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Dental Disease, Inflammation, Cardiovascular Disease, Nutrition and Nutritional Supplements
Published in Stephen T. Sinatra, Mark C. Houston, Nutritional and Integrative Strategies in Cardiovascular Medicine, 2022
Douglas G. Thompson, Gregori M. Kurtzman, Chelsea Q. Watkins
Numerous studies have demonstrated that in addition to the bacteria in the biofilm, periodontal disease severity in adults is intricately linked with increases in local inflammatory mediators due to genetic mutations of genes regulating the production of inflammatory cytokines. One commonly recognized inflammatory cytokine is interleukin-1. A mutation of the interleukin-1 (IL-1) gene can cause overexpression of IL-1 making it a key player in the inflammatory process and a prime candidate for a genetic association with periodontal disease.88–90 Thirty percent of the population can be identified with IL-1 polymorphisms.91,92 The presence of the IL-1 genotype does not confer an expected periodontal disease diagnosis. However, this gene mutation has been implicated as a contributory factor to the host’s immunoinflammatory response contributing to the severity of adult periodontitis.93 The IL-1 gene has also been connected to atherothrombosis.94
Myocarditis
Published in Mary N. Sheppard, Practical Cardiovascular Pathology, 2022
IL (interleukin)-1 is a pivotal proinflammatory cytokine amplifying the innate immune response. Upstream of IL-1 is the inflammasome, a cytosolic molecular structure composed of an adaptor protein, procaspase-1, and a sensor molecule. The best-characterized inflammasome has a sensor molecule called NLRP3 (nucleotide-binding domain and leucine-rich repeat pyrin domain containing-3). Biological treatments that block the IL-1 pathway, including the IL-Ra (IL-1 receptor antagonist) anakinra, the fully human IgG1 anti–IL-1β monoclonal antibody, canakinumab, and colchicine are potential candidates to treat myocarditis.
Immune Modulation In Sepsis
Published in Thomas F. Kresina, Immune Modulating Agents, 2020
Janet M. J. Hammond, Peter D. Potgieter
Interleukin 1 plays an early proximal role in mediating the inflammatory response either by itself or, more commonly, in concert with the other proinflamma-tory cytokines. The release of IL-6, IL-8, and the colony stimulating factors are particularly induced by IL-1. All the same substances that promote TNF release, including bacterial endotoxins and exotoxins, viruses, parasites, and fungi, as well as TNF itself, promote the release of IL 1 (see Figure 1). Interleukin 1 is produced by numerous cells, including macrophages, monocytes, neutrophils, lymphocytes, endothelial cells, synovial lining cells, fibroblasts, astrocytes, microglia, and dendritic cells [62].
Amyloid nomenclature 2022: update, novel proteins, and recommendations by the International Society of Amyloidosis (ISA) Nomenclature Committee
Published in Amyloid, 2022
Joel N. Buxbaum, Angela Dispenzieri, David S. Eisenberg, Marcus Fändrich, Giampaolo Merlini, Maria J. M. Saraiva, Yoshiki Sekijima, Per Westermark
Interleukin-1 is a prominent proinflammatory cytokine which is over-expressed in a number of inflammatory diseases, e.g. in auto-inflammatory disorders and in rheumatoid arthritis. Interleukin-1 receptor antagonist protein is expressed as a 177 aa protein including a 25 aa signal peptide. Anakinra is a recombinant analog, which binds to the IL-1 receptor and thereby exerts anti-inflammatory properties and is used therapeutically in rheumatoid arthritis and a variety of inflammatory disorders. The drug is given subcutaneously with one daily dose 100 mg which may vary according to the patients’ clinical status. In a recent report two patients were described with pronounced localised subcutaneous amyloid deposits at the site of injections [21]. Mass spectrometric analyses showed these to be of Interleukin-1 receptor antagonist protein nature. The name of the amyloid fibril protein is AIL1RAP.
Association between Interleukin-1β Polymorphism at Rs16944 and Glucose Metabolism: A Cohort Study
Published in Immunological Investigations, 2022
Xiaoling Cheng, Yiying Liu, Nengbo Lin, Sijie Deng, Qin Wan
Diabetes mellitus (DM) is a chronic systemic metabolic disease that has attracted worldwide attention. It not only severely reduces quality of life due to the multi-system complications, caused by it, but also brings a heavy economic burden onto human society with a rapid global growth rate (Hu et al. 2015; IDF 2017). According to the results of the 2019 International Diabetes Federation (IDF 2019) Epidemiological Survey, 1 in 11 people worldwide have diabetes on average, with China having the most cases worldwide. Schmidt et al. (Schmidt et al. 1999) first proposed that inflammatory mediators can predict the occurrence of type 2 diabetes mellitus (T2DM). As one of the key mediators of the inflammatory response, interleukin 1 (IL-1) is widely involved in the occurrence and development of various diseases in the body(Conti et al. 2017). A -C/T single-base mutation in the rs16944 site of the IL-1β gene has been shown to affect the expression level of IL-1β(Mishra et al. 2015) and participate in the pathogenesis of diabetes. At present, many lateral studies have reported that the IL-1β gene rs16944 polymorphism is related to the incidence of diabetes. However, there is still no follow-up research conducted in this area. Therefore, this study examines the effects of the IL-1β gene rs16944 polymorphism on glucose metabolism after a follow-up period to deepen the existing research and provide a theoretical basis for new techniques that might be used in the prevention of diabetes.
A novel nasal co-loaded loratadine and sulpiride nanoemulsion with improved downregulation of TNF-α, TGF-β and IL-1 in rabbit models of ovalbumin-induced allergic rhinitis
Published in Drug Delivery, 2021
Soad A. Mohamad, Mohamed A. Safwat, Mahmoud Elrehany, Sherif A. Maher, Ahmed M. Badawi, Heba F. Mansour
Different inflammatory parameters were determined prior and post treatment to assess the efficacy of the selected nanoemulsion (F3). These parameters include TNF-α that is a powerful pro-inflammatory cytokine having fundamental responsibilities in stimulating leukocyte staffing to injured spots via provocation of expression of inflammatory chemokines and adhesion molecules. Another inflammatory parameter is TGF-β that is known as a very effective immunosuppressive and anti-inflammatory cytokine, conflicting TNF-α activities, stimulating the production of T regulatory cells, and facilitating the anti-inflammatory activities of these cells (Ohno et al., 1992; Hamaguchi et al., 1994; MULLOU et al., 1995). Interleukin-1 (IL-1) also is a cytokine that is essential for triggering the inherent immune response, facilitating the staffing, stimulation, and adherence of phagocytes (macrophages and neutrophils), and ending the inherent immune response is the same as TNF-α (Ott et al., 2007).