Rabbit Anti-Human IL8 (a.a. 23-99) Polyclonal antibody

Name: Rabbit Anti-Human IL8 (a.a. 23-99) Polyclonal antibody
SKU: DPABH-04383
Rating: 5 (1 reviews)

Rabbit Anti-Human IL8 (a.a. 23-99) Polyclonal antibody for ELISA, IHC, WB

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COA

SDS

Datasheet

Key features and details

Target: Human IL8
Host: Rabbit
Application: ELISA, IHC, WB
Species Reactivity: Human

Summary

Specifications

Antibody Isotype

IgG

Species Reactivity

Human

Immunogen

E. coli - derived recombinant Human IL8/CXCL8 (Ala23-Ser99).

Conjugate

Unconjugated

Applications

Application Notes

ELISA: 1:4000-1:8000
IHC: 1:50-1:100
WB: 1:1000-1:4000

General Notes

This product (Catalog No. DPABH-04383) is a rabbit-derived polyclonal antibody raised against human IL8, targeting the amino acid region 23–99 of the protein. It has been affinity purified by Protein A. The protein encoded by this gene is a member of the CXC chemokine family and is a major mediator of the inflammatory response. The encoded protein is commonly referred to as interleukin-8 (IL-8). IL-8 is secreted by mononuclear macrophages, neutrophils, eosinophils, T lymphocytes, epithelial cells, and fibroblasts. It functions as a chemotactic factor by guiding the neutrophils to the site of infection. Bacterial and viral products rapidly induce IL-8 expression. IL-8 also participates with other cytokines in the proinflammatory signaling cascade and plays a role in systemic inflammatory response syndrome (SIRS). This gene is believed to play a role in the pathogenesis of the lower respiratory tract infection bronchiolitis, a common respiratory tract disease caused by the respiratory syncytial virus (RSV). The overproduction of this proinflammatory protein is thought to cause the lung inflammation associated with csytic fibrosis. This proinflammatory protein is also suspected of playing a role in coronary artery disease and endothelial dysfunction. This protein is also secreted by tumor cells and promotes tumor migration, invasion, angiogenesis and metastasis. This chemokine is also a potent angiogenic factor. The binding of IL-8 to one of its receptors (IL-8RB/CXCR2) increases the permeability of blood vessels and increasing levels of IL-8 are positively correlated with increased severity of multiple disease outcomes (eg, sepsis). This gene and other members of the CXC chemokine gene family form a gene cluster in a region of chromosome 4q.
DPABH-04383 is suitable for use in ELISA (1:4,000–1:8,000), IHC (1:50–1:100), Western blot (WB) (1:1,000–1:4,000) applications.
DPABH-04383 is supplied as a liquid formulation in 0.01M PBS, pH 7.4, 50% Glycerol, 0.05% Proclin 300. For long-term storage, keep at −20 °C. For short-term use, store at 2–8 °C. Avoid repeated freeze–thaw cycles to maintain antibody integrity and performance.

Target

Alternative Names

IL8; CXCL8; AMCF-I; interleukin-8; IL-8; C-X-C motif chemokine 8; chemokine (C-X-C motif) ligand 8; alveolar macrophage chemotactic factor I; alveolar macrophage-derived chemotactic factor-I

UniProt ID

P10145

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Interleukin 1 beta and Prostaglandin E2 affect expression of DNA methylating and demethylating enzymes in human gingival fibroblasts

INTERNATIONAL IMMUNOPHARMACOLOGY

Authors: Seutter, Sara; Winfield, Jacquay; Esbitt, Alexis; Snyder, Samantha; Magner, Anastasia; Kim, Kristine; Carcuffe, Craig; Schmoyer, Jeremy; Kamrani, Payvand; Mercando, Jason; Shamseddin, Seyed M.; Green, Kevan; Borghaei, Ruth C.

Abstract

Periodontitis is a common chronic inflammatory condition that results in increased levels of inflammatory cytokines and inflammatory mediators. In addition to oral disease and tooth loss, it also causes low-grade systemic inflammation that contributes to development of systemic conditions including cardiovascular disease, pre-term birth, diabetes and cancer. Chronic inflammation is associated with epigenetic change, and it has been suggested that such changes can alter cell phenotypes in ways that contribute to both ongoing inflammation and development of associated pathologies. Here we show that exposure of human gingival fibroblasts to IL-1 beta increases expression of maintenance methyltransferase DNMT1 but decreases expression of de novo methyltransferase DNMT3a and the demethylating enzyme TET1, while exposure to PGE2 decreases expression of all three enzymes. IL-1 beta and PGE2 both affect global levels of DNA methylation and hydroxymethylation, as well as methylation of some specific CpG in inflammation-associated genes. The effects of IL-1 beta are independent of its ability to induce production of PGE2, and the effects of PGE2 on DNMT3a expression are mediated by the EP4 receptor. The finding that exposure of fibroblasts to IL-1 beta and PGE2 can result in altered expression of DNA methylating/demethylating enzymes and in changing patterns of DNA methylation suggests a mechanism through which inflammatory mediators might contribute to the increased risk of carcinogenesis associated with inflammation.

Deepwater Horizon oil alone and in conjunction with Vibrio anguillarum exposure modulates immune response and growth in red snapper (Lutjanus campechanus)

AQUATIC TOXICOLOGY

Authors: Rodgers, Maria L.; Takeshita, Ryan; Griffitt, Robert J.

Abstract

This study examined the impacts of Macondo oil from the Deepwater Horizon oil spill, both alone and in conjunction with exposure to the known fish pathogen Vibrio anguillarum, on the expression of five immune-related gene transcripts of red snapper (il8, il10, tnfa, il1b, and igm). In order to elucidate this impact, six different test conditions were used: one Control group (No oil/No pathogen), one Low oil/No pathogen group (tPAH50 = 0.563 mu g/L), one High oil/No pathogen group (tPAH50 = 17.084 mu g/L, one No oil/Pathogen group, one Low oil/Pathogen group (tPAH50 = 0.736 mu g/L), and one High oil/Pathogen group (tPAH50 = 15.799 mu g/ L). Fish were exposed to their respective oil concentrations for one week. On day 7 of the experiment, all fish were placed into new tanks (with or without V. anguillarwn) for one hour. At three time points (day 8, day 10, and day 17), fish organs were harvested and placed into RNAlater, and qPCR was run for examination of the above specific immune genes as well as cyp1a1. Our results suggest that cyp1a1 transcripts were upregulated in oil-exposed groups throughout the experiment, confirming oil exposure, and that all five immune gene transcripts were upregulated on day 8, but were generally downregulated or showed no differences from controls on days 10 and 17. Finally, both oil and pathogen exposure had impacts on growth.