Sandwich ELISA, Biotin-labelled antibody
Serum, Plasma-EDTA, Plasma-Heparin, Plasma-Citrate, Saliva
At ambient temperature. Upon receipt, store the product at the temperature recommended below.
Store the complete kit at 2–8°C. Under these conditions, the kit is stable until the expiration date (see label on the box).
1.25 – 80 pg/ml
Limit of Detection
CV = 3.5 %
CV = 6.0 %
Serum: 83 %
Saliva: 104 %
Serum: 102 %
Saliva: 96 %
- It is intended for research use only
- The total assay time is less than 4 hours
- The kit measures IL-1 Beta in serum, plasma (EDTA, heparin, citrate) and saliva
- Assay format is 96 wells
- Standard is recombinant protein based
- Components of the kit are provided ready to use, concentrated or lyophilized
Cardiovascular disease, Coronary artery disease, Cytokines and chemokines and related molecules, Diabetology - Other Relevant Products, Immune Response, Infection and Inflammation, Neural tissue markers, Oncology, Transplantation, Animal studies
IL-1 Beta is a polypeptide cytokine and represents one of the most important mediators of inflammation and host responses to infections. This protein is a member of the interleukin-1 cytokine family, which is closely linked to the innate immune response. Mature form of IL-1 beta has molecular weight of 17.5 kDa and exists in monomeric form. Expression of the gene that encodes IL-1 beta is induced by various proinflammatory stimuli such as bacterial and viral products, other cytokines, cellular injury, monosodium urate crystals and hypoxia. IL-1 beta is produced by many cell types of both the peripheral and central immune system, including lymphocytes and monocytes. The synthesis and release of IL-1 Beta is tightly regulated. IL-1 beta is secreted only upon inflammatory signals and is not present in homeostatic conditions. IL-1 beta is synthetized as biologically inactive 35 kDa cytosolic precursor. Processing of bioactive IL-1 beta depends on activation of caspase-1 by protein complexes termed the inflammasomes. Most of the IL-1 beta remains intracellular; an additional signal such as ATP is needed for its secretion. Even low concentrations of IL-1 beta cause fever, hypotension and production of additional proinflammatory chemokines/cytokines, such as IL-6. IL-1 beta exerts biological effects by binding the membrane-bound type I IL-1 receptor (IL-1R), which then associates with the IL-1-receptor accessory protein (IL-1RAcP) to form a complex capable of intracellular signaling. This signalling controls expression of a number of inflammatory and catabolic genes. Besides its favorable role in mediating host responses to microbial invasion, IL-1 beta has also harmful effects. IL-1 beta can promote tumor invasiveness, tumor angiogenesis and metastasis. IL-1 beta also exacerbates damage during chronic diseases and acute tissue injury. Overexpression of IL-1 beta was observed in the pathophysiological changes that occur during different diseases, such as rheumatoid arthritis, neuropathic pain, inflammatory bowel disease, osteoarthritis, multiple sclerosis and neurodegenerative diseases. It was observed that IL-1 beta impairs insulin-producing Beta-cell function. Macrophage-derived IL-1 beta production in insulin-sensitive organs leads to progression of inflammation and induction of insulin resistance in obesity. Regarding other biofluids, it was found that IL-1 beta is one of the most abundant cytokine in saliva. It was observed that salivary level of IL-1 beta was higher in the patients with periodontitis compared to periodontally healthy subjects.