Canine IL-8 (CXCL8) (Yeast-derived Recombinant Protein) - 5 micrograms

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Interleukin-8 (IL-8), also known as CXCL8, is a CXC family member chemokine produced by macrophages and other cell types such as epithelial cells. There have been 17 different CXC chemokines described in mammals, that are subdivided into two categories, those with a specific amino acid sequence (or motif) of glutamic acid-leucine-arginine (or ELR for short) immediately before the first cysteine of the CXC motif (ELR-positive), and those without an ELR motif (ELR-negative). ELR-positive CXC chemokines such as IL-8 specifically induce the migration of neutrophils, and interact with chemokine receptors CXCR1 and CXCR2.

Alternate Names - CXCL8, chemokine (C-X-C motif) ligand 8, GCP-1, GCP1, LECT, LUCT, LYNAP, MDNCF, MONAP, NAF, NAP-1, NAP1, IL8, C-X-C motif chemokine ligand 8, Interleukin-8, SCYB8

Homology Across Species
Canis lupus familiaris (dog) IL-8 – 100%
Canis lupus dingo (dingo) IL-8 – 100%
Vulpes vulpes (red fox) IL-8 – 100%
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Canine IL-8 (CXCL8) (Yeast-derived Recombinant Protein) - 5 micrograms
Catalog No.:
5 ug
The Canine IL-8 recombinant protein was produced in yeast and therefore does not have endotoxin, is naturally folded, and post-translationally modified.
The Canine IL-8 (CXCL8) recombinant protein has a predicted molecular weight of 8.6 kDa.
Protein Sequence:
Country of Origin:
The Canine IL-8 (CXCL8) endotoxin-free recombinant protein can be used in cell culture, as an IL-8 ELISA Standard, and as a Western Blot Control.


Interleukin-1β, tumour necrosis factor-α and lipopolysaccharide induce C-type natriuretic peptide from canine aortic endothelial cells.

Osterbur K, Yu DH, Declue AE.

Res Vet Sci. 2012 Nov 8. doi:pii: S0034-5288(12)00305-0. 10.1016/j.rvsc.2012.10.002.

Applications: Stimulation of canine aortic endothelial cells

The N-terminal portion of pro C-type natriuretic peptide (NT-pCNP) has shown promise as a biomarker for sepsis in humans and dogs, however the mechanism of NT-pCNP production in dogs is unknown. Canine aortic endothelial cells were stimulated with lipopolysaccharide, lipoteichoic acid, peptidoglycan, TNF-α, IL-1β, IL-6, IL-10, IL-21, CXCL-8, IFN-γ, VEGF-A or control (PBS), and NT-pCNP production was measured. Lipopolysaccharide, TNF-α, and IL-1β significantly stimulated NT-pCNP production in a dose and time dependent manner; IL-1β resulted in the greatest NT-pCNP concentrations. The other stimulants did not result in significant NT-pCNP production. The addition of serum to the cell culture model did not alter lipopolysaccharide, lipoteichoic acid or peptidoglycan induced NT-pCNP production. These data indicate that lipopolysaccharide, TNF-α and IL-1β regulate CNP production from canine vascular endothelium and of the stimulants tested, IL-1β is the predominant inducing factor. These data provide some initial insight into the mechanisms of CNP regulation in dogs.

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