Evidence map›Paper›PMID 28612844›Full record

ArticleMucosal immunology2018

NLRP3 inflammasome pathway has a critical role in the host immunity against clinically relevant Acinetobacter baumannii pulmonary infection.

N Dikshit, S D Kale, H J Khameneh, V Balamuralidhar, C Y Tang, P Kumar, T P Lim, T T Tan, A L Kwa, A Mortellaro and 1 more

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Mucosal immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

38 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. MARCH E3 Ligases: Understudied Regulators of Pulmonary Immune Function.Journal of respiratory biology and translational medicine · 2026
    Article
  7. Article
  8. Antivirulence drugs against Acinetobacter baumannii: where do they stand?World journal of microbiology & biotechnology · 2025
    Review
  9. Current research in microbial sciences · 2025
    Article
  10. Article
  11. Review
  12. Virulence Factors and Pathogenicity Mechanisms ofAntibiotics (Basel, Switzerland) · 2023
    Review
  13. Value of T6SS Core GeneIndian journal of microbiology · 2023
    Article
  14. Article
  15. ReplicativebioRxiv : the preprint server for biology · 2023
    Article
  16. Deciphering the virulence factors, regulation, and immune response toFrontiers in cellular and infection microbiology · 2023
    Review
  17. Article
  18. Article
  19. Epithelial Pyroptosis in Host Defense.Journal of molecular biology · 2022
    Review
  20. Article
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 at 5 institutions in 1 country.

N DikshitProgram in Emerging Infectious Diseases, Duke-NUS Medical School, Singapore, Singapore.
S D KaleProgram in Emerging Infectious Diseases, Duke-NUS Medical School, Singapore, Singapore.
H J KhamenehSingapore Immunology Network (SIgN), Agency for Science, Technology and Research (A*STAR), Singapore, Singapore.
V BalamuralidharProgram in Emerging Infectious Diseases, Duke-NUS Medical School, Singapore, Singapore.
C Y TangLife Sciences Institute, National University of Singapore, Singapore, Singapore.
P KumarProgram in Emerging Infectious Diseases, Duke-NUS Medical School, Singapore, Singapore.
T P LimDepartment of Pharmacy, Singapore General Hospital, Singapore.
T T TanDepartment of Infectious Diseases, Singapore General Hospital, Singapore, Singapore.
A L KwaProgram in Emerging Infectious Diseases, Duke-NUS Medical School, Singapore, Singapore.
A MortellaroSingapore Immunology Network (SIgN), Agency for Science, Technology and Research (A*STAR), Singapore, Singapore.
B SukumaranProgram in Emerging Infectious Diseases, Duke-NUS Medical School, Singapore, Singapore.
Duke-NUS Medical School · SGAgency for Science, Technology and Research · SGSingHealth · SGNational University of Singapore · SGSingapore General Hospital · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The opportunistic Gram-negative bacterium Acinetobacter baumannii (AB) is a leading cause of life-threatening nosocomial pneumonia. Outbreaks of multidrug resistant (MDR)-AB belonging to international clones (ICs) I and II with limited treatment options are major global health threats. However, the pathogenesis mechanisms of various AB clonal groups are understudied. Although inflammation-associated interleukin-1β (IL-1β) levels and IL-1 receptor antagonist polymorphisms were previously implicated in MDR-AB-related pneumonia in patients, whether inflammasomes has any role in the host defense and/or pathogenesis of clinically relevant A. baumannii infection is unknown. Using a sublethal mouse pneumonia model, we demonstrate that an extensively drug-resistant clinical isolate (ICII) of A. baumannii exhibits reduced/delayed early pulmonary neutrophil recruitment, higher lung persistence, and, most importantly, elicits enhanced IL-1β/IL-18 production and lung damage through NLRP3 inflammasome, in comparison with A. baumannii-type strain. A. baumannii infection-induced IL-1β/IL-18 production is entirely dependent on NLRP3-ASC-caspase-1/caspase-11 pathway. Using Nlrp3

Indexed as

Acinetobacter baumanniiAcinetobacter InfectionsAnimalsCaspasesCells, CulturedCross InfectionDisease Models, AnimalDrug Resistance, MultipleFemaleHumansInflammasomesLungMiceMice, Inbred C57BLMice, KnockoutNLR Family, Pyrin Domain-Containing 3 ProteinCaspasesInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouse

Identifiers

PMID28612844
OpenAlexW2624735087

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.