Taken together, it is possible that
CCL3 will play a pivotal role in OP progression.
IFN-[gamma] (a), TNF-[alpha] (b), GM-CSF (c),
CCL3 (d), IL-17 (e), CCL5 (f), IL-4 (g), and CCL4 (h) secretion from in vitro stimulated [CD4.sup.+] T cells.
We assessed protein levels of 22 cytokines and chemokines associated with innate and adaptive immune responses (innate: TNF, IL-1[beta], IL-6, IL-10, granulocyte-macrophage colony-stimulating factor, IL-8, IFN-[alpha], CCL2,
CCL3, and CCL19; adaptive-Thl: IFN-[gamma], IL-12p40, IL-12p70, cysteine-X-cysteine motif cytokine ligand 9 (CXCL9), and CXCL10; adaptive-Th17: IL-17A, IL-17F, IL-21, IL-22, IL-23, IL-25, and IL-27) in culture supernatants by using bead-based Luminex (EMD-Millipore, Darmstadt, Germany) multiplex assays.
Similarly, the expression of 18 cytokine genes (IL-7, IL-10, TNFAIP8, SPP2, TNFAIP3, IFNB, CCL19, TNFAIP8L1, IL-16, CNTF, CXCL13, TNFAIP8L3, TNFSF13B, IL-34, TGFB1, TNFAIP2,
CCL3, and ADIPOQ) and 39 cytokine receptor genes (CXCR7, CSF2RA, IL-1RL1, I-L1R2, IL-17RA, IFNAR1, IL-18RAP, IL-31RA, IL-9R, IL-18R1, IL-20RB, IL-21R, IL-2RG, IL-20RA, IL-4I1, LILRB1, TLR1, IL-17REL, LILRB5, TGFBR1, TLR6, TNFRSF13B, XCR1, TLR7, TNFRSF13C, TLR15 etc.) was also markedly upregulated by 2.03- to 8.41-fold and 2.08- to 9.12-fold, respectively, in chicken line 7.2 with p < 0.01 and fold [greater than or equal to] 2 (Supplementary Table S4, Figures 4 and 5).
We found that in addition to TNF-a, the proinflammatory chemokine CC chemokine ligand 3 (
CCL3) also was downregulated by rolipram whereas the anti-inflammatory cytokine interleukin-1 receptor antagonist (IL-1Ra) was upregulated.
The CCl4 induced hepatotoxicity is a well proven experimental model for inducing acute liver injury is bio-transformed by hepatic microsomal cytochrome P450 to trichloromethyl-free radical (
CCl3 or CCl3OO) (Weber et al.
CCL3 (chemokine ligand 3, also known as macrophage inflammatory protein-1a), CCL4 (macrophage inflammatory protein-1b) and CCL5 (also known as RANTES--regulated on activation normal T cell expressed and secreted) [7].
The gene profiling analysis revealed the modulation of several genes including cytokines (e.g., IL-1[alpha], IL-1[beta], IL-6, TNF-[alpha], IFN-[beta]1 and G-CSF), chemokines (e.g.,
CCL3, CCL4, CCRL2, CXCL2 and CXCL10), as well as several co-stimulatory molecules (e.g., CD14, CD40, CD69, CD82, CD83 and CD274).
Available at http://water.epa.gov/scitech/drinkingwater/dws/ccl/
ccl3.cfm.
In particular, we evaluated PDGF-[beta][beta], IL-1[beta], IL-1ra, IL-2, IL-4, IL-5, IL-6, IL-7, IL-8, IL-9, IL-10, IL-12, IL-13, IL-15, IL-17, Eotaxin, FGF basic, GCSF, GM-CSF, INF-[gamma], IP-10, MCP-1, MIP-1a (
CCL3), MIP-1[beta] (CCL4), Rantes, TNF-[alpha], and VEGF.
Sera were separated from blood and analysed for 14 different molecules: interleukin (IL)-2, IL-6, IL-10, IL-12p70, interferon (IFN)-[gamma] macrophage migration inhibitory factor (MIF), tumor necrosis factor (TNF)-[alpha], TNF-related apoptosis inducing ligand (TRAIL), sFas and Fas ligand (sFasL), and chemokines CXCL10, CCL2,
CCL3, and CCL4 as previously described [26].
Plasma concentration of cytokines/chemokines, IFN-[gamma], IL-6, IL-12p40, TNF, sCD40L, IL-1[beta], IL-4, IL-10, IL-13, IL-RA, MCP-1, fractakine, eotaxin, IL-15, IL-17A, TGF-[alpha], macrophage inflammatory proteins-1[alpha], (MIP-1[alpha] or
CCL3), Macrophage inflammatory proteins-1[beta] (MIP-1[beta] or CCL4), and rAnTES and metabolic hormone panel containing leptin, C-peptide, GLP-1 (active) glucagon, insulin, pancreatic peptide, and PYY (total) were measured using the Multiplex MAP Magnetic Bead-based immunoassay kits (Millipore Corp.