Evidence map›Paper›PMID 24766550›Full record

ArticleImmunology2014

Nod2 and Rip2 contribute to innate immune responses in mouse neutrophils.

Yu-Jin Jeong, Min-Jung Kang, Sang-Jin Lee, Chang-Hwan Kim, Jee-Cheon Kim, Tae-Hyoun Kim, Dong-Jae Kim, Donghyun Kim, Gabriel Núñez, Jong-Hwan Park

Open access · bronzeAbstract read
In one paragraph

Article in Immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

39 citing papers in PubMed, 65 citations in OpenAlex.

  1. Review
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  16. Isomer-Specific Effects ofAnimals : an open access journal from MDPI · 2021
    Article
  17. Review
  18. Frontiers in cellular and infection microbiology · 2021
    Article
  19. Article
  20. Immunologic mechanism of fungal keratitis.International journal of ophthalmology · 2021
    Review
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

10 authors at 4 institutions in 2 countries.

Yu-Jin JeongDepartment of Biochemistry, College of Medicine, Konyang University, Daejeon, Korea.
Min-Jung Kang
Sang-Jin Lee
Chang-Hwan Kim
Jee-Cheon Kim
Tae-Hyoun Kim
Dong-Jae Kim
Donghyun Kim
Gabriel Núñez
Jong-Hwan Park
Konyang University · KRAgency for Defense Development · KRMichigan Center for Translational Pathology · USUniversity of Michigan · US

Funding

Nod2: A Susceptibility Gene for Crohn's DiseaseR01DK061707 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI NUNEZ, GABRIEL · 2002 to 2017
$4.7M
NIDDK NIH HHS DK61707NIDDK NIH HHS R01 DK061707
6 · The paper itself

Abstract

Nod-like receptors are a family of innate immune receptors that link cytosolic sensing of microbial and danger stimuli to the activation of immune responses. Two Nod-like receptor family members, Nod1 and Nod2, recognize bacterial peptidoglycan and activate immune responses via nuclear factor-κB (NF-κB) and mitogen-activated protein kinase (MAPK). The function of Nod1 and Nod2 has been largely studied in macrophages, but the role of these receptors in other innate immune cells remains unclear. In this study, we examined the function of Nod1 and Nod2 in innate immune responses of neutrophils. Mice were injected intraperitoneally with thioglycollate, and then peritoneal neutrophils were isolated 4 hr after injection. Tri-DAP and muramyl-dipeptide (MDP) were used as Nod1 and Nod2 agonists, respectively. The level of cytokines [interleukin-6 (IL-6) and tumour necrosis factor-α (TNF-α)] and chemokines (CXCL1 and CCL2) was increased by MDP, but not Tri-DAP in wild-type (WT) neutrophils. Increased production of cytokines and chemokines with MDP was abolished in Nod2- and Rip2-deficient neutrophils. MDP also induced the activation of NF-κB and MAPK in WT neutrophils, but not in Nod2- and Rip2-deficient cells. Flow cytometry analysis showed that L-selectin shedding was induced by MDP in WT neutrophils, but not in Nod2- and Rip2-deficient cells. MDP and Toll-like receptor (TLR) agonists (Pam3 CSK4 and lipopolysaccharide) exerted synergistic effects on the production of IL-6 and CXCL1 in neutrophils. Moreover, Nod2 and TLR4 cooperated to produce IL-6, TNF-α, CXCL1 and CCL2 in neutrophils in response to Gram-negative bacteria. Our findings suggest that the Nod2-Rip2 axis may contribute to the innate immune response of neutrophils against bacterial infection.

Indexed as

Immunity, InnateNeutrophil ActivationAcetylmuramyl-Alanyl-IsoglutamineAnimalsCells, CulturedChemokine CCL2Chemokine CXCL1Diaminopimelic AcidInterleukin-6LipopolysaccharidesListeria monocytogenesL-SelectinMiceMice, Inbred C57BLMice, KnockoutMitogen-Activated Protein KinasesAcetylmuramyl-Alanyl-IsoglutamineCcl2 protein, mouseChemokine CCL2Chemokine CXCL1Cxcl1 protein, mouseDiaminopimelic AcidInterleukin-6interleukin-6, mouseL-Ala-gamma-D-Glu-meso-diaminopimelic acidlipopolysaccharide, Escherichia coli O111 B4LipopolysaccharidesL-SelectinMitogen-Activated Protein KinasesNF-kappa BNod1 protein, mouseNod1 Signaling Adaptor ProteinNod2 protein, mouseNod2 Signaling Adaptor ProteinOligopeptidesReceptor-Interacting Protein Serine-Threonine Kinase 2Receptor-Interacting Protein Serine-Threonine KinasesRipk2 protein, mouseTlr4 protein, mouseToll-Like Receptor 4Tumor Necrosis Factor-alphaimmune responsemuramyl dipeptideneutrophilsNod2Rip2

Identifiers

PMID24766550
PMCPMC4172142
OpenAlexW2075783181

What OpenQuestion holds

Textmetadata
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.