o IL-1?, IL-1?, IL-2, IL-4, IL-6,
IL-8, IL-10, IFN-?, TNF-?
RT-qPCR analyses were then performed with SYBR Green Master mix kit (Applied Biosystems, Foster City, CA, USA) and primers for GAPDH, IL-1[sz], TNF-a, IL-6,
IL-8, and IL-33.
The production of reactive oxygen species (ROS) is required to induce the microbicidal activity mediated by vitamin D and cathelicidin, and cathelicidin enhances the production of ROS and proinflammatory cytokines, such as TNF-[alpha],
IL-8, and IL-6 [99].
A comparative analysis of the relative gene expression by fold difference before and after HAART revealed that the IRIS group had higher NFAT1, IL-6,
IL-8, and TNF-[alpha] expression in [CD3.sup.+] T cells after receiving HAART for 1 month.
It also showed that the concentrations of IL6 and
IL-8 increased during the fever stage, and continued to increase during the hypotension stage, reaching their peak during the oliguria stage.
Cells treated with IL-15 and
IL-8 showed marked expression of IL-15R.
Conclusions.--Our data demonstrate that anti-IL-8 autoantibody:
IL-8 complexes are present in lung tissues of patients with ARDS, and are attached to Fc[gamma]RIIa.
Blood samples were drawn onto sodium EDTA from the following subjects after informed consent: For determination of the reference range of total
IL-8, blood was collected from 103 healthy subjects (46 males and 57 females) who underwent routine examination by a company physician.
Thus, IL-36 ligands not only act as effector cytokines of the IL23/Th17 axis, but also induce several proinflammatory mediators (including IL-6,
IL-8, and IL-23) that reinforce the Th17-driven inflammatory milieu [25, 59, 60, 63].
The aim of this study was to evaluate (a)
IL-8 production in both plasma and ascitic fluid in cirrhotic patients with SBP and sterile ascites (SA); (b) the correlation of these values with neutrophil count in ascitic fluid; (c) the effect of therapy on
IL-8; and (d) the sensitivity and specificity of ascitic fluid
IL-8 in cirrhotic patients with ascites for detecting SBP patients.
The disease progression depends on the increased production of proinflammatory cytokines (IL-1[alpha], IL-1[beta], IL-6,
IL-8, and TNF[alpha]), metalloproteinases, and prostaglandins or decreased production of anti-inflammatory cytokines (IL-10, TGF[beta]) and inhibitors of metalloproteinases [2].