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Crystalline Arthritis
Published in Jason Liebowitz, Philip Seo, David Hellmann, Michael Zeide, Clinical Innovation in Rheumatology, 2023
Anti-IL-1β biologics have limited gastrointestinal, renal, and metabolic adverse effects but are costlier than traditional agents. In a trial comparing anakinra to usual care (colchicine, naproxen, or prednisone) for treating gout flares, anakinra was noninferior with respect to pain reduction.26 Similarly, canakinumab in the β-RELIEVED and β-RELIEVED-II trials demonstrated efficacy for treating and preventing gout flares in those with frequent flares (≥ 3/year) for whom traditional agents were deemed inappropriate. One dose of canakinumab 150 mg was superior to triamcinolone acetonide 40 mg to prevent new and delay subsequent flares, although cytopenias and infections were more common with canakinumab.27
Immediate Cytokine Responses to Endotoxin: Tumor Necrosis Factor-α and the lnterleukin-1 Family
Published in Helmut Brade, Steven M. Opal, Stefanie N. Vogel, David C. Morrison, Endotoxin in Health and Disease, 2020
Although the systemic effects of TNF-α and IL-1β have been studied in animals, there are now data on the effects and sensitivity of humans to IL-1 and TNF-α. In general, the effects are similar to either cytokine. Acute toxicities of either IL-1α or IL-1β were greater following intravenous compared to subcutaneous injection; subcutaneous injection was associated with significant local pain, erythema, and swelling (19,20). Chills and fever are observed in nearly all patients, even in the 1 ng/kg dose group (21). The febrile response increased in magnitude with increasing doses (22–26), and chills and fever were abated with indo-methacin treatment (27). In patients receiving IL-1α (25,26) or IL-1α (22,23), nearly all subjects experienced significant hypotension at doses of 100 ng/kg or greater. Systolic blood pressure fell steadily and reached a nadir of 90 mmHg or less 3–-5 hours after the infusion of IL-1. At doses of 300 ng/kg, most patients required intravenous pressors. By comparison, in a trial of 16 patients given IL-1β 4–32 ng/kg subcutaneously, there was only one episode of hypotension at the highest dose level (19). These results suggest that the hypotension is probably due to induction of NO, and elevated levels of serum nitrate have been measured in patients with IL-1-induced hypotension (26).
Physiology of veins and lymphatics
Published in Ken Myers, Paul Hannah, Marcus Cremonese, Lourens Bester, Phil Bekhor, Attilio Cavezzi, Marianne de Maeseneer, Greg Goodman, David Jenkins, Herman Lee, Adrian Lim, David Mitchell, Nick Morrison, Andrew Nicolaides, Hugo Partsch, Tony Penington, Neil Piller, Stefania Roberts, Greg Seeley, Paul Thibault, Steve Yelland, Manual of Venous and Lymphatic Diseases, 2017
Ken Myers, Paul Hannah, Marcus Cremonese, Lourens Bester, Phil Bekhor, Attilio Cavezzi, Marianne de Maeseneer, Greg Goodman, David Jenkins, Herman Lee, Adrian Lim, David Mitchell, Nick Morrison, Andrew Nicolaides, Hugo Partsch, Tony Penington, Neil Piller, Stefania Roberts, Greg Seeley, Paul Thibault, Steve Yelland
Cytokines are either antior pro-inflammatory. Anti-inflammatory cytokines promote healing and reduce inflammation, whereas pro-inflammatory cytokines, though necessary for healing, generally make disease worse and can cause auto-immune conditions.Anti-inflammator y cytokines that regulate this response include interleukin (IL)-1 receptor antagonist, IL-4, IL-10, IL-11, and IL-13.Pro-inflammatory cytokines include interleukins (IL-1β, IL-6) and tumour necrosis factor (TNF-α). IL-1β is released primarily by monocytes, macrophages, fibroblasts and endothelial cells during cell injury, infection and inflammation. Once released, they induce a cascade of further cytokine production.Various cytokines termed chemokines induce activation and migration of leukocytes. They include monocyte che-moattractant protein (MCP-1), monocyte inflammatory protein (MIP-1α, MIP-1β) and growth related oncogene (GRO/KC).
Obesity, Inflammation, and Advanced Prostate Cancer
Published in Nutrition and Cancer, 2021
Armando Olivas, Ramona Salcedo Price
The pro-inflammatory cytokine IL-1β is transcribed via the IL1B gene and is produced by a variety of cell types including monocytes, dendritic cells, endothelial cells, tissue macrophages, and fibroblasts (72). Stimuli inducing transcription include cytokines, including IL-1β, and molecules produced by microbes (72). IL-1β binds to the ubiquitously expressed IL-1 receptor type 1 (IL-1RI) (73). Ligand-binding to IL-1RI results in recruitment of IL-1 receptor-associated kinase (IRAK)-1 and tumor necrosis factor receptor-associated factor (TRAF) six onto the cytoplasmic domain of IL-1RI (73). Recruitment of IRAK-1 and TRAF6 potentiates expression of genes relating to cytokine and chemokine production, cell survival, proliferation, apoptosis, and other factors that can promote carcinogenesis and disease progression, primarily via NF-κB activation (72). In breast cancer, IL-1β has also been shown to stimulate matrix metalloproteinase-9 production thus facilitating invasion and metastasis (74). Pathways involved in mediating IL-1β signaling include MAPK, NF-κB, Toll—like Receptor (TLR), and NOD-like Receptor (NLR) signaling pathways (75,76).
Neutrophil Extracellular Trapping Network Promotes the Pathogenesis of Neutrophil-associated Asthma through Macrophages
Published in Immunological Investigations, 2021
Xi Chen, Yuanyuan Li, Ling Qin, Ruoxi He, Chengping Hu
Interestingly, the interaction between NETs and macrophages which indirectly induces the production of large amounts of inflammatory cytokines might be an essential step for NETs to induce disease (Pham et al. 2017; Wright et al. 2016). As a major source of pro-inflammatory mediators in the airway cavity and bronchial mucosa, macrophages were found to produce more TNF-α, IL-1β, IL-6, and IL-8 in asthmatic patients. Among them, TNF-α and IL-1β-mediated signaling pathways are directly related to the occurrence of NA (Baines et al. 2011). IL-1β is the central mediator of the inflammatory response. IL-1β directly stimulates the secretion of IL-6 and IL-8 by bronchial epithelial cells, thereby recruiting neutrophils to infiltrate the airway and participating in neutrophilic airway inflammation (Peebles 2017). Since we observed the significant increase in IL-1β level in NA mice, we speculate that NETs might promote the production of IL-1β by acting on macrophages, thereby inducing NA. As expected, either IL-1β neutralizing antibody or macrophage scavenger (CL) significantly reduced the formation of NETs, improved the severity of NA symptoms in mice, and attenuated NA mice inflammation. These findings suggest that macrophages might promote neutrophil infiltration in the airway by mediating the secretion of inflammatory factors such as IL-1β, thereby promoting the formation of NETs and ultimately leading to the occurrence of NA.
Effects of Jian Pi Qing Chang Hua Shi decoction on mucosal injuries in a 2,4,6-trinitrobenzene sulphonic acid-induced inflammatory bowel disease rat model
Published in Pharmaceutical Biology, 2021
Huicun Zhang, Na Ta, Hong Shen, Hongbing Wang
When inflammatory cell infiltration occurs, IBD is induced in the colonic tissue and TNF-α and IL-1β are released by inflammatory cells. TNF-α, an important mediator of biological immune defences and homeostasis, is closely related to IBD injury (Perrier and Rutgeerts 2011). TNF-α induces inflammatory cell aggregation by binding to high-affinity receptors on vascular endothelial cells, thereby upregulating the expression of IL-6 and adhesion molecules (Akanda et al. 2018). IL-1β is mainly produced by monocytes and macrophages. When patients with IBD have crypt inflammation, the content of IL-1β in intestinal fluids increases significantly. IL-1β interacts with antigens to activate CD4+ T cells, express IL-2R, and promote the activation and growth of B cells. IL-1β promotes the expression of antigen-presenting cells, such as monocytes and macrophages, and attracts neutrophils to aggregate and release inflammatory transmitters (Evgenikos et al. 2002). IL-6 is a cytokine that mediates the pathogenesis of IBD. The imbalance in pro-inflammatory cytokines, including TNF-α and IL-1β, plays a key role in the signalling cascade of the inflammatory pathway. TNF-α and IL-1β are the therapeutic targets of IBD therapy (Pedersen et al. 2014; Wallace et al. 2014).