A5042707107- Inflammasome and immune disorders
- IL-33, ST2, and ILC Pathways
- Gastrointestinal motility and disorders
- interferon and immune responses
- Heme Oxygenase-1 and Carbon Monoxide
- Ubiquitin and proteasome pathways
- Advanced Glycation End Products research
- Pneumocystis jirovecii pneumonia detection and treatment
- Helicobacter pylori-related gastroenterology studies
- Mycobacterium research and diagnosis
- Alzheimer's disease research and treatments
- Inflammatory mediators and NSAID effects
- Toxoplasma gondii Research Studies
- Drug-Induced Adverse Reactions
- Cancer, Stress, Anesthesia, and Immune Response
- Streptococcal Infections and Treatments
Centre for Inflammation Research
2016-2023
University of Manchester
2016-2023
Manchester Academic Health Science Centre
2018-2021
Université Claude Bernard Lyon 1
2018-2019
Centre National de la Recherche Scientifique
2018-2019
École Normale Supérieure de Lyon
2018-2019
Inserm
2018-2019
Article11 September 2018Open Access Source DataTransparent process USP7 and USP47 deubiquitinases regulate NLRP3 inflammasome activation Pablo Palazón-Riquelme Division of Infection, Immunity Respiratory Medicine, Faculty Biology, Medicine Health, Manchester Collaborative Centre Inflammation Research, Academic Health Science Centre, Core Technology Facility, School Biological Sciences, University Manchester, UK Search for more papers by this author Jonathan D Worboys Jack Green Neuroscience...
Interleukin (IL)-1 family cytokines potently regulate inflammation, with the majority of IL-1 proteins being secreted from immune cells via unconventional pathways. In many cases, secretion appears to be closely coupled cell death, yet secretory mechanisms involved remain poorly understood. Here, we studied three best-characterized members superfamily, IL-1α, IL-1β, and IL-18, in a range conditions types, including murine bone marrow–derived peritoneal macrophages, human monocyte–derived...
Non-steroidal anti-inflammatory drugs (NSAIDs) exert detrimental effects on the intestine, mainly through an involvement of enteric bacteria This study examined pathophysiology NSAID-associated intestinal lesions in a rat model diclofenac-enteropathy and evaluated effect rifaximin small bowel damage. Enteropathy was induced 40-week-old male rats by intragastric diclofenac (4 mg/kg BID, 14 days). Rifaximin (delayed release formulation) administered (50 BID) 1 hour before NSAID. At end...
Increasing evidence suggests that intestinal dysfunctions may represent early events in Alzheimer’s disease and contribute to brain pathology. This study examined the relationship between onset of cognitive impairment colonic a spontaneous AD model before full development SAMP8 mice underwent Morris water maze assessment faecal output at four, six eight months age. In vitro motility was examined. Faecal Aβ, tau proteins, α-synuclein IL-1β were assessed by ELISA. Colonic citrate synthase...
Background and Purpose Enteric neurogenic/inflammation contributes to bowel dysmotility in obesity. We examined the role of NLRP3 colonic neuromuscular dysfunctions mice with high‐fat diet (HFD)‐induced Experimental Approach Wild‐type C57BL/6J NLRP3‐KO ( Nlrp3 −/− ) were fed HFD or standard for 8 weeks. The activation inflammasome pathways tissues from obese was assessed. vivo transit vitro tachykininergic contractions substance P distribution evaluated. effect on signalling tested cultured...
Background. Non-steroidal anti-inflammatory drugs can exert detrimental effects on the intestine, mainly through an involvement of enteric bacteria. This study examined rifaximin small bowel mucosal integrity and inflammation as well gut microbiota in rats with diclofenac-induced enteropathy.