We detected IL-1[sz], IL-33, IL-6, IL-8, and TNF-a.
Therefore, if we increase the level of IL-33 in RASFs, soluble ST2 may play a negative role on more cytokines, such as IL-6, IL-8, and TNF-a.
NFAT can bind to the promoter/enhancer of various cytokine genes and can contribute to the expression of IL-2, IL-3, IL-4, IL-5, IL-6, IL-8
, IL-10, IL-13, IFN-[gamma], and TNF-[alpha].
The concentrations of urine IL-6, IL-8
, and TNF increased significantly at the fever stage.
However, the cells which were treated with IL-8
seem to show a little more IL-15R a mRNA expression than other treatments.
(19,20) Importantly, our studies indicate that immune complexes containing a functional homolog of IL-8
(mouse [KC.sup.21]) and anti-KC autoantibodies are deposited in the lungs of mice (A.K., unpublished observations, 2005), and contribute to lung inflammation and injury.
was measured with the enzyme immunoassay IMMULITE IL-8
(test code, 18; DPC Biermann) performed fully automated on the IMMULITE system.
Furthermore, IL-6 secretion results in secondary production of chemokines such as IL-8
and MCP-1 by mononuclear cells/macrophages as well as expression of ICAM-1 and other adhesion molecules on endothelial cells, leading to enhanced neutrophil migration [75, 77, 79].
Statistically significant differences for IL-8
and other values in ascitic fluid and in plasma between groups were studied with the Mann-Whitney U-test.
Our results showed that the stimulation of IL-17 could significantly increase the mRNA expressions of HBD-2, 3, IL-8
, CCL-20, and TNF-[alpha], but not the expression of HBD-1, CXCL-9, -10, -11, CCL-5, and IL-6 in HOK cells.
Using ICCs, poor agreement was found between plasma and serum in IL-1[beta], IL-4, IL-5, IL-6, IL-7, IL-8
, TNF-[alpha], IFN-[gamma], IL-12p70, IL-13, IL-17, G-CSF, MCP-1, and MIP-1[beta].