Cutting edge: IL-1β processing during Pseudomonas aeruginosa infection is mediated by neutrophil serine proteases and is independent of NLRC4 and caspase-1.
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Impact of Microbiota on Resistance to Ocular Pseudomonas aeruginosa-Induced KeratitisNeutrophil elastase promotes interleukin-1β secretion from human coronary endothelium.Dietary modulation of the microbiome affects autoinflammatory diseaseLocalization and functionality of the inflammasome in neutrophilsTransient infection of the zebrafish notochord with E. coli induces chronic inflammationAlveolar macrophages and neutrophils are the primary reservoirs for Legionella pneumophila and mediate cytosolic surveillance of type IV secretion.Distinct contributions of interleukin-1α (IL-1α) and IL-1β to innate immune recognition of Pseudomonas aeruginosa in the lung.The interleukin-1β/CXCL1/2/neutrophil axis mediates host protection against group B streptococcal infection.Host response and bacterial virulence factor expression in Pseudomonas aeruginosa and Streptococcus pneumoniae corneal ulcers.IKKα negatively regulates ASC-dependent inflammasome activation.Neutrophil IL-1β processing induced by pneumolysin is mediated by the NLRP3/ASC inflammasome and caspase-1 activation and is dependent on K+ efflux.Caspase-1-independent interleukin-1β is required for clearance of Bordetella pertussis infections and whole-cell vaccine-mediated immunityLactobacillus plantarum CECT 7315/7316 intake modulates the acute and chronic innate inflammatory response.Caspase-8 as an Effector and Regulator of NLRP3 Inflammasome SignalingNeutrophils Directly Recognize Group B Streptococci and Contribute to Interleukin-1β Production during Infection.Differential ASC requirements reveal a key role for neutrophils and a noncanonical IL-1β response to Pseudomonas aeruginosa.Antimicrobial Blue Light Therapy for Infectious Keratitis: Ex Vivo and In Vivo Studies.Pseudomonas aeruginosa Triggers Macrophage Autophagy To Escape Intracellular Killing by Activation of the NLRP3 Inflammasome.Neutrophil P2X7 receptors mediate NLRP3 inflammasome-dependent IL-1β secretion in response to ATP.The inflammasome NLRP3 plays a protective role against a viral immunopathological lesion.IL-1α signaling initiates the inflammatory response to virulent Legionella pneumophila in vivoLithium chloride promotes host resistance against Pseudomonas aeruginosa keratitis.Host defense at the ocular surfaceIL-17 promotes neutrophil entry into tumor-draining lymph nodes following induction of sterile inflammation.NLRP1 is an inflammasome sensor for Toxoplasma gondii.Bacterial Secretant from Pseudomonas aeruginosa Dampens Inflammasome Activation in a Quorum Sensing-Dependent Manner.Subversion of inflammasome activation and pyroptosis by pathogenic bacteria.Novel roles for caspase-8 in IL-1β and inflammasome regulation.Clinical Isolates of Pseudomonas aeruginosa from Chronically Infected Cystic Fibrosis Patients Fail To Activate the Inflammasome during Both Stable Infection and Pulmonary Exacerbation.Evasion and interference: intracellular pathogens modulate caspase-dependent inflammatory responses.Neutral serine proteases of neutrophils.A motive for killing: effector functions of regulated lytic cell death.α-Linoleic acid enhances the capacity of α-1 antitrypsin to inhibit lipopolysaccharide-induced IL-1β in human blood neutrophilsFracture initiates systemic inflammatory response syndrome through recruiting polymorphonuclear leucocytes.Corneal Fibroblasts as Sentinel Cells and Local Immune Modulators in Infectious Keratitis.Neutrophil pyroptosis mediates pathology of P. aeruginosa lung infection in the absence of the NADPH oxidase NOX2.Neutrophil extracellular traps induce IL-1β production by macrophages in combination with lipopolysaccharide.NLRC4 regulates caspase-1 and IL-1beta production in a CD11blowLy6Glow population of cells required for resistance to Pseudomonas aeruginosa keratitis.Contributions of MyD88-dependent receptors and CD11c-positive cells to corneal epithelial barrier function against Pseudomonas aeruginosa.Mycobacterial infection induces higher interleukin-1β and dysregulated lung inflammation in mice with defective leukocyte NADPH oxidase.
P2860
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P2860
Cutting edge: IL-1β processing during Pseudomonas aeruginosa infection is mediated by neutrophil serine proteases and is independent of NLRC4 and caspase-1.
description
2012 nî lūn-bûn
@nan
2012年の論文
@ja
2012年学术文章
@wuu
2012年学术文章
@zh-cn
2012年学术文章
@zh-hans
2012年学术文章
@zh-my
2012年学术文章
@zh-sg
2012年學術文章
@yue
2012年學術文章
@zh
2012年學術文章
@zh-hant
name
Cutting edge: IL-1β processing ...... endent of NLRC4 and caspase-1.
@ast
Cutting edge: IL-1β processing ...... endent of NLRC4 and caspase-1.
@en
type
label
Cutting edge: IL-1β processing ...... endent of NLRC4 and caspase-1.
@ast
Cutting edge: IL-1β processing ...... endent of NLRC4 and caspase-1.
@en
prefLabel
Cutting edge: IL-1β processing ...... endent of NLRC4 and caspase-1.
@ast
Cutting edge: IL-1β processing ...... endent of NLRC4 and caspase-1.
@en
P2093
P2860
P356
P1476
Cutting edge: IL-1β processing ...... endent of NLRC4 and caspase-1.
@en
P2093
Amy G Hise
Arne Rietsch
Eric Pearlman
Mausita Karmakar
P2860
P304
P356
10.4049/JIMMUNOL.1201447
P407
P577
2012-09-28T00:00:00Z