Neutrophil mobilization from the bone marrow during polymicrobial sepsis is dependent on CXCL12 signaling. - Wikidata - wikimedia - TriplyDB

Neutrophil mobilization from the bone marrow during polymicrobial sepsis is dependent on CXCL12 signaling.

Neutrophil mobilization from the bone marrow during polymicrobial sepsis is dependent on CXCL12 signaling.

http://www.wikidata.org/entity/Q30419805

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Immunological cells and functions in Gaucher disease Administration of a CXCL12 Analog in Endotoxemia Is Associated with Anti-Inflammatory, Anti-Oxidative and Cytoprotective Effects In Vivo Administration of AMD3100 in endotoxemia is associated with pro-inflammatory, pro-oxidative, and pro-apoptotic effects in vivo Localized bacterial infection induces systemic activation of neutrophils through Cxcr2 signaling in zebrafish.Infection mobilizes hematopoietic stem cells through cooperative NOD-like receptor and Toll-like receptor signaling.Elevated plasma stromal-cell-derived factor-1 protein levels correlate with severity in patients with community-acquired pneumonia.TRIF-dependent innate immune activation is critical for survival to neonatal gram-negative sepsis.Delayed emergency myelopoiesis following polymicrobial sepsis in neonates.Dietary supplementation with Lactobacilli improves emergency granulopoiesis in protein-malnourished mice and enhances respiratory innate immune response Early severe impairment of hematopoietic stem and progenitor cells from the bone marrow caused by CLP sepsis and endotoxemia in a humanized mice model Touch of chemokines.Acute-Phase Deaths from Murine Polymicrobial Sepsis Are Characterized by Innate Immune Suppression Rather Than Exhaustion Sex-specific regulation of chemokine Cxcl5/6 controls neutrophil recruitment and tissue injury in acute inflammatory states.Early sensing of Yersinia pestis airway infection by bone marrow cells.Sepsis-induced immune dysfunction: can immune therapies reduce mortality?Role of G-CSF in monophosphoryl lipid A-mediated augmentation of neutrophil functions after burn injury.Persistent Inflammation, Immunosuppression, and Catabolism: Evolution of Multiple Organ Dysfunction.Persistent inflammation and immunosuppression: a common syndrome and new horizon for surgical intensive care New strategy for sepsis: Targeting a key role of platelet-neutrophil interaction.Homologous lactoferrin triggers mobilization of the myelocytic lineage of bone marrow in experimental mice.The Role of the Bone Marrow Stromal Compartment in the Hematopoietic Response to Microbial Infections.The transcriptional repressor BLIMP1 curbs host defenses by suppressing expression of the chemokine CCL8.Natural nitration of CXCL12 reduces its signaling capacity and chemotactic activity in vitro and abrogates intra-articular lymphocyte recruitment in vivo.Regulation of neutrophil trafficking from the bone marrow.Current insights into neutrophil homeostasis.Inflammatory response following neutrophil recovery postchemotherapy in acute myeloid leukemia cases without evidence of infection: role of homing of neutrophils.Neutrophil migration under normal and sepsis conditions.Pharmacological modulation of C-X-C motif chemokine receptor 4 influences development of acute respiratory distress syndrome after lung ischemia-reperfusion injury.Obesity alters the lung myeloid cell landscape to enhance breast cancer metastasis through IL5 and GM-CSF.White Blood Cell Counts, Alcoholism, and Cirrhosis in Pneumococcal Pneumonia The immune system's role in sepsis progression, resolution, and long-term outcome.Neutrophil dysregulation during sepsis: an overview and update.Human Brain Chemokine and Cytokine Expression in Sepsis: A Report of Three Cases.Surgical and immune reconstitution murine models in bone marrow research: Potential for exploring mechanisms in sepsis, trauma and allergy.Targeting ADAM17 in leukocytes increases neutrophil recruitment and reduces bacterial spread during polymicrobial sepsis.Improved emergency myelopoiesis and survival in neonatal sepsis by caspase-1/11 ablation.Combined treatment with a CXCL12 analogue and antibiotics improves survival and neutrophil recruitment and function in murine sepsis.Establishment of a novel mouse model of ulcerative colitis with concomitant cytomegalovirus infection: in vivo identification of cytomegalovirus persistent infected cells.Diabetes and Sepsis: Risk, Recurrence, and Ruination.CXCR4 blockade decreases CD4+ T cell exhaustion and improves survival in a murine model of polymicrobial sepsis.

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P2860

Neutrophil mobilization from the bone marrow during polymicrobial sepsis is dependent on CXCL12 signaling.

http://www.wikidata.org/entity/Q30419805

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2011 nî lūn-bûn

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2011 թուականի Յունիսին հրատարակուած գիտական յօդուած

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2011 թվականի հունիսին հրատարակված գիտական հոդված

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2011年の論文

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Neutrophil mobilization from t ...... dependent on CXCL12 signaling.

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Neutrophil mobilization from t ...... dependent on CXCL12 signaling.

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Neutrophil mobilization from t ...... dependent on CXCL12 signaling.

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Neutrophil mobilization from t ...... dependent on CXCL12 signaling.

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Neutrophil mobilization from t ...... dependent on CXCL12 signaling.

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JIMMUNOL.1100588

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Journal of Immunology

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Neutrophil mobilization from t ...... dependent on CXCL12 signaling.

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P2093

Alex G Cuenca

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Clayton E Mathews

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Drake Laface

http://www.w3.org/2001/XMLSchema#string

Elizabeth Warner

http://www.w3.org/2001/XMLSchema#string

Kerri A O'Malley

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Kindra M Kelly-Scumpia

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Lyle L Moldawer

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Matthew J Delano

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Paul G Heyworth

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Philip A Efron

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P2860

Epidemiology of severe sepsis in the United States: analysis of incidence, outcome, and associated costs of care

The epidemiology of sepsis in the United States from 1979 through 2000

The pathophysiology and treatment of sepsis

Lymphoid organ development and cell migration.

CXCR2 and CXCR4 antagonistically regulate neutrophil trafficking from murine bone marrow

Rapid mobilization of murine and human hematopoietic stem and progenitor cells with AMD3100, a CXCR4 antagonist

Increased natural CD4+CD25+ regulatory T cells and their suppressor activity do not contribute to mortality in murine polymicrobial sepsis.

Treatment with GITR agonistic antibody corrects adaptive immune dysfunction in sepsis.

Cecal ligation and puncture.

Adoptive transfer of apoptotic splenocytes worsens survival, whereas adoptive transfer of necrotic splenocytes improves survival in sepsis.

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911-918

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scholarly article

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10.4049/JIMMUNOL.1100588

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2

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187

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2011-06-20T00:00:00Z

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51235658

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21690321

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3635667

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