ArticleAmerican journal of physiology. Lung cellular and molecular physiology2015
Differential ASC requirements reveal a key role for neutrophils and a noncanonical IL-1β response to Pseudomonas aeruginosa.
Article in American journal of physiology. Lung cellular and molecular physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 32 citations in OpenAlex.
- ExoS effector in Pseudomonas aeruginosa Hyperactive Type III secretion system mutant promotes enhanced Plasma Membrane Rupture in Neutrophils.PLoS pathogens · 2025Article
- Inflammasome-triggered IL-18 controls skin inflammation in the progression of Buruli ulcer.PLoS pathogens · 2023Article
- NADPH oxidase 2 limits amplification of IL-1β-G-CSF axis and an immature neutrophil subset in murine lung inflammation.Blood advances · 2023Article
- Role of toll-like receptors and nod-like receptors in acute lung infection.Frontiers in immunology · 2023Review
- Bactericidal/Permeability-Increasing Protein Preeminently Mediates Clearance ofFrontiers in immunology · 2021Article
- ATP Facilitates Staphylococcal Enterotoxin O Induced Neutrophil IL-1β SecretionFrontiers in immunology · 2021Article
- The PANoptosome: A Deadly Protein Complex Driving Pyroptosis, Apoptosis, and Necroptosis (PANoptosis).Frontiers in cellular and infection microbiology · 2020Review
- Gamma Interferon and Interleukin-17A Differentially Influence the Response of Human Macrophages and Neutrophils to Pseudomonas aeruginosa Infection.Infection and immunity · 2019Article
- Lung Defense through IL-8 Carries a Cost of Chronic Lung Remodeling and Impaired Function.American journal of respiratory cell and molecular biology · 2018Article
- Myeloid-specific Acat1 ablation attenuates inflammatory responses in macrophages, improves insulin sensitivity, and suppresses diet-induced obesity.American journal of physiology. Endocrinology and metabolism · 2018Article
- ASC acts in a caspase-1-independent manner to worsen acute pneumonia caused by Pseudomonas aeruginosa.Journal of medical microbiology · 2018Article
- The inflammasome potentiates influenza/Staphylococcus aureus superinfection in mice.JCI insight · 2018Article
- Acidosis exacerbates in vivo IL-1-dependent inflammatory responses and neutrophil recruitment during pulmonary Pseudomonas aeruginosa infection.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Small Molecule Inhibitor of Type Three Secretion System Belonging to a Class 2,4-disubstituted-4H-[1,3,4]-thiadiazine-5-ones Improves Survival and Decreases Bacterial Loads in an AirwayBioMed research international · 2018Article
- Autophagy Mediates Interleukin-1β Secretion in Human Neutrophils.Frontiers in immunology · 2018Article
- NAIP/NLRC4 inflammasome activation in MRP8Nature communications · 2017Article
- Preferential pattern of mouse neutrophil cell death in response to various stimulants.In vitro cellular & developmental biology. Animal · 2017Article
- Interleukin 7 immunotherapy improves host immunity and survival in a two-hit model of Pseudomonas aeruginosa pneumonia.Journal of leukocyte biology · 2017Article
- Bacterial secretion systems and regulation of inflammasome activation.Journal of leukocyte biology · 2017Review
- Inflammation: A Double-Edged Sword in the Response to Pseudomonas aeruginosa Infection.Journal of innate immunity · 2017Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The NLRC4 inflammasome is responsible for IL-1β processing by macrophages in response to Pseudomonas aeruginosa infection. We therefore hypothesized that mice that lack ASC, an NLRC4 inflammasome adaptor protein necessary for in vitro IL-1β production by macrophages, would be preferentially protected from a hyperinflammatory lethal challenge that is dependent on bacterial type three secretion system (T3SS) activity. We report herein that lack of ASC does not confer preferential protection in response to P. aeruginosa acute infection and that ASC(-/-) mice are capable of producing robust amounts of IL-1β comparable with C57BL/6 mice. We now identify that neutrophils represent the ASC-independent source of IL-1β production during the acute phases of infection both in models of acute pneumonia and peritonitis. Consequently, depletion of neutrophils in ASC(-/-) mice leads to a marked deficit in IL-1β production in vivo. The pulmonary neutrophil IL-1β response is predominantly dependent on caspase-1, which contrasts with data derived from ocular infection. These studies therefore identify a noncanonical mechanism of IL-1β production by neutrophils independent of ASC and demonstrate the first physiological contribution of neutrophils as an important source of IL-1β in response to acute P. aeruginosa infection during acute pneumonia and peritonitis.
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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.