Evidence map›Paper›PMID 31539400›Full record

ArticlePloS one2019

Mice deficient in NKLAM have attenuated inflammatory cytokine production in a Sendai virus pneumonia model.

Donald W Lawrence, Laurie P Shornick, Jacki Kornbluth

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

10 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. The RING finger protein family in health and disease.Signal transduction and targeted therapy · 2022
    Review
  7. Review
  8. Annals of translational medicine · 2021
    Article
  9. Article
  10. 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

3 authors at 2 institutions in 1 country.

Donald W LawrenceDepartment of Pathology, Saint Louis University School of Medicine, Saint Louis, Missouri, United States of America.ORCID 0000-0001-5912-6992
Laurie P ShornickDepartment of Biology, Saint Louis University, Saint Louis, Missouri, United States of America.
Jacki KornbluthDepartment of Pathology, Saint Louis University School of Medicine, Saint Louis, Missouri, United States of America.ORCID 0000-0001-7726-781X
Saint Louis University · USVA St. Louis Health Care System · US

Funding

NKLAM: An RBR E3 Ubiquitin Ligase Essential for Regulation of Innate ImmunityI01BX000705 · VA · ST. LOUIS VA MEDICAL CENTER · PI KORNBLUTH, JACKI · 2012 to 2020
–
BLRD VA I01 BX000705
6 · The paper itself

Abstract

Recent studies have begun to elucidate a role for E3 ubiquitin ligases as important mediators of the innate immune response. Our previous work defined a role for the ubiquitin ligase natural killer lytic-associated molecule (NKLAM/RNF19b) in mouse and human innate immunity. Here, we present novel data describing a role for NKLAM in regulating the immune response to Sendai virus (SeV), a murine model of paramyxoviral pneumonia. NKLAM expression was significantly upregulated by SeV infection. SeV-infected mice that are deficient in NKLAM demonstrated significantly less weight loss than wild type mice. In vivo, Sendai virus replication was attenuated in NKLAM-/- mice. Autophagic flux and the expression of autophagy markers LC3 and p62/SQSTM1 were also less in NKLAM-/- mice. Using flow cytometry, we observed less neutrophils and macrophages in the lungs of NKLAM-/- mice during SeV infection. Additionally, phosphorylation of STAT1 and NFκB p65 was lower in NKLAM-/- than wild type mice. The dysregulated phosphorylation profile of STAT1 and NFκB in NKLAM-/- mice correlated with decreased expression of numerous proinflammatory cytokines that are regulated by STAT1 and/or NFκB. The lack of NKLAM and the resulting attenuated immune response is favorable to NKLAM-/- mice receiving a low dose of SeV; however, at a high dose of virus, NKLAM-/- mice succumbed to the infection faster than wild type mice. In conclusion, our novel results indicate that NKLAM plays a role in regulating the production of pro-inflammatory cytokines during viral infection.

Indexed as

Disease Models, AnimalAnimalsCytokinesHumansImmunity, InnateInflammation MediatorsMacrophagesMembrane ProteinsMice, 129 StrainMice, Inbred C57BLMice, KnockoutPhosphorylationPneumoniaRespirovirus InfectionsSendai virusSequestosome-1 ProteinCytokinesInflammation MediatorsMembrane ProteinsNK lytic-associated moleculeSequestosome-1 ProteinSqstm1 protein, mouseTranscription Factor RelA

Identifiers

PMID31539400
PMCPMC6754162
OpenAlexW2973752249

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.