Evidence map›Paper›PMID 39533032›Full record

ArticleCommunications biology2024

Interferon signalling and non-canonical inflammasome activation promote host protection against multidrug-resistant Acinetobacter baumannii.

Fei-Ju Li, Lora Starrs, Anukriti Mathur, Daniel Enosi Tuipulotu, Si Ming Man, Gaetan Burgio

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. Review
  2. Article
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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

6 authors.

Fei-Ju LiDivision of Immunology and Infectious Disease, The John Curtin School of Medical Research, the Australian National University, Canberra, Australian Capital Territory, Australia.
Lora StarrsDivision of Immunology and Infectious Disease, The John Curtin School of Medical Research, the Australian National University, Canberra, Australian Capital Territory, Australia.
Anukriti MathurDivision of Immunology and Infectious Disease, The John Curtin School of Medical Research, the Australian National University, Canberra, Australian Capital Territory, Australia.ORCID 0000-0002-7004-301X
Daniel Enosi TuipulotuDivision of Immunology and Infectious Disease, The John Curtin School of Medical Research, the Australian National University, Canberra, Australian Capital Territory, Australia.ORCID 0000-0002-6442-4633
Si Ming ManDivision of Immunology and Infectious Disease, The John Curtin School of Medical Research, the Australian National University, Canberra, Australian Capital Territory, Australia.ORCID 0000-0002-5079-2857
Gaetan BurgioDivision of Immunology and Infectious Disease, The John Curtin School of Medical Research, the Australian National University, Canberra, Australian Capital Territory, Australia. Gaetan.burgio@anu.edu.au.ORCID 0000-0002-7434-926X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multidrug-resistant (MDR) Acinetobacter baumannii are of major concern worldwide due to their resistance to last resort carbapenem and polymyxin antibiotics. To develop an effective treatment strategy, it is critical to better understand how an A. baumannii MDR bacterium interacts with its mammalian host. Pattern-recognition receptors sense microbes, and activate the inflammasome pathway, leading to pro-inflammatory cytokine production and programmed cell death. Here, we examined the effects of a systemic MDR A. baumannii infection and found that MDR A. baumannii activate the NLRP3 inflammasome complex predominantly via the non-canonical caspase-11-dependent pathway. We show that caspase-1 and caspase-11-deficient mice are protected from a virulent MDR A. baumannii strain by maintaining a balance between protective and deleterious inflammation. Caspase-11-deficient mice also compromise between effector cell recruitment, phagocytosis, and programmed cell death in the lung during infection. Importantly, we found that cytosolic immunity - mediated by guanylate-binding protein 1 (GBP1) and type I interferon signalling - orchestrates caspase-11-dependent inflammasome activation. Together, our results suggest that non-canonical inflammasome activation via the (Interferon) IFN pathway plays a critical role in the host response against MDR A. baumannii infection.

Indexed as

Acinetobacter baumanniiAcinetobacter InfectionsCaspases, InitiatorDrug Resistance, Multiple, BacterialInflammasomesMice, Inbred C57BLSignal TransductionAnimalsCaspase 1CaspasesMiceMice, KnockoutNLR Family, Pyrin Domain-Containing 3 ProteinCasp1 protein, mouseCasp4 protein, mouseCaspase 1CaspasesCaspases, InitiatorInflammasomesNLR Family, Pyrin Domain-Containing 3 Protein

Identifiers

PMID39533032
PMCPMC11557958

What OpenQuestion holds

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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.