IL8 Antibody - #DF6998

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Product: IL8 Antibody
Catalog: DF6998
Description: Rabbit polyclonal antibody to IL8
Application: WB IHC
Reactivity: Human
Mol.Wt.: 11kDa; 11kD(Calculated).
Uniprot: P10145
RRID: AB_2838954

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MSDS
Data Sheet
COA
Protocols
WB Handbook
IHC Protocol
IF/ICC Protocol

Product Info

Source:
Rabbit
Application:
WB 1:500-1:2000, IHC 1:50-1:200
*The optimal dilutions should be determined by the end user.
*Tips:

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

Reactivity:
Human
Clonality:
Polyclonal
Specificity:
IL8 Antibody detects endogenous levels of total IL8.
RRID:
AB_2838954
Cite Format: Affinity Biosciences Cat# DF6998, RRID:AB_2838954.
Conjugate:
Unconjugated.
Purification:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
Storage:
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
Alias:

Fold/Unfold

(Ala-IL-8)77; (Ser-IL-8)72; 9E3; Beta thromboglobulin like protein; C-X-C motif chemokine 8; CEF-4; chemokine, CXC motif, ligand 8; CXCL8; Emoctakin; GCP-1; GCP/IL-8 protein I; GCP/IL-8 protein II; GCP/IL-8 protein III; GCP/IL-8 protein IV; GCP/IL-8 protein V; GCP/IL-8 protein VI; GCP1; Granulocyte chemotactic protein 1; IL-8; IL-8(1-77); IL-8(9-77); IL8; IL8/NAP1 form I; IL8/NAP1 form II; IL8/NAP1 form III; IL8/NAP1 form IV; IL8/NAP1 form V; IL8/NAP1 form VI; IL8_HUMAN; Inteleukin 8; LECT; LUCT; Lymphocyte-derived neutrophil-activating factor; LYNAP; MDNCF; MDNCF-b; MDNCF-c; MONAP; Monocyte-derived neutrophil chemotactic factor; Monocyte-derived neutrophil-activating peptide; NAF; NAP-1; NAP1; Neutrophil activating peptide 1; Neutrophil activating protein 1; Neutrophil-activating factor; Neutrophil-activating protein 1; Protein 3 10C; Protein 3-10C; SCYB8; Small inducible cytokine subfamily B member 8; T cell chemotactic factor; T-cell chemotactic factor; TSG1;

Immunogens

Immunogen:
Uniprot:

P10145(IL8_HUMAN) >>Visit HPA database.

Gene(ID):
CXCL8(3576)
Description:
The protein encoded by this gene is a member of the CXC chemokine family. This chemokine is one of the major mediators of the inflammatory response. This chemokine is secreted by several cell types. It functions as a chemoattractant, and is also a potent angiogenic factor. This gene is believed to play a role in the pathogenesis of bronchiolitis, a common respiratory tract disease caused by viral infection. This gene and other ten members of the CXC chemokine gene family form a chemokine gene cluster in a region mapped to chromosome 4q.
Sequence:
MTSKLAVALLAAFLISAALCEGAVLPRSAKELRCQCIKTYSKPFHPKFIKELRVIESGPHCANTEIIVKLSDGRELCLDPKENWVQRVVEKFLKRAENS

Research Backgrounds

Function:

IL-8 is a chemotactic factor that attracts neutrophils, basophils, and T-cells, but not monocytes. It is also involved in neutrophil activation. It is released from several cell types in response to an inflammatory stimulus. IL-8(6-77) has a 5-10-fold higher activity on neutrophil activation, IL-8(5-77) has increased activity on neutrophil activation and IL-8(7-77) has a higher affinity to receptors CXCR1 and CXCR2 as compared to IL-8(1-77), respectively.

PTMs:

Several N-terminal processed forms are produced by proteolytic cleavage after secretion from at least peripheral blood monocytes, leukcocytes and endothelial cells. In general, IL-8(1-77) is referred to as interleukin-8. IL-8(6-77) is the most promiment form.

Citrullination at Arg-27 prevents proteolysis, and dampens tissue inflammation, it also enhances leukocytosis, possibly through impaired chemokine clearance from the blood circulation.

Subcellular Location:

Secreted.

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Subunit Structure:

Homodimer.

Family&Domains:

Belongs to the intercrine alpha (chemokine CxC) family.

Research Fields

· Cellular Processes > Cell growth and death > Cellular senescence.   (View pathway)

· Environmental Information Processing > Signaling molecules and interaction > Cytokine-cytokine receptor interaction.   (View pathway)

· Environmental Information Processing > Signal transduction > NF-kappa B signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > Phospholipase D signaling pathway.   (View pathway)

· Human Diseases > Endocrine and metabolic diseases > Non-alcoholic fatty liver disease (NAFLD).

· Human Diseases > Infectious diseases: Bacterial > Epithelial cell signaling in Helicobacter pylori infection.

· Human Diseases > Infectious diseases: Bacterial > Shigellosis.

· Human Diseases > Infectious diseases: Bacterial > Salmonella infection.

· Human Diseases > Infectious diseases: Bacterial > Pertussis.

· Human Diseases > Infectious diseases: Bacterial > Legionellosis.

· Human Diseases > Infectious diseases: Parasitic > Chagas disease (American trypanosomiasis).

· Human Diseases > Infectious diseases: Parasitic > Malaria.

· Human Diseases > Infectious diseases: Parasitic > Amoebiasis.

· Human Diseases > Infectious diseases: Viral > Hepatitis C.

· Human Diseases > Infectious diseases: Viral > Hepatitis B.

· Human Diseases > Infectious diseases: Viral > Influenza A.

· Human Diseases > Cancers: Overview > Pathways in cancer.   (View pathway)

· Human Diseases > Cancers: Overview > Transcriptional misregulation in cancer.

· Human Diseases > Cancers: Specific types > Bladder cancer.   (View pathway)

· Human Diseases > Immune diseases > Rheumatoid arthritis.

· Organismal Systems > Immune system > Chemokine signaling pathway.   (View pathway)

· Organismal Systems > Immune system > Toll-like receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > NOD-like receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > RIG-I-like receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > IL-17 signaling pathway.   (View pathway)

References

1). HIF-1α/JMJD1A signaling regulates inflammation and oxidative stress following hyperglycemia and hypoxia-induced vascular cell injury. CELLULAR & MOLECULAR BIOLOGY LETTERS, 2021 (PubMed: 34479471) [IF=8.3]

Application: WB    Species: Human    Sample: HUVECs

Fig. 3 Effects of inhibition of HIF-1α on expression of inflammation after hyperglycemic and hypoxia. a Cells were treated with glucose (25 mM) or with combined exposure to high glucose and hypoxia for 6, 12, 24, and 48 h. Exposure to glucose alone or combined stimulation with hypoxia significantly increased gene expression of HIF-1α. b Cells were treated with KC7F2 (10 µM) or si-HIF-1α for 48 h following combined stimulation, and IL-6, IL-8, ICAM-1, MCP-1, and c HIF-1α levels were analyzed. The relative density of IL-6, IL-8, ICAM-1, and MCP-1 (d) was normalized according to GAPDH expression. Importantly, the downregulation of HIF-1α decreased the secretion of IL-6, IL-8, ICAM-1 and MCP-1 based on ELISA and qRT-PCR assays (e–f). n = 3; *p < 0.05 and **p < 0.01 vs. DMSO. DMSO-treated cells, DMSO; HIF-1α inhibitors KC7F2 (10 µM)-treated cells, KC7F2 (10 µM); si-HIF-1α, small interfering RNA HIF-1α; HG, high glucose; HG + Hypoxia, combined stimulus with high glucose and hypoxia; NG, control

Application: WB    Species: human    Sample: HUVECs

Fig. 3 | Efects of inhibition of HIF-1α on expression of infammation after hyperglycemic and hypoxia.b Cells were treated with KC7F2 (10 µM) or si-HIF-1α for 48 h following combined stimulation, and IL-6, IL-8, ICAM-1, MCP-1, and c HIF-1α levels were analyzed. The relative density of IL-6, IL-8,ICAM-1, and MCP-1 (d) was normalized according to GAPDH expression.
2). FGF21 Attenuates Neurodegeneration though Modulating Neuroinflammation and Oxidant-stress. BIOMEDICINE & PHARMACOTHERAPY, 2020 (PubMed: 32768941) [IF=7.5]

Application: IHC    Species: mouse    Sample: brains

Fig. 5. |FGF21 attenuates neurodegeneration through anti-inflammation in aging mice (n = 7-8/group). (D) The injury levels were exhibited by H&E staining (10X magnification, bar = 100 μm) and IL6, IL8 levels were exhibited by immunohistochemistry (40X magnification, bar = 20 μm) in the brains of each group mice. The FGF21 (1.0 mg/kg) and metformin (20 mg/kg)were used. The data were performed using one-way analysis of variance (ANOVA), followed by the two-tailed t test. Significant as compared to young mice. *p＜0.05.Significant as compared to aging mice. #p＜0.05.

Application: WB    Species: mouse    Sample: brains

Fig. 3. |FGF21 attenuates the expression of NF-κB, Iba1, IL6 and IL8 in the brains of diabetic mice (n = 10/group). (A)The IL6 levels of each group mice were exhibited by immunohistochemistry (40X magnification, bar = 20 μm). (B) The levels of NF-κB, Iba1, IL6 and IL8 in the brains were measured by Western blot.
3). Pyrogallol enhances therapeutic effect of human umbilical cord mesenchymal stem cells against LPS-mediated inflammation and lung injury via activation of Nrf2/HO-1 signaling. Free radical biology & medicine, 2022 (PubMed: 36028178) [IF=7.4]
4). BML-111 inhibits EMT, migration and metastasis of TAMs-stimulated triple-negative breast cancer cells via ILK pathway. International Immunopharmacology, 2020 (PubMed: 32485356) [IF=5.6]

Application: IHC    Species: mouse    Sample: tumor

Fig.7. The inhibitory effect of BML-111 on the tumor growth of 4T1-MIND model mice in vivo (A) Representative images of the tumor tissue dissected from 4T1-MIND model mice. *P = 0.0271 BML-111 group vs. control group. (F) The expression of IL-8 in tumor cells and stroma of BML-111 group was compared with that in control group. Scale bar, 200 μm. ****P < 0.0001.
5). Rosmarinic acid treatment protects against lethal H1N1 virus-mediated inflammation and lung injury by promoting activation of the h-PGDS-PGD2-HO-1 signal axis. Chinese medicine, 2023 (PubMed: 37891648) [IF=4.9]

Application: IF/ICC    Species: Mouse    Sample:

Fig. 2 Effects of RosA on the H1N1 virus-triggered pro-inflammatory response. A Representative immunofluorescence images of IL-6, IL-8 (pink) and TNF-α, MCP-1 (red) in lung SpC+ (green) alveolar epithelial cells. B Quantitative analysis of fluorescence intensities for IL-6, TNF-α, IL-8 and MCP-1 in SpC+ alveolar epithelial cells. C Levels of pro-inflammatory mediators (IL-6, MCP-1, RANTES and TNF-α) in the lung homogenates were determined by Luminex assay. D Levels of pro-inflammatory mediators (IL-6, IL-8, IP-10, MCP-1, RANTES and TNF-α) were determined by Luminex assay.
6). An Extracellular Matrix-Mimicking Hydrogel for Full Thickness Wound Healing in Diabetic Mice. MACROMOLECULAR BIOSCIENCE, 2018 (PubMed: 29737012) [IF=4.6]

Application: IHC    Species: rat    Sample: inflammatory cell

Figure 6. |Immunohistochemical staining of a) IL-8 and b) MCP-1 in the wound bed on day 3, 7, and 14. Scale bars represent 100 µm. c) Semiquantitative analysis of IL-8 and MCP-1, double-blind analysis by using a four-point scale (0, no positive cells; 1, low number of positive cells; 2, moderate number of positive cells; and 3, high number of positive cells). The level of IL-8 in the HA-GEL group was significantly lower than that in the other two groups at day 7 (p < 0.05). On day 3, both alginate and HA-GEL groups could significantly reduce the expression of MCP-1. On day 7, the level of MCP-1 in the HA-GEL group remained significantly lower than that in the alginate group and control.
7). Interaction with tumor‑associated macrophages promotes PRL‑3‑induced invasion of colorectal cancer cells via MAPK pathway‑induced EMT and NF‑κB signaling‑induced angiogenesis. ONCOLOGY REPORTS, 2019 (PubMed: 30864736) [IF=4.2]

Application: WB    Species: mouse    Sample: TAMs

Figure 2. |PRL‑3‑induced activation of IL‑6 and IL‑8 by initiating JNK and ERK pathways in TAMs. (A) After co‑culture with colorectal cancer cells, IL‑6, IL‑8, p‑JNK, and p‑ERK levels in TAMs were examined using western blot assays.
8). Whole-Transcriptome Analysis of Non-Coding RNA Alteration in Porcine Alveolar Macrophage Exposed to Aflatoxin B1. Toxins, 2022 (PubMed: 35737034) [IF=4.2]

Application: IF/ICC    Species: pig    Sample: 3D4/2 cells

Figure 5 Cell immunofluorescence assay of the expression of CXCL8 and GADD45G proteins. (A) The fluorescence intensity and positive percentages of CXCL8. Nuclear staining (blue) and CXCL8-positive cells (green). (B) The fluorescence intensity and positive percentages of GADD45G. Nuclear staining (blue) and GADD45G-positive cells (red). ** Indicates extremely significant differences (p < 0.01). All experiments were repeated 3 times.
9). Transcriptional Profiling Reveals the Regulatory Role of CXCL8 in Promoting Colorectal Cancer. Frontiers in Genetics, 2020 (PubMed: 32038715) [IF=3.7]

Application: IHC    Species: human    Sample: tumor

FIGURE 3 | Expression levels of CXCL8 in the clinical cohort. (A) The levels of CXCL8 mRNA in the normal (N = 81), colorectal cancer (CRC)-early stage (N = 44)and CRC-advanced stage (N = 37) groups. (B) The levels of CXCL8 protein in normal (N = 87), CRC-early stage (N = 48), and CRC-advanced stage (N = 39)groups. (C) Immunohistochemical staining of normal, CRC-early stage and CRC-advanced stage groups.
10). Alamandine, a new member of the renin-angiotensin system (RAS), attenuates collagen-induced arthritis in mice via inhibiting cytokine secretion in synovial fibroblasts. PEPTIDES, 2022 (PubMed: 35609788) [IF=3.0]

Application: WB    Species: Mouse    Sample: synovial fibroblasts

Fig. 4. Effect of Alamandine on the mRNA and protein expression of inflammatory cytokines in synovial fibroblasts. MH7A cells (A) or primary FLS from RA patients (B) were cultured with the indicated concentrations of alamandine in the presence of TNF-α (10 ng/ml) for 24 h, mRNA levels of inflammation related genes were analyzed with real time PCR and protein levels in MH7A cells were validated with western blotting (C). (D) MH7A cells were treated with alamandine 10 μg/ml for 6 h, and further stimulated with TNF-a (10 ng/ml) for 30 min. The phosphorylated expression of JNK, p38, ERK and NF-κB p65 were evaluated by wester blotting. (E) The expression of MrgD in MH7A cells (upper) and primary RA FLS (lower) were detected by immunofluorescent staining. The magnification is × 400. Results from three independent experiments are shown as mean ± SEM. * P < 0.05, * * P < 0.01.
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