Evidence map›Paper›PMID 27725770›Full record

SynthesisScientific reports2016

Genetic dissection of host immune response in pneumonia development and progression.

Tamara V Smelaya, Olesya B Belopolskaya, Svetlana V Smirnova, Artem N Kuzovlev, Viktor V Moroz, Arkadiy M Golubev, Noel A Pabalan, Lyubov E Salnikova

Open access · goldAbstract readMeta-Analysis
In one paragraph

Synthesis in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

13 citing papers in PubMed, 29 citations in OpenAlex.

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  4. Influence ofInternational journal of molecular sciences · 2022
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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

8 authors at 4 institutions in 2 countries.

Tamara V SmelayaV. A. Negovsky Research Institute of General Reanimatology, Russian Academy of Sciences, 25 Petrovka str., build.2, Moscow 107031, Russia.
Olesya B BelopolskayaN.I. Vavilov Institute of General Genetics, Russian Academy of Sciences, 3 Gubkin street, Moscow 117971, Russia.
Svetlana V SmirnovaN.I. Vavilov Institute of General Genetics, Russian Academy of Sciences, 3 Gubkin street, Moscow 117971, Russia.
Artem N KuzovlevV. A. Negovsky Research Institute of General Reanimatology, Russian Academy of Sciences, 25 Petrovka str., build.2, Moscow 107031, Russia.
Viktor V MorozV. A. Negovsky Research Institute of General Reanimatology, Russian Academy of Sciences, 25 Petrovka str., build.2, Moscow 107031, Russia.
Arkadiy M GolubevV. A. Negovsky Research Institute of General Reanimatology, Russian Academy of Sciences, 25 Petrovka str., build.2, Moscow 107031, Russia.
Noel A PabalanCenter for Research and Development, Angeles University Foundation, Angeles City 2009, Philippines.
Lyubov E SalnikovaV. A. Negovsky Research Institute of General Reanimatology, Russian Academy of Sciences, 25 Petrovka str., build.2, Moscow 107031, Russia.
Russian Academy of Sciences · RUVavilov Institute of General Genetics · RUAngeles University Foundation · PHV.A. Negovsky Scientific Research Institute of General Reanimatology · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The role of host genetic variation in pneumonia development and outcome is poorly understood. We studied common polymorphisms in the genes of proinflammatory cytokines (IL6 rs1800795, IL8 rs4073, IL1B rs16944), anti-inflammatory cytokines (IL10 rs1800896, IL4 rs2243250, IL13 rs20541) and toll-like receptors (TLR2 rs5743708 and rs4696480, TLR4 rs4986791, TLR9 rs352139, rs5743836 and rs187084) in patients with community-acquired pneumonia (CAP) (390 cases, 203 controls) and nosocomial pneumonia (355 cases, 216 controls). Experimental data were included in a series of 11 meta-analyses and eight subset analyses related to pneumonia susceptibility and outcome. TLR2 rs5743708 minor genotype appeared to be associated with CAP/Legionnaires' disease/pneumococcal disease. In CAP patients, the IL6 rs1800795-C allele was associated with severe sepsis/septic shock/severe systemic inflammatory response, while the IL10 rs1800896-A allele protected against the development of these critical conditions. To contribute to deciphering of the above results, we performed an in silico analysis and a qualitative synthesis of literature data addressing basal and stimulated genotype-specific expression level. This data together with database information on transcription factors' affinity changes caused by SNPs in putative promoter regions, the results of linkage disequilibrium analysis along with SNPs functional annotations supported assumptions about the complexity underlying the revealed associations.

Indexed as

Community-Acquired InfectionsComputer SimulationCross InfectionDisease ProgressionGenetic Predisposition to DiseaseHumansInterleukin-10Interleukin-6Legionnaires' DiseaseLinkage DisequilibriumPneumoniaPolymorphism, Single NucleotidePromoter Regions, GeneticToll-Like Receptor 2Transcription FactorsIL10 protein, humanIL6 protein, humanInterleukin-10Interleukin-6TLR2 protein, humanToll-Like Receptor 2Transcription Factors

Identifiers

PMID27725770
PMCPMC5057148
OpenAlexW2530014922

What Socratic 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 Socratic graph.