Disease relevance of IL-18

• In cell culture, murine T241 fibrosarcoma cells are insensitive to recombinant IL-18 at concentrations that significantly inhibit endothelial cell proliferation [1].
• Systemic and intralesional administrations of IL-18 produce a significant suppression of the growth of murine T241 fibrosarcoma in syngeneic C57Bl6/J and immunodeficient SCID mice [1].
• In vivo, IL-18 is sufficiently potent to suppress the fibroblast growth factor-induced corneal neovascularization by systemic administration in mice [1].
• Construction and immunogenicity of recombinant fowlpox vaccines coexpressing HA of AIV H5N1 and chicken IL18 [2].
• The rFPV-H5-H7-IL18 vaccinated group displayed significantly increased weight gain relative to the rFPV-H5HA group [2].

High impact information on IL-18

• In this study, we characterize a Th1-like regulatory system focusing on the IL-18-regulated IFN-gamma secretion [3].
• In contrast, PBL were unresponsive to IL-18 in the presence or absence of macrophages, but IFN-gamma secretion was stimulated by suboptimal anti-TCR cross-linking combined with IL-18 [3].
• Both cytokines activated the splenocytes as demonstrated by increased size and MHC class II Ag up-regulation in the case of IL-18 [3].
• Using real-time quantitative RT-PCR, we characterized the expression of IFN-gamma, IL-1beta, IL-2, IL-6, IL-8, IL-15, and IL-18 in thyroids from OS birds and control CB line birds, both in the embryo just before hatch (embryonic day 20) and at 3 and 5 days posthatch [4].
• Predicted proteins with putative functions involving immune evasion included eight natural killer cell receptors, four CC chemokines, three G-protein-coupled receptors, two beta nerve growth factors, transforming growth factor beta, interleukin-18-binding protein, semaphorin, and five serine proteinase inhibitors (serpins) [5].

Chemical compound and disease context of IL-18

• We found that rHis-ChIL-18 significantly enhanced antibody responses to Clostridium perfringens alpha-toxoid and Newcastle disease virus (NDV) antigens, comparable to the Al(OH)3-gel, Miglyol and chitosan adjuvant [6].

Biological context of IL-18

• By searching a chicken EST database, we identified a cDNA clone that appeared to contain the entire open reading frame (ORF) of chicken interleukin-18 (ChIL-18) [7].
• We propose that rChIL-2 could be priming heterophils solely to function as more efficient innate effector cells to limit bacterial growth through the selective increase of IL-8 and IL-18 gene expression [8].
• The deduced amino acid sequence has 99% and 95% similarity with the IL-18 sequences of cattle and sheep, respectively [9].
• There are two amino acid substitutions at positions 132 and 182 in buffalo IL-18 compared with that of cattle [9].
• However, antibody responses were lower than water-in-oil (w/o) emulsions and combinations of rHis-ChIL-18 with Al(OH)3-gel, Miglyol or chitosan [6].

Anatomical context of IL-18

• In addition, splenic macrophages were activated and had temporarily increased levels of mRNA transcripts of pro-inflammatory mediators, including IL-1beta, IL-6, IL-18, and iNOS [10].
• To characterize the intracellular distribution of ChIL-18, ChIL-18-F and ChIL-18-M were each fused to the enhanced green fluorescent protein gene, and expressed in Vero cells [11].
• Nitric oxide inducing function and intracellular movement of chicken interleukin-18 in cultured cells [11].
• IL-18 stimulates the proliferation and IFN-gamma release of CD4+ T cells in the chicken: conservation of a Th1-like system in a nonmammalian species [3].
• Breed effect was significant (P<0.05) for CXCLi2, IL-10, IL-12alpha, and CCLi2 mRNA expression in the spleen, and for IL-12alpha, IL-12beta, IL-18, and CCLi2 mRNA expression in the cecum [12].

Other interactions of IL-18

• Compared to unvaccinated infected chickens, vaccinated protected birds had lower expression of interleukin (IL)-6, IL-10 and IL-18 genes in spleen [13].
• Heterophils from SE-resistant chickens (A and D) had significantly higher levels of pro-inflammatory cytokine (interleukin (IL)-6, IL-8, and IL-18) mRNA expression upon treatment with all agonists compared to heterophils from SE-susceptible lines (B and C) [14].
• In B19-2D8 cells, cytoplasmically stored interferon-gamma is quickly secreted in response to interleukin-18 exposure [15].
• We now describe a sensitive bioassay that is based on interleukin-18-induced release of interferon (IFN)-gamma by a permanent chicken cell line [15].

Analytical, diagnostic and therapeutic context of IL-18

• However, bLF markedly elevated IL-18 concentration in serum by oral administration, but not by intraperitoneal administration [16].
• A sensitive bioassay for chicken interleukin-18 based on the inducible release of preformed interferon-gamma [15].

References