Evidence map›Paper›PMID 33474883›Full record

ReviewSichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition2021

[Analysis of the Development Mechanism of Cytokine Storm in Severe Burn Patients Complicated with Infection].

Yuan-Yang Tang, Gao-Xing Lou, Wei-Feng He

Open access · greenAbstract readReview
In one paragraph

Review in Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.2field-weighted citation impact, top 51% 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

4 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Detection ofInfection and drug resistance · 2025
    Article
  3. Review
  4. [Research advances on severe burn infection and cytokine storm].Zhonghua shao shang yu chuang mian xiu fu za zhi · 2023
    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 1 institution in 1 country.

Yuan-Yang TangState Key Laboratory of Trauma, Burns, and Combined Injury, Institute of Burn Research, the First Affiliated Hospital of Army Medical University (the Third Military Medical University), Chongqing Key Laboratory for Disease Proteomics, Chongqing 400038, China.
Gao-Xing LouState Key Laboratory of Trauma, Burns, and Combined Injury, Institute of Burn Research, the First Affiliated Hospital of Army Medical University (the Third Military Medical University), Chongqing Key Laboratory for Disease Proteomics, Chongqing 400038, China.
Wei-Feng HeState Key Laboratory of Trauma, Burns, and Combined Injury, Institute of Burn Research, the First Affiliated Hospital of Army Medical University (the Third Military Medical University), Chongqing Key Laboratory for Disease Proteomics, Chongqing 400038, China.
Chongqing University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the early stage of infection in severe burn patients, the killing function of the natural immune cells is continuously low, which causes the immune system to continuously and compensatorily secrete a large amount of cytokines to improve the ability to resist bacterial infection. Once the cytokine secretion is out of control, a cytokine storm will form. In the late stage of severe burn infection, the bone marrow mobilization caused by continuous acute myelodysplasia will be exhausted, the level of immune response will be low, and the secretion of anti-inflammatory factors promoting repair will be increased, which will lead to immune suppression. Cytokine storm after burn infection is caused by excessive proinflammatory stimulation, inadequate inflammatory regulation, or a combination of the two. From the perspective of immunology, this review will briefly summarize the changing process of immune response against pathogenic bacteria after severe burn infection, cytokine storm in the early stage of severe burn infection and the mechanism of occurrence and transformation of immunosuppression in the late stage of severe burn infection. We suggest that future research direction from the following aspects: Mechanism of low bacterial killing function of innate immune cells after severe burns; The mechanism by which acute myeloid hyperplasia leads to myeloid inhibitory cells (MDSC) and nucleated erythrocytosis during the development of cytokine storms; The key regulatory mechanism between macrophage phagocytic dysfunction and cytokine hyperactivity; The role and key regulatory mechanism of destruction of the dynamic balance of M1/M2 macrophages and effector/regulatory T cells in triggering immune suppression.

Indexed as

BurnsCytokine Release SyndromeCytokinesHumansImmune ToleranceMacrophagesCytokinesBurn infectionCytokine stormImmunosuppression

Identifiers

PMID33474883
PMCPMC10408939
OpenAlexW3123562705

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.