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Singh, V.K. et al.

Singh, Seed, Kumar,

N-palmitoylation of the radioprotective domain of interleukin-1 affords inhibition of LPS-induced nitric oxide generation.

Interleukin-1beta (IL-1beta), a cytokine involved in homeostatic processes such as the immune system and inflammatory reactions, is a potent inducer of nitric oxide. The nonapeptide of human IL-1beta (VQGEESNDK, position 163-171, specific radioprotective domain--SRD) has been shown to retain radioprotective, immunostimulatory, and adjuvant activities of the native molecule without any inflammatory and pyrogenic properties. Unlike the parent IL-1, SRD did not induce nitric oxide (NO) in control or irradiated RAW 264.7 cells nor did it affect inducible nitric oxide synthase ( iNOS) as shown by ELISA based mRNA assay (Quantikine). A lipophillic derivative of the SRD (a palmitoyl residue at the amino terminus of the SRD) was synthesized (palmitoyl specific radioprotective domain, P-SRD) to find out if this structural derivatization would restore the NO-inducing ability of IL-1. Surprisingly, P-SRD not only did not induce NO, but significantly inhibited lipopolysaccharide (LPS) stimulated nitric oxide (NO) production. Quantikine studies indicated that P-SRD also inhibited iNOS in LPS stimulated macrophage cells, suggesting that decrease in NO production in the presence of P-SRD was the result of iNOS mRNA inhibition. These results indicate that N-palmitoylation of SRD may effectively ameliorate potentially fatal symptoms of LPS-induced endotoxemic hypotensive shock associated with IL-1 without inflammatory and pyrogenic toxic side effects.[1]

References

N-palmitoylation of the radioprotective domain of interleukin-1 affords inhibition of LPS-induced nitric oxide generation. Singh, V.K., Seed, T.M., Kumar, K.S. Immunopharmacology and immunotoxicology. (2004) [Pubmed]

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