Evidence map›Paper›PMID 20937845›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2010

CXCL1 regulates pulmonary host defense to Klebsiella Infection via CXCL2, CXCL5, NF-kappaB, and MAPKs.

Shanshan Cai, Sanjay Batra, Sergio A Lira, Jay K Kolls, Samithamby Jeyaseelan

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

91 citing papers in PubMed, 123 citations in OpenAlex.

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  15. Phagocytosis is a primary determinant of pulmonary clearance of clinicalFrontiers in cellular and infection microbiology · 2023
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  16. Thirty-five years since the discovery of chemotactic cytokines, interleukin-8 and MCAF: A historical overview.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2023
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31 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 1 country.

Shanshan CaiDepartment of Pathobiological Sciences,Louisiana State University, Baton Rouge, LA 70803, USA.
Sanjay Batra
Sergio A Lira
Jay K Kolls
Samithamby Jeyaseelan
Louisiana State University · USIcahn School of Medicine at Mount Sinai · USLouisiana 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
NHLBI NIH HHS R01 HL-091958NHLBI NIH HHS R01 HL091958NHLBI NIH HHS R01 HL-091958S1
6 · The paper itself

Abstract

Pulmonary bacterial infections are a leading cause of death. Since the introduction of antibiotics, multidrug-resistant Klebsiella pneumoniae became an escalating threat. Therefore, development of methods to augment antibacterial defense is warranted. Neutrophil recruitment is critical to clear bacteria, and neutrophil migration in the lung requires the production of ELR(+) CXC chemokines. Although lung-specific CXCL1/keratinocyte cell-derived chemokine (KC) transgene expression causes neutrophil-mediated clearance of K. pneumoniae, the mechanisms underlying KC-mediated host defense against K. pneumoniae have not been explored. In this study, we delineated the host defense functions of KC during pulmonary K. pneumoniae infection using KC(-/-) mice. Our findings demonstrate that KC is important for expression of CXCL2/MIP-2 and CXCL5/LPS-induced CXC chemokine, and activation of NF-κB and MAPKs in the lung. Furthermore, KC derived from both hematopoietic and resident cells contributes to host defense against K. pneumoniae. Neutrophil depletion in mice before K. pneumoniae infection reveals no differences in the production of MIP-2 and LPS-induced CXC chemokine or activation of NF-κB and MAPKs in the lung. Using murine bone marrow-derived and alveolar macrophages, we confirmed KC-mediated upregulation of MIP-2 and activation of NF-κB and MAPKs on K. pneumoniae infection. Moreover, neutralizing KC in bone marrow-derived macrophages before K. pneumoniae challenge decreases bacteria-induced production of KC and MIP-2, and activation of NF-κB and MAPKs. These findings reveal the importance of KC produced by hematopoietic and resident cells in regulating pulmonary host defense against a bacterial pathogen via the activation of transcription factors and MAPKs, as well as the expression of cell adhesion molecules and other neutrophil chemoattractants.

Indexed as

AnimalsBlotting, WesternChemokine CXCL1Chemokine CXCL2Chemokine CXCL5Enzyme ActivationEnzyme-Linked Immunosorbent AssayGene Expression RegulationIntercellular Adhesion Molecule-1Klebsiella InfectionsLung DiseasesMiceMice, Inbred C57BLMice, KnockoutMitogen-Activated Protein KinasesNF-kappa BChemokine CXCL1Chemokine CXCL2Chemokine CXCL5Intercellular Adhesion Molecule-1Mitogen-Activated Protein KinasesNF-kappa BVascular Cell Adhesion Molecule-1

Identifiers

PMID20937845
PMCPMC2974054
OpenAlexW2159545888

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.