mediates helminth killing through L-arginine depletion. These studies indicate that recruited monocytes are selectively programmed in the pulmonary environment to express AM markers and an anti-helminth phenotype.

| S-EPMC9403845 | biostudies-literature

Cancer cell-derived arginine fuels polyamine biosynthesis in tumor-associated macrophages to promote immune evasion

Project description:Cancer cell metabolic reprogramming reshapes the tumor microenvironment (TME) into a pro-tumor niche. Arginine metabolism plays complex roles in regulating tumor progression through metabolic cross-feeding among various cell types within the TME, but the primary intercellular communication dominating the collective impact of arginine on tumor progression remains unclear. Here, we investigated the role of arginine metabolism in breast cancer progression using clinical analysis, single-cell RNA sequencing data analysis, and in vivo animal models. We found that the metabolic interplay between cancer cells and macrophages exerts a predominant influence on breast cancer progression mediated by arginine metabolism. Breast cancer cells act as the major source of arginine within the TME, where this tumor-derived arginine fosters a pro-tumor shift in tumor-associated macrophages (TAMs), leading them to suppress the anti-tumor activity of CD8+ T cells. Notably, this cancer cell-macrophage interaction overrides the stimulatory effect of arginine on the anti-tumor capability of CD8+ T cells. Mechanistically, polyamines derived from arginine metabolism mediate TAM polarization via TDG-mediated DNA demethylation, driven by p53 signaling. Importantly, inhibiting the arginine-polyamine-TDG axis across cancer cells to macrophages effectively suppresses breast cancer growth by modulating the immune microenvironment, suggesting therapeutic potential in targeting this axis for breast cancer therapy.

2025-06-30 | GSE285794 | GEO

Streptococcus pneumoniae D39 wild-type grown in CDM+10 mM arginine compared to D39 wild type grown in CDM + 0.05 mM arginine

Project description:Comparison of Streptococcus pneumoniae D39 wild-type grown in CDM+10 mM arginine compared to D39 wild type grown in CDM + 0.05 mM arginine to define the genome-wide transcriptional response to arginine. Details described in Kloosterman TG and Kuipers OP. ArgR1 and AhrC Mediate Arginine-Dependent Regulation of Arginine Acquisition- and Virulence Genes in the Human Pathogen Streptococcus pneumoniae. JBC 2011 Two condition design comparison of wild type strain

2011-11-02 | E-GEOD-33036 | 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

Influenza-induced activation of recruited alveolar macrophages during the early inflammatory phase drives lung injury and lethality

Project description:we identify gene expression patterns associated with three distinct phases (Infiltrating, Early Inflammatory, Late Inflammatory) in the influenza A virus response of recruited alveolar macrophages. In the Early Inflammatory phase, recruited macrophages begin expressing pro-inflammatory genes, driving cytokine-mediated lung damage and contributing to the morbidity observed in influenza-infected wild-type mice. In mice lacking vimentin (Vim-/-), genes associated with the Early Inflammatory phase are suppressed, while the expression of the Infiltrating Phase genes is maintained, which is associated with protection from influenza-induced injury. Using a bone-marrow chimera mouse model, we validate that Vim-/- recruited alveolar macrophages are sufficient to confer protection from influenza-induced mortality. Our results define the temporal dynamics of gene expression in recruited alveolar macrophages, which shape the host response to infection with respiratory viruses.

2024-08-01 | GSE182637 | GEO

Macrophages mediate systemic tissue health after remote injury

Project description:Macrophages mediate systemic tissue health after remote injury

| PRJNA412396 | ENA

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

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