| Protein Name: | Interleukin-8 (P10145) |
|---|---|
| Gene Name: | IL8 |
| Description: | Interleukin-8 precursor (IL-8) (CXCL8) (Monocyte-derived neutrophil chemotactic factor) (MDNCF) (T-cell chemotactic factor) (Neutrophil- activating protein 1) (NAP-1) (Protein 3-10C) (Granulocyte chemotactic protein 1) (GCP-1) (Monocyte-derived neutrophil |
| PDB ID: | 1ICW |
| Protein Family: | |
| Protein Category: | Secreted Protein |
This panel provides drug-protein interaction and their ADRs along with references
| Interacting Drugs | Toxicity | Mechanism | Reference |
|---|---|---|---|
| Epinephrine | Inflammation | Epinephrine-induced enhancement of IL-8 production@which may be relevant for the understanding of endogenous and therapeutic stress hormone influences on IL-8 mediated inflammation [ ADR Type 5 ] | Lipopolysaccharide-induced interleukin 8 production by human whole blood is enhanced by epinephrine and inhibited by hydrocortisone |
| Hydrocortisone | Inflammation | Hydrocortisone dose-dependently inhibited LPS-induced IL-8 production@which may be relevant for the understanding of endogenous and therapeutic stress hormone influences on IL-8 mediated inflammation [ ADR Type 1 ] | Lipopolysaccharide-induced interleukin 8 production by human whole blood is enhanced by epinephrine and inhibited by hydrocortisone |
| Ibritumomab | Pathogenesis Of Side-Effects | Infusion of rituximab induced rapid complement activation@ preceding the release of TNF-alpha@ IL-6 and IL-8@which is correlated with pathogenesis of side-effects [ ADR Type 5 ] | Complement activation plays a key role in the side-effects of rituximab treatment |
| Nicotine | Ulcerative Colitis | Transdermal nicotine decreases mucosal IL-8 expression@which lead to ulcerative colitis [ ADR Type 5 ] | Transdermal nicotine decreases mucosal IL-8 expression but has no effect on mucin gene expression in ulcerative colitis Inflamm Bowel Dis 1 |
This panel provides information on drug category
| Toxicity | Source |
|---|