Evidence map›Paper›PMID 23637040›Full record

ArticleClinical and vaccine immunology : CVI2013

Toll-like receptor 4 agonistic antibody promotes innate immunity against severe pneumonia induced by coinfection with influenza virus and Streptococcus pneumoniae.

Akitaka Tanaka, Shigeki Nakamura, Masafumi Seki, Kenji Fukudome, Naoki Iwanaga, Yoshifumi Imamura, Taiga Miyazaki, Koichi Izumikawa, Hiroshi Kakeya, Katsunori Yanagihara and 1 more

Abstract read
In one paragraph

Article in Clinical and vaccine immunology : CVI, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

11 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Association between TLR4 A299G polymorphism and pneumonia risk: a meta-analysis.Medical science monitor : international medical journal of experimental and clinical research · 2015
    Pooled it
  2. Article
  3. Review
  4. Inhibitory effects and related molecular mechanisms of total flavonoids in Mosla chinensis Maxim against H1N1 influenza virus.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018
    Article
  5. Article
  6. Influenza A Virus as a Predisposing Factor for Cryptococcosis.Frontiers in cellular and infection microbiology · 2017
    Article
  7. Lethal Synergism between Influenza andJournal of infectious pulmonary diseases · 2016
    Article
  8. Article
  9. Article
  10. Review
  11. 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

11 authors.

Akitaka TanakaDepartment of Molecular Microbiology and Immunology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki University School of Medicine, Nagasaki, Japan.
Shigeki Nakamura
Masafumi Seki
Kenji Fukudome
Naoki Iwanaga
Yoshifumi Imamura
Taiga Miyazaki
Koichi Izumikawa
Hiroshi Kakeya
Katsunori Yanagihara
Shigeru Kohno

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Coinfection with bacteria is a major cause of mortality during influenza epidemics. Recently, Toll-like receptor (TLR) agonists were shown to have immunomodulatory functions. In the present study, we investigated the effectiveness and mechanisms of the new TLR4 agonistic monoclonal antibody UT12 against secondary pneumococcal pneumonia induced by coinfection with influenza virus in a mouse model. Mice were intranasally inoculated with Streptococcus pneumoniae 2 days after influenza virus inoculation. UT12 was intraperitoneally administered 2 h before each inoculation. Survival rates were significantly increased and body weight loss was significantly decreased by UT12 administration. Additionally, the production of inflammatory mediators was significantly suppressed by the administration of UT12. In a histopathological study, pneumonia in UT12-treated mice was very mild compared to that in control mice. UT12 increased antimicrobial defense through the acceleration of macrophage recruitment into the lower respiratory tract induced by c-Jun N-terminal kinase (JNK) and nuclear factor kappaB (NF-κB) pathway-dependent monocyte chemoattractant protein 1 (MCP-1) production. Collectively, these findings indicate that UT12 promoted pulmonary innate immunity and may reduce the severity of severe pneumonia induced by coinfection with influenza virus and S. pneumoniae. This immunomodulatory effect of UT12 improves the prognosis of secondary pneumococcal pneumonia and makes UT12 an attractive candidate for treating severe infectious diseases.

Indexed as

Immunity, InnateAnimalsAntibodies, BacterialBody WeightCoinfectionDisease Models, AnimalHistocytochemistryHumansMaleMiceMice, Inbred C3HMice, Inbred CBAOrthomyxoviridaeOrthomyxoviridae InfectionsPneumococcal InfectionsPneumoniaAntibodies, BacterialTlr4 protein, mouseToll-Like Receptor 4

Identifiers

PMID23637040
PMCPMC3697446

What OpenQuestion holds

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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.