Evidence map›Paper›PMID 38454980›Full record

ArticleNarra J2023

The role of mediator suppressor of cytokine signaling (SOCS), toll-like receptor 3 (TLR-3) and nuclear factor kappa B (NFκB) on cytokine production during dengue virus infection.

Sri Masyeni, Kuntaman Kuntaman, Aryati Aryati, Muchlis Au Sofro, Usman Hadi, Gondo Mastutik, Windu Purnomo, Agus Santosa, Muhammad Iqhrammullah, Benediktus Yohan and 2 more

Open access · diamondAbstract read
In one paragraph

Article in Narra J, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

2 citing papers in PubMed, 5 citations in OpenAlex.

  1. Trial
  2. 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

12 authors at 6 institutions in 1 country.

Sri MasyeniDepartement of Internal Medicine, Faculty of Medicine and Health Sciences, Universitas Warmadewa, Bali, Indonesia.
Kuntaman KuntamanDepartment of Medical Microbiology, Faculty of Medicine, Airlangga University, Surabaya, Indonesia.
Aryati AryatiDepartment of Clinical Pathology, School of Medicine and Institute of Tropical Disease, Universitas Airlangga, Surabaya,Indonesia.
Muchlis Au SofroDepartment of Internal Medicine, Faculty of Medicine, Diponegoro University, Semarang, Indonesia.
Usman HadiDepartment of Internal Medicine, Faculty of Medicine, Airlangga University, Surabaya, Indonesia.
Gondo MastutikDepartment of Anatomical Pathologic, Faculty of Medicine, Airlangga University, Surabaya, Indonesia.
Windu PurnomoDepartment of Biostatistics, Faculty of Public Health, Universitas Airlangga Surabaya, Indonesia.
Agus SantosaDepartement of Internal Medicine, Faculty of Medicine and Health Sciences, Universitas Warmadewa, Bali, Indonesia.
Muhammad IqhrammullahFaculty of Public Health, Universitas Muhammadiyah Aceh, Banda Aceh, Indonesia.
Benediktus YohanEijkman Research Center for Molecular Biology, Jakarta, Indonesia.
Erni J NelwanDivision of Tropical and Infectious Disease, Department of Internal Medicine, Cipto Mangunkusumo Hospital, Universitas Indonesia, Jakarta, Indonesia.
R Tedjo SasmonoEijkman Research Center for Molecular Biology, Jakarta, Indonesia.
Airlangga University · IDEijkman Institute for Molecular Biology · IDWarmadewa University · IDDiponegoro University · IDUniversitas Muhammadiyah Aceh · IDUniversity of Indonesia · ID

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inability to understand the pathogenesis of severe dengue, in particular the control mechanism of immune responses, has led to high mortality rate for patients with dengue shock syndrome (DSS). The aim of this study was to determine the control mechanism of cytokine production by mediator suppressor of cytokine signaling (SOCS), toll-like receptor 3 (TLR-3) and nuclear factor kappa B (NFκB) during DENV infection. Peripheral blood mononuclear blood cells (PBMC), isolated from healthy individuals, were infected with dengue virus (DENV)-2 strain SJN-006 Cosmopolitan genotype (isolated from Bali, Indonesia). The relative gene expression of SOCS-3, TLR-3, NFκB, and the cytokine genes (interleukin (IL)-6, IL-8, interferon inducible protein 10 (IP-10), and macrophage inflammatory protein-1 beta (MIP-1β)) were measured using qRT-PCR at 6, 12 and 24 hours post infection (hpi). Student t-test and Mann-Whitney test were used to compare the gene expressions while causal correlations were analyzed using regression test and path analyses. DENV-2 infection increased the gene expression of SOCS-3, TLR-3, and NFκB after 12 and 24 hpi. The expression of IL-6, IL-8, IP-10, and MIP-1β genes was increased and peaked at different times post-infection. NFκB and SOCS-3 genes likely have role in the upregulation of IL-8 and IL-6 gene expression, respectively. MIP-1β gene expression was significantly induced by both NFκB and SOCS-3. In conclusion, our study suggested that SOCS-3, TLR-3, and NFκB are important in regulating the production of IL-6, IL-8, IP-10, MIP-1β during early phase of DENV-2 infection. This enriches our understanding on pathogenesis pathway of DENV-associated cytokine storm.

Indexed as

cytokine stormDengueNFκBSOCS-3TLR-3

Identifiers

PMID38454980
PMCPMC10919718
OpenAlexW4384560583

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

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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.