Evidence map›Paper›PMID 25172493›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2014

CXCL1 contributes to host defense in polymicrobial sepsis via modulating T cell and neutrophil functions.

Liliang Jin, Sanjay Batra, David Nobuhiro Douda, Nades Palaniyar, Samithamby Jeyaseelan

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
3.5field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

70 citing papers in PubMed, 112 citations in OpenAlex.

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  16. HMGB1 released by mesothelial cells drives the development of asbestos-induced mesothelioma.Proceedings of the National Academy of Sciences of the United States of America · 2023
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10 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 2 countries.

Liliang JinLaboratory of Lung Biology, Department of Pathobiological Sciences, Center for Experimental Infectious Disease Research, Louisiana State University School of Veterinary Medicine, Baton Rouge, LA 70803;
Sanjay BatraLaboratory of Lung Biology, Department of Pathobiological Sciences, Center for Experimental Infectious Disease Research, Louisiana State University School of Veterinary Medicine, Baton Rouge, LA 70803;
David Nobuhiro DoudaProgram in Physiology and Experimental Medicine, SickKids Research Institute, Toronto, Ontario M5G 1X8, Canada; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario M5S 1A8, Canada; and.
Nades PalaniyarProgram in Physiology and Experimental Medicine, SickKids Research Institute, Toronto, Ontario M5G 1X8, Canada; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario M5S 1A8, Canada; and.
Samithamby JeyaseelanLaboratory of Lung Biology, Department of Pathobiological Sciences, Center for Experimental Infectious Disease Research, Louisiana State University School of Veterinary Medicine, Baton Rouge, LA 70803; Division of Pulmonary and Critical Care Medicine, Department of Medicine, Louisiana State University Health Sciences Center, New Orleans, LA 70112 jey@lsu.edu.
Louisiana State University · USUniversity of Toronto · CALouisiana State University Health Sciences Center New Orleans · US

Funding

Neutrophil Accumulation in Bacterial PneumoniaR01HL091958 · NHLBI · LOUISIANA STATE UNIV A&M COL BATON ROUGE · PI JEYASEELAN, SAMITHAMBY · 2008 to 2017
$3.8M
NOD-Like Receptor Signaling is Critical to Secondhand Smoke-Induced Immunity andR15ES023151 · NIEHS · SOUTHERN UNIV A&M COL BATON ROUGE · PI BATRA, SANJAY · 2013 to 2016
$369k
NHLBI NIH HHS 2R01 HL-091958NHLBI NIH HHS R01 HL091958NIEHS NIH HHS 1R15ES023151-01
6 · The paper itself

Abstract

Severe bacterial sepsis leads to a proinflammatory condition that can manifest as septic shock, multiple organ failure, and death. Neutrophils are critical for the rapid elimination of bacteria; however, the role of neutrophil chemoattractant CXCL1 in bacterial clearance during sepsis remains elusive. To test the hypothesis that CXCL1 is critical to host defense during sepsis, we used CXCL1-deficient mice and bone marrow chimeras to demonstrate the importance of this molecule in sepsis. We demonstrate that CXCL1 plays a pivotal role in mediating host defense to polymicrobial sepsis after cecal ligation and puncture in gene-deficient mice. CXCL1 appears to be essential for restricting bacterial outgrowth and death in mice. CXCL1 derived from both hematopoietic and resident cells contributed to bacterial clearance. Moreover, CXCL1 is essential for neutrophil migration, expression of proinflammatory mediators, activation of NF-κB and MAPKs, and upregulation of adhesion molecule ICAM-1. rIL-17 rescued impaired host defenses in cxcl1(-/-) mice. CXCL1 is important for IL-17A production via Th17 differentiation. CXCL1 is essential for NADPH oxidase-mediated reactive oxygen species production and neutrophil extracellular trap formation. This study reveals a novel role for CXCL1 in neutrophil recruitment via modulating T cell function and neutrophil-related bactericidal functions. These studies suggest that modulation of CXCL1 levels in tissues and blood could reduce bacterial burden in sepsis.

Indexed as

AnimalsCell DifferentiationCell MovementChemokine CXCL1Extracellular Signal-Regulated MAP KinasesInterleukin-17MAP Kinase Signaling SystemMiceMice, KnockoutNeutrophilsNF-kappa BSepsisTh17 CellsChemokine CXCL1Cxcl1 protein, mouseExtracellular Signal-Regulated MAP KinasesIl17a protein, mouseInterleukin-17NF-kappa B

Identifiers

PMID25172493
PMCPMC4170008
OpenAlexW1711544787

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.