IL-1 beta Protein, Human (CHO)

IL-1 beta is a potent proinflammatory cytokine expressed by monocytes, macrophages, and dendritic cells. IL-1 beta plays a key role in inflammation and immunologic reactions^[1][2].  IL-1 beta Protein, Human (CHO) is produced in  CHO cells, and consists of 153 amino acids (A117-S269).

Interleukin-1β (IL-1β) is one of the pro-inflammatory cytokines and is produced and secreted by a variety of cell types although the vast majority of studies have focussed on its production within cells of the innate immune system, such as monocytes and macrophages^[1][2].
IL-1β is produced as inactive pro-IL-1β (encoded by pro-Il-1b) in response to inflammatory stimuli, including both microbial products and endogenous danger-associated molecules. IL-1β gene expression and synthesis of pro-IL-1β occurs after activation of pattern recognition receptors (PRRs). Inflammatory stimuli also drive activation of cytosolic CARD and PYHIN domain-containing PRRs that recruit ASC and caspase-1 (Casp-1) to assemble into the multiprotein complex inflammasome. Pro-Casp-1 (encoded by pro-Casp-1), activated by the inflammasome, cleaves pro-IL-1β into the bioactive IL-1β. IL-1β acts in an autocrine/paracrine manner via the type I IL-1 receptor (IL-1R1)^[1][2][3].
IL-1β could regulate the inflammatory response, and is involved in a variety of cellular activities, including cell proliferation, differentiation, and apoptosis. IL-1β also plays a significant regulator of reproduction in females^[1][2][3].

IL-1β (1-15625 pg/mL; 12 hours) dose-dependently increases production of the NF-κB-dependent inflammatory cytokine TNF-α, and a significant effect of IL-1β is observed at concentrations as low as 5 pg/mL in immortalized murine RAW264.7 macrophages^[1].
IL-1β (1, 10 and 100 ng/mL; 24 hours) results in a dose-dependent increase of cell proliferation in pig heart cells. IL-1β increases the gene expression of caspase-3, and increases the enzymatic activities of MMP-2 and MMP-9^[2].

IL-1β (8 ng; i.p.; daily; for 3 days) rescues Casp1^−/− mice, restores survival and reduces lung bacterial load (i.e. days 0, 1, and 2 post-infection) in Chlamydia pneumoniae infected Casp1^−/− mice. Yet, mice treated later (days 2, 3 and 4 post-infection) shows significantly increased bacterial counts relative to early-treated mice^[3].

1.The ED₅₀ is <10 pg/mL as measured by D10S cells, corresponding to a specific activity of >1.0 × 10⁸ units/mg.
2.Measured in a cell proliferation assay using CTLL-2 mouse T lymphocyte. The ED₅₀ this effect is 2.877 pg/mL, corresponding to a specific activity is 3.47×10⁵ units/mg.

Human

CHO

Tag Free

P01584 (A117-S269)

3553  [NCBI]

APVRSLNCTLRDSQQKSLVMSGPYELKALHLQGQDMEQQVVFSMSFVQGEESNDKIPVALGLKEKNLYLSCVLKDDKPTLQLESVDPKNYPKKKMEKRFVFNKIEINNKLEFESAQFPNWYISTSQAENMPVFLGGTKGGQDITDFTMQFVSS

16-23 kDa

Greater than 95% as determined by reducing SDS-PAGE.

Lyophilized powder.

Lyophilized after extensive dialysis against PBS or 20 mM PB, 150 mM NaCl, pH 7.4.

<0.2 EU/μg, determined by LAL method.

It is not recommended to reconstitute to a concentration less than 100 μg/mL in ddH₂O. For long term storage it is recommended to add a carrier protein (0.1% BSA, 5% HSA, 10% FBS or 5% Trehalose).

Stored at -20°C for 2 years. After reconstitution, it is stable at 4°C for 1 week or -20°C for longer (with carrier protein). It is recommended to freeze aliquots at -20°C or -80°C for extended storage.

Room temperature in continental US; may vary elsewhere.

• [1]. Jan Petrasek, et al. IL-1 receptor antagonist ameliorates inflammasome-dependent alcoholic steatohepatitis in mice. J Clin Invest. 2012 Oct;122(10):3476-89.  [Content Brief]

  [2]. Karina Zitta, et al. Interleukin-1beta regulates cell proliferation and activity of extracellular matrix remodelling enzymes in cultured primary pig heart cells. Biochem Biophys Res Commun. 2010 Sep 3;399(4):542-7.  [Content Brief]

  [3]. Kenichi Shimada, et al. Caspase-1 dependent IL-1β secretion is critical for host defense in a mouse model of Chlamydia pneumoniae lung infection. PLoS One. 2011;6(6):e21477.  [Content Brief]