David Brough

Priming of macrophages with lipopolysaccharide potentiates P2X7-mediated cell death via a caspase-1-dependent mechanism, independently of cytokine production.

Purinergic (P2X7) receptor activation of microglia induces cell death via an interleukin-1-independent mechanism.

Extracellular ATP and P2X7 receptors in neurodegeneration.

Role of P2X7 receptors in ischemic and excitotoxic brain injury in vivo.

Ca2+ stores and Ca2+ entry differentially contribute to the release of IL-1 beta and IL-1 alpha from murine macrophages.

Interleukin-18 induces expression and release of cytokines from murine glial cells: interactions with interleukin-1 beta.

The structural integrity of the endoplasmic reticulum, and its possible regulation by inositol 1,3,4,5-tetrakisphosphate.

Caspase-1-dependent processing of pro-interleukin-1beta is cytosolic and precedes cell death.

Mechanisms of regulation for interleukin-1beta in neurodegenerative disease.

A selective, non-peptide caspase-1 inhibitor, VRT-018858, markedly reduces brain damage induced by transient ischemia in the rat.

Neuronal injury induces the release of pro-interleukin-1beta from activated microglia in vitro.

The dynamics and mechanisms of interleukin-1alpha and beta nuclear import.

Pannexin-1-dependent caspase-1 activation and secretion of IL-1beta is regulated by zinc.

Nuclear retention of IL-1 alpha by necrotic cells: a mechanism to dampen sterile inflammation.

Regulation of interleukin-1 in acute brain injury.

Understanding the mechanism of IL-1β secretion.

Efficient discovery of anti-inflammatory small-molecule combinations using evolutionary computing.

Two zinc uptake systems contribute to the full virulence of Listeria monocytogenes during growth in vitro and in vivo.

Sphingosine regulates the NLRP3-inflammasome and IL-1β release from macrophages.

Interleukin-1α expression precedes IL-1β after ischemic brain injury and is localised to areas of focal neuronal loss and penumbral tissues.

Obese mice exhibit an altered behavioural and inflammatory response to lipopolysaccharide.

Inhibition of calpain blocks the phagosomal escape of Listeria monocytogenes.

Interleukin-1 receptor antagonist is beneficial after subarachnoid haemorrhage in rat by blocking haem-driven inflammatory pathology.

NLRP3-Inflammasome Activating DAMPs Stimulate an Inflammatory Response in Glia in the Absence of Priming Which Contributes to Brain Inflammation after Injury.

Deubiquitinases regulate the activity of caspase-1 and interleukin-1β secretion via assembly of the inflammasome.

Microglia and macrophages differentially modulate cell death after brain injury caused by oxygen-glucose deprivation in organotypic brain slices.

Acidosis drives damage-associated molecular pattern (DAMP)-induced interleukin-1 secretion via a caspase-1-independent pathway.

The role of inflammation and interleukin-1 in acute cerebrovascular disease.

Release of interleukin-1α or interleukin-1β depends on mechanism of cell death.

The NLRP3 inflammasome is released as a particulate danger signal that amplifies the inflammatory response.

Dendritic cell IL-1α and IL-1β are polyubiquitinated and degraded by the proteasome.

Apoptosis-associated speck-like protein containing a CARD forms specks but does not activate caspase-1 in the absence of NLRP3 during macrophage swelling.

AIM2 and NLRC4 inflammasomes contribute with ASC to acute brain injury independently of NLRP3.

Interleukin-1α and brain inflammation.

P2X7R activation drives distinct IL-1 responses in dendritic cells compared to macrophages.

Interleukin-1 as a pharmacological target in acute brain injury.

Acid-dependent Interleukin-1 (IL-1) Cleavage Limits Available Pro-IL-1β for Caspase-1 Cleavage.

Potassium efflux fires the canon: Potassium efflux as a common trigger for canonical and noncanonical NLRP3 pathways.

Inhibiting the Inflammasome: A Chemical Perspective.

Molecular and Translational Classifications of DAMPs in Immunogenic Cell Death.

Investigating IL-1β Secretion Using Real-Time Single-Cell Imaging.

Novel perspectives on non-canonical inflammasome activation.

Inflammasomes link vascular disease with neuroinflammation and brain disorders.

Fenamate NSAIDs inhibit the NLRP3 inflammasome and protect against Alzheimer's disease in rodent models.

P2X7 receptor-dependent tuning of gut epithelial responses to infection.

Inflammasomes as therapeutic targets for Alzheimer's disease.

Unconventional Pathways of Secretion Contribute to Inflammation.

Salmonella typhimurium-induced IL-1 release from primary human monocytes requires NLRP3 and can occur in the absence of pyroptosis.

An emerging case for membrane pore formation as a common mechanism for the unconventional secretion of FGF2 and IL-1β.

Boron-Based Inhibitors of the NLRP3 Inflammasome.

Assessing Inflammation in Acute Intracerebral Hemorrhage with PK11195 PET and Dynamic Contrast-Enhanced MRI.

CRISPR/Cas9 mediated mutation of mouse IL-1α nuclear localisation sequence abolishes expression.

Microglial Priming as Trained Immunity in the Brain.

Design, Synthesis and Evaluation of Oxazaborine Inhibitors of the NLRP3 Inflammasome.

Synthesis and antibacterial activities of enamine derivatives of dehydroacetic acid.

Redefining the ancestral origins of the interleukin-1 superfamily.

Development of a characterised tool kit for the interrogation of NLRP3 inflammasome-dependent responses.

Targeting the IL33-NLRP3 axis improves therapy for experimental cerebral malaria.

Is Targeting the Inflammasome a Way Forward for Neuroscience Drug Discovery?

USP7 and USP47 deubiquitinases regulate NLRP3 inflammasome activation.

Chloride regulates dynamic NLRP3-dependent ASC oligomerization and inflammasome priming.

Small, Thin Graphene Oxide Is Anti-inflammatory Activating Nuclear Factor Erythroid 2-Related Factor 2 via Metabolic Reprogramming.

Improving the Gene Ontology Resource to Facilitate More Informative Analysis and Interpretation of Alzheimer's Disease Data.

The three cytokines IL-1β, IL-18, and IL-1α share related but distinct secretory routes.

Cathelicidin is a "fire alarm", generating protective NLRP3-dependent airway epithelial cell inflammatory responses during infection with Pseudomonas aeruginosa.

Extent of Ischemic Brain Injury After Thrombotic Stroke Is Independent of the NLRP3 (NACHT, LRR and PYD Domains-Containing Protein 3) Inflammasome.