The Human IL-8 ELISA kit is designed to detect and quantify the level of Human IL-8 in cell culture supernatant, serum, and plasma.
Contents of Kit
1. Microwell plate: 1 x 96 wells 2. Human IL-8 Standard: 2 bottles 3. Assay Solution: 1 x 25 mL 4. Human IL-8 Biotin Conjugate: 1 x 11 mL 5. Streptavidin-horseradish peroxidase (HRP) Concentrate (100x): 1 x 150 μL 6. Streptavidin-HRP Diluent: 1 x 12 mL 7. Wash Solution Concentrate (10x): 2 x 75 mL 8. Chromogen Solution: 1 x 12 mL 9. Stop Solution: 1 x 12 mL
Storage
Store the reagents at 2-8°C until expiration date. For more detailed information, please download the following document on our website.
Sensitivity
< 1 pg/mL
Standard Curve
Citations
Publication ()
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Background
Interleukin-8 (IL-8) (CXCL8) is a typical chemotactic chemokine of the CXC chemokine family released mostly by monocyte macrophages. Adult IL-8 comes in four species (given relative molecular weight) of which IL-8 contains 72 amino acids, which are the most potent. Other cells can also release IL-8, and different cells including neutrophils, endothelial cells, fibroblasts and some tumour cells can produce IL-8 when the right environment and other triggers lead to this. IL-8 is almost imperceptible in the natural state, but it is amplified 10-100-fold when induced by conditions external to the body. It turned out that IL-8 wasn't just widespread in inflammatory conditions, but also contributed to the formation of many kinds of tumours.
IL-8 is mainly dependent on its specific binding to specific cell surface G protein-coupled receptors to exert its corresponding effects. The 2 main classes of IL-8 receptors are CXCR1 and CXCR2. Both are G protein-coupled receptors and occur mainly on endothelial, epithelial, leukocyte and neuron cells. Most widely used pro-inflammatory factor is IL-8. Inflammation changes the microenvironment in which cells reside, and microenvironment changes can induce pathological cell growth or oncogene and suppressor gene mutations that can cause tumourigenesis. And, in fact, IL-8 is strongly associated with cancer cell growth and metastasis, as well as angiogenesis.
Epithelial mesenchymal transition (EMT) regulates tumor cell invasion and metastasis via cell morphology and deadherination loss, epithelial and mesenchymal signature factors, EMT transcription factors (absence of E-cadherin, growth of N-cadherin, fibrillin, matrix metalloproteinases) responsible for the tumor cell invasion and metastasis. IL-8 has been shown to be closely associated with tumor EMT. MiR-520c-3p was shown to down-regulate IL-8 expression in breast cancer and E-cadherin levels were increased, and fibronectin levels decreased, indicating that IL-8 plays a role in EMT of breast cancer cells. Sohlh2, a transcription factor of ovarian cancer superfamily, blocks EMT in breast cancer cells by preventing IL-8 expression and so inhibits tumour cell invasion in vitro and metastasis in vivo. Not only can IL-8 be recruited by other stimuli to cause tumor EMT, it can in itself or by interacting with its receptor induce tumour EMT. In human ovarian cancer SKOV3 cells, IL-8 decreased E-cadherin expression and enhanced invasion and migration by the SKOV3 cells; therefore, IL-8 can cause EMT and improve invasion and migration by ovarian cancers.
Figure 1. Effects of IL-8 on the tumor and microenvironment (Source: David JM, et al. 2016)
Alternative Names
Human Interleukin-8 ELISA Kit Human IL 8 ELISA Kit Human CXCL8 ELISA Kit
References
1. Matsushima K, et al. Interleukin-8: An evolving chemokine. Cytokine. 2022 May;153:155828.
2. David JM, et al. The IL-8/IL-8R Axis: A Double Agent in Tumor Immune Resistance. Vaccines (Basel). 2016 Jun 24;4(3):22.
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References
The Axin2-snail axis promotes bone invasion by activating cancer-associated fibroblasts in oral squamous cell carcinoma
BMC CANCER
Authors: An, Yin-Zhe; Cho, Eunae; Ling, Junqi; Zhang, Xianglan
BackgroundIn bone-invasive oral squamous cell carcinoma (OSCC), cancer-associated fibroblasts (CAFs) infiltrate into bony tissue ahead of OSCC cells. In the present study, we aimed to investigate the role of the Axin2-Snail axis in the biological behaviour of CAFs and bone invasion in OSCC.MethodsThe clinicopathological significance of Axin2 and Snail expression was investigated by immunohistochemistry in an OSCC cohort containing 217 tissue samples from patients with long-term follow-up. The influence of the Axin2-Snail axis on the biological behaviour of OSCC cells and CAFs was further investigated both in vitro and in vivo.ResultsAxin2 expression was significantly associated with Snail expression, the desmoplasia status, and bone invasion in patients with OSCC. In multivariate analysis, lymph node metastasis, desmoplasia, Axin2 expression, and Snail expression were independent poor prognostic factors in our cohort. Consistent with these findings, OSCC cells demonstrated attenuated oncogenic activity as well as decreased expression of Snail and various cytokines after Axin2 knockdown in vitro. Among the related cytokines, C-C motif chemokine ligand 5 (CCL5) and interleukin 8 (IL8) demonstrated a strong influence on the biological behaviour of CAFs in vitro. Moreover, both the desmoplastic reaction and osteolytic lesions in the calvaria were predominantly decreased after Axin2 knockdown in OSCC cells in vivo using a BALB/c athymic nude mouse xenograft model.ConclusionsOncogenic activities of the Axin2-Snail axis are not limited to the cancer cells themselves but rather extend to CAFs via regulation of the cytokine-mediated cancer-stromal interaction, with further implications for bone invasion as well as a poor prognosis in OSCC.
In vitro preconditioning of equine adipose mesenchymal stem cells with prostaglandin E-2, substance P and their combination changes the cellular protein secretomics and improves their immunomodulatory competence without compromising stemness
VETERINARY IMMUNOLOGY AND IMMUNOPATHOLOGY
Authors: Cabezas, J.; Rojas, D.; Wong, Y.; Telleria, F.; Manriquez, J.; Mancanares, A. C. F.; Rodriguez-Alvarez, Ll; Castro, F. O.
Mesenchymal stem cells (MSC) are modern tools in regenerative therapies of humans and animals owed to their immunomodulatory properties, which are activated in a pro-inflammatory environment. Different preconditioning strategies had been devised to enhance the immunomodulatory properties of MSC. In this research, we evaluated the immunological attributes of equine adipose MSC (eAMSC) before and after preconditioning in vitro with prostaglandin E-2 (PGE2), substance P (SP), their combination and IFN gamma. PGE(2)/SP was the best combination to keep or enhance the mesodermal lineage differentiation of eAMSC. Alongside with this, preconditioning of eMSC with PGE(2) and SP did not affect expression of stemness MSC surface phenotype: CD90(+), CD44(+), MHC class I+, MHC class II- and CD45(-), assessed by cytometry. Both naive and preconditioned eAMSC expressed genes related with immune properties, such as MHC-I, PTGES, IL6, IL1A, TNF alpha and IL8 assessed by qPCR. Only TNF alpha was under expressed in treated cells, while the other markers were either overexpressed or not changed. In no cases MHC-II expression was detected. The antiproliferative effect of preconditioned eAMSC exposed to activated peripheral blood mononuclear cells (PBMC) showed that SP treatment significantly inhibited proliferation of LPS stimulated PBMC. When eAMSC were stimulated with Poly I:C, all the treatments significantly inhibited proliferation of stimulated PBMC (p < 0.05). Direct contact (coculture) between the preconditioned eAMSC and PBMC, induced a shift of significantly more (CD4/CD25/FOXP3)(+) T-regulatory PBMC than naive eAMSC. In the experiments of this research, we investigated the secreted proteomic profile of naive and preconditioned eAMSC, 42 up-regulated and 40 down-regulated proteins were found in the proteomic assay. Our proteomic data revealed profound changes in the secretory pattern of MSC exposed to different treatments, compared to naive eAMSC as well as among treatments. In overall, compared to naive cells, the protein profile of preconditioned cells resembled the mesenchymal-epithelial transition (MET). Here we showed that the combined use of PGE(2) and SP provoked in overall the highest expression of anti-inflammatory markers as well as lead to an increased acquisition of a T-regulatory phenotype in preconditioned eAMSC without affecting their "stemness".