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Interleukin-1β (IL-1 beta) is one of a family of biologically active small protein molecules known as cytokines. Cytokines are produced by a number of different cell types, including macrophages, monocytes, fibroblasts, and dendritic cells. (1,2,3) IL-1β is an example of a pro-inflammatory cytokine, since it is involved in the body’s inflammatory response to acute or chronic infections, or to conditions that are associated with a persistent low-grade inflammatory state, such as obesity. (4,5) IL-1β is therefore frequently used as a bio-marker of inflammation. (6,7) A study with normal mouse parotid acinar cells has shown that they synthesize IL-1β and store it in secretory granules. IL-1β is released from the granules following α- and β-adrenergic stimulation. (8) Relationships between IL-1β levels in blood and saliva are not fully understood.
*Add 300 µl to the total volume of all tests for liquid handling
IL-1 Beta may be Flow Rate Dependent
3.13 pg/mL - 200 pg/mL
0.05 - 2256 pg/mL
Collect Saliva Samples
IL-1 BETA SALIVA COLLECTION CONSIDERATIONS
Better results begin with better saliva collection. This collection protocol features general considerations to maximize salivary IL-1 Beta analysis. Use this analyte specific collection protocol to plan your collection methodology and sampling schemes.
Considerations for adding Salivary DNA to analyte Studies:
You can combine salivary analytes with easy, accurate, and affordable genomic testing using Salimetrics SalivaLab and the same sample that you are already collecting – no specialized saliva collection devices or additional samples are required.
Don’t know what SNPs are right for you? The SalivaLab’s DNA team specializes in genetic testing services, we recommend you Request a DNA Consult (gratis) to learn more about common considerations such as # of samples, participant ethnicity, and IRB Approval.
Giannobile, W.V., Beikler, T., Kinney, J.S., et al. (2009). Saliva as a diagnostic tool for periodontal disease: Current state and future directions. Periodontology 2000, 50, 52-64.
Pirhonen, J., Sareneva, R., Kurimoto, M., et al. (1999). Virus infection activates IL-1β and IL-18 production in human macrophages by a caspase-1-dependent pathway. J Immunol, 162(12), 7322-29.
Park, D.R., Thomsen, A.R., Frevert, C.W. et al. (2003). Fas (CD95) induces proinflammatory cytokine responses by human monocytes and monocyte-derived macrophages. J Immunol, 170(12), 6209-16.
Hernández-Rodríguez, J., Segarra, M., Vilardell, C., et al. (2004). Tissue production of pro-inflammatory cytokines (IL-1β, TNFα, and IL-6) correlates with the intensity of the systemic inflammatory response and with corticosteroid requirements in giant-cell arteritis. Rheumatology (Oxf.), 43(3), 294-301.
Southerland, J.H., Taylor, G.W., Moss, K., et al. (2006). Commonality in chronic inflammatory diseases: Periodontitis, diabetes, and coronary artery disease. Periodontology 2000, 40, 130-43.
Tzouvelekis, A., Pneumatikos, I, Bouros, D. (2005). Serum biomarkers in acute respiratory distress syndrome an ailing prognosticator. Respir Res, 6, 62.
Miller, C.S., King C.P., Langub, M.C., et al. (2006). Salivary biomarkers of existing periodontal disease: A cross-sectional study. J Am Dent Assoc, 137(3), 322-29.
Tanda, N., Ohyama, H., Yamakawa, M., et al. (1998). IL-1β and IL-6 in mouse parotid acinar cells: Characterization of synthesis, storage, and release. Am J Physiol, 274(1 Pt1), G147-56.