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Erroneous efferocytosis of live neutrophils during infection prevents the resolution of inflammation [RNAseq_dual_species]

ABSTRACT: Erroneous efferocytosis of live neutrophils during infection prevents the resolution of inflammation [RNAseq_dual_species]

PROVIDER: PRJNA1103070 | ENA |

REPOSITORIES: ENA

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Erroneous efferocytosis of live neutrophils during infection prevents the resolution of inflammation

Project description:Erroneous efferocytosis of live neutrophils during infection prevents the resolution of inflammation

| PRJNA1103064 | ENA

Erroneous efferocytosis of live neutrophils during infection prevents the resolution of inflammation [RNAseq_single_species]

Project description:Erroneous efferocytosis of live neutrophils during infection prevents the resolution of inflammation [RNAseq_single_species]

| PRJNA1103071 | ENA

Erroneous efferocytosis of live neutrophils during infection prevents the resolution of inflammation [RNAseq_dual_species]

Project description:Here, we show that neutrophils infected with the bacterial pathogenPorphyromonas gingivalis (Pg) are internalized alive by macrophages in a manner that bypasses all known efferocytic receptor-ligand interactions. Live cell uptake was mediated by the proteolysis of neutrophil granule proteins by the Pg protease RgpB. Subsequent translocation and recognition of these RgpB-generated efferocytic ligands by macrophage complement receptor 3 (CR3) receptors led to the internalization of live neutrophils by macrophages. Contrary to the immunosuppression induced by apoptotic cells, efferocytosis of live neutrophils was highly inflammatory. Thus, our data show a novel immune subversion strategy employed by a bacterial pathogen that utilizes a previously unknown receptor-ligand interaction for the efferocytosis of live cells and consequently dysregulates the resolution of inflammation.

2025-08-25 | GSE264523 | GEO

Erroneous efferocytosis of live neutrophils during infection prevents the resolution of inflammation [RNAseq_single_species]

2025-08-25 | GSE264522 | GEO

Atypical efferocytosis of live neutrophils dysregulates inflammation during P. gingivalis infection

Project description:Here, we show that neutrophils infected with the bacterial pathogen Porphyromonas gingivalis (Pg) are internalized alive by macrophages in a manner that bypasses all known efferocytic receptor-ligand interactions with highly inflammatory outcomes. Mechanistically, proteolytic cleavage of neutrophil granule proteins by the Pg protease RgpB generated non-canonical ligands that were recognized by macrophage aMb2 (CR3) receptors, facilitating the efferocytosis of live neutrophils. Contrary to the immunosuppression induced by apoptotic cells, efferocytosis of Pg-infected or RgpB-treated live neutrophils was highly inflammatory, with significant delays in efferosomal maturation. Thus, our data show a novel immune subversion strategy employed by a bacterial pathogen that utilizes a previously unknown receptor-ligand interaction for the efferocytosis of live cells and consequently dysregulates the resolution of inflammation.

2025-07-14 | PXD051073 | Pride

Erroneous efferocytosis of live neutrophils during infection prevents the resolution of inflammation

Project description:This SuperSeries is composed of the SubSeries listed below.

2025-08-25 | GSE264524 | GEO

Suppression of Notch during efferocytosis prevents macrophages inflammatory polarization

Project description:Suppression of Notch during efferocytosis prevents macrophages inflammatory polarization

| PRJNA1194505 | ENA

Study of human macrophage reprogramming toward a pro-resolving profile by efferocytosis

Project description:Inﬂammation is a physiopathological process triggered by infection or tissue damage. Immune system initiates coordinated sequential steps in response to these danger signals. Once the threat has been contained inflammation has to be subsequently shut down. Inflammation resolution is initiated by the reprogramming of pro-inflammatory macrophages toward a pro-resolving profile. This reprogramming is induced in particular by the non-phlogistic engulfment of apoptotic cells, mostly apoptotic neutrophils, a process called efferocytosis. As a matter of fact, macrophages are an essential linchpin regulating both inflammation triggering and sustaining and inflammation resolution. This duality can be achieved through the tremendous plasticity of these innate immune cells. Indeed, depending on microenvironmental signals (cytokines, efferocytosis, growth factors…) macrophages can adopt numerous diverse and sometimes antagonistic phenotypes. The mechanisms governing these transitions remain relatively scattered especially in human. With this project we propose to explore the mechanisms involved in human macrophage reprogramming toward a pro-resolving profile after efferocytosis. The stakes are high due to the estimated prevalence of chronic inflammatory diseases in Western society is 5 to 7%. Chronic inflammation is a burden to patient due to life-long debilitating illness and increased mortality and is also a burden to society due to high costs for therapy and care. Finding new therapies to limit chronic inflammation establishment and persistence is thus a highly valuable goal.

2021-12-01 | E-MTAB-8885 | biostudies-arrayexpress

Suppression of Notch during efferocytosis prevents macrophages inflammatory polarization [RNA-seq.HumanMouse]

Project description:Suppression of Notch during efferocytosis prevents macrophages inflammatory polarization [RNA-seq.HumanMouse]

| PRJNA1194507 | ENA

Suppression of Notch during efferocytosis prevents macrophages inflammatory polarization [SLAM-seq]

Project description:Suppression of Notch during efferocytosis prevents macrophages inflammatory polarization [SLAM-seq]

| PRJNA1194508 | ENA