Evidence map›Paper›PMID 32849610›Full record

ReviewFrontiers in immunology2020

Pulmonary Innate Immune Response Determines the Outcome of Inflammation During Pneumonia and Sepsis-Associated Acute Lung Injury.

Vijay Kumar

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05862675 (The Role and Mechanism of Immune Regulation in Acute Lung Injury in Children), which is not on this map. Cited by 372 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
372citing papers in PubMed, 1 pooled it
36.5field-weighted citation impact, top 1% 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.

NCT05862675 withdrawnnot on this mapstarted 2023, after this paper: background citation

The Role and Mechanism of Immune Regulation in Acute Lung Injury in Children

Typeobservational_patient_registrySponsorChildren's Hospital of Chongqing Medical UniversityRan2023 to 2026Enrolled0ConditionsAcute Lung InjuryArmsRNA sequencing of blood samples
3 · Its place in the literature

Who cites it

372 citing papers in PubMed, 1 synthesis or guideline pooled it, 651 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. TMEM16F deficiency alleviates sepsis-induced acute lung injury through regulating macrophage polarization.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Fecal microbiota transplantation alleviates sepsis-induced acute lung injury by improving mitochondrial function.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026
    Article
  9. Article
  10. Article
  11. Article
  12. PKM2: A gatekeeper in macrophage metabolic reprogramming.Journal of pharmaceutical analysis · 2026
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Assessment of Noninvasive Measurement Techniques and Histologic Findings in a Mouse Model of LPS-Induced Acute Lung Injury.Journal of the American Association for Laboratory Animal Science : JAALAS · 2026
    Article
  18. Article
  19. Article
  20. Alveolar macrophage-neutrophil crosstalk in acute lung injury: mechanisms, feedback loops, and therapeutic opportunities.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review

312 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

Vijay KumarChildren's Health Queensland Clinical Unit, Faculty of Medicine, School of Clinical Medicine, Mater Research, University of Queensland, Brisbane, QLD, Australia.
University of Queensland · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The lung is a primary organ for gas exchange in mammals that represents the largest epithelial surface in direct contact with the external environment. It also serves as a crucial immune organ, which harbors both innate and adaptive immune cells to induce a potent immune response. Due to its direct contact with the outer environment, the lung serves as a primary target organ for many airborne pathogens, toxicants (aerosols), and allergens causing pneumonia, acute respiratory distress syndrome (ARDS), and acute lung injury or inflammation (ALI). The current review describes the immunological mechanisms responsible for bacterial pneumonia and sepsis-induced ALI. It highlights the immunological differences for the severity of bacterial sepsis-induced ALI as compared to the pneumonia-associated ALI. The immune-based differences between the Gram-positive and Gram-negative bacteria-induced pneumonia show different mechanisms to induce ALI. The role of pulmonary epithelial cells (PECs), alveolar macrophages (AMs), innate lymphoid cells (ILCs), and different pattern-recognition receptors (PRRs, including Toll-like receptors (TLRs) and inflammasome proteins) in neutrophil infiltration and ALI induction have been described during pneumonia and sepsis-induced ALI. Also, the resolution of inflammation is frequently observed during ALI associated with pneumonia, whereas sepsis-associated ALI lacks it. Hence, the review mainly describes the different immune mechanisms responsible for pneumonia and sepsis-induced ALI. The differences in immune response depending on the causal pathogen (Gram-positive or Gram-negative bacteria) associated pneumonia or sepsis-induced ALI should be taken in mind specific immune-based therapeutics.

Indexed as

Immunity, InnateAcute Lung InjuryAnimalsHost-Pathogen InteractionsHumansInflammasomesInflammation MediatorsLungPneumonia, BacterialSepsisSignal TransductionToll-Like ReceptorsInflammasomesInflammation MediatorsToll-Like ReceptorsALIILCsmacrophagesneutrophilspneumoniasepsis

Identifiers

PMID32849610
PMCPMC7417316
OpenAlexW3047284551

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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.