Evidence map›Paper›PMID 29163464›Full record

ArticleFrontiers in immunology2017

NLRP3 Inflammasome Mediates Dormant Neutrophil Recruitment following Sterile Lung Injury and Protects against Subsequent Bacterial Pneumonia in Mice.

Xiaoli Tian, He Sun, Amy-Jo Casbon, Edward Lim, Kevin P Francis, Judith Hellman, Arun Prakash

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

21 citing papers in PubMed, 39 citations in OpenAlex.

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  15. Sterile inflammation in thoracic transplantation.Cellular and molecular life sciences : CMLS · 2021
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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

7 authors at 2 institutions in 1 country.

Xiaoli TianDepartment of Anesthesia and Perioperative Care, University of California, San Francisco, San Francisco, CA, United States.
He SunDepartment of Anesthesia and Perioperative Care, University of California, San Francisco, San Francisco, CA, United States.
Amy-Jo CasbonDepartment of Anatomy, University of California, San Francisco, San Francisco, CA, United States.
Edward LimPreclinical Imaging, PerkinElmer, Hopkinton, MA, United States.
Kevin P FrancisPreclinical Imaging, PerkinElmer, Hopkinton, MA, United States.
Judith HellmanDepartment of Anesthesia and Perioperative Care, University of California, San Francisco, San Francisco, CA, United States.
Arun PrakashDepartment of Anesthesia and Perioperative Care, University of California, San Francisco, San Francisco, CA, United States.
University of California, San Francisco · USPerkinElmer (United States) · US

Funding

Role of Innate Immune Cells and Pathways in Ventilated Lung Ischemia ReperfusionK08GM110497 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI PRAKASH BUDDE, ARUN · 2015 to 2018
$791k
NIGMS NIH HHS K08 GM110497
6 · The paper itself

Abstract

Sterile lung injury is an important clinical problem that complicates the course of severely ill patients. Interruption of blood flow, namely ischemia-reperfusion (IR), initiates a sterile inflammatory response in the lung that is believed to be maladaptive. The rationale for this study was to elucidate the molecular basis for lung IR inflammation and whether it is maladaptive or beneficial. Using a mouse model of lung IR, we demonstrate that sequential blocking of inflammasomes [specifically, NOD-, LRR-, and pyrin domain-containing 3 (NLRP3)], inflammatory caspases, and interleukin (IL)-1β, all resulted in an attenuated inflammatory response. IL-1β production appeared to predominantly originate in conjunction with alveolar type 2 epithelial cells. Lung IR injury recruited unactivated or dormant neutrophils producing less reactive oxygen species thereby challenging the notion that recruited neutrophils are terminally activated. However, lung IR inflammation was able to limit or reduce the bacterial burden from subsequent experimentally induced pneumonia. Notably, inflammasome-deficient mice were unable to alter this bacterial burden following IR. Thus, we conclude that the NLRP3 inflammasome, through IL-1β production, regulates lung IR inflammation, which includes recruitment of dormant neutrophils. The sterile IR inflammatory response appears to serve an important function in inducing resistance to subsequent bacterial pneumonia and may constitute a critical part of early host responses to infection in trauma.

Indexed as

and pyrin domain-containing 3inflammasomeinflammationinterleukin-1βischemia–reperfusionLRR-lung injuryneutrophil activationNOD-

Identifiers

PMID29163464
PMCPMC5671513
OpenAlexW2766855969

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.