Essential involvement of interleukin-8 (IL-8) in acute inflammation

TLDR

Neutrophil infiltration is a hallmark of acute inflammation, driven by locally produced chemotactic factors such as the leukocyte‑activating cytokine interleukin‑8 (IL‑8), which is produced by various cells in response to inflammatory stimuli. The study aimed to provide definitive evidence for IL‑8’s role in recruiting and activating neutrophils within lesions of diverse acute inflammatory reactions. Researchers administered a highly specific neutralizing antibody against IL‑8 in models of LPS‑induced dermatitis, LPS/IL‑1 arthritis, lung reperfusion injury, and immune‑complex glomerulonephritis. Anti‑IL‑8 treatment blocked neutrophil infiltration and prevented neutrophil‑dependent tissue damage, demonstrating that IL‑8 causatively drives acute inflammation. J Leukoc Biol 56:559‑564; 1994.

Abstract

Abstract Neutrophil infiltration into inflammatory sites is one of the hallmarks of acute inflammation. Locally produced chemotactic factors are presumed to mediate the sequence of events leading to the infiltration at inflammatory sites. Interleukin-8 (IL-8), a novel leukocyte chemotactic activating cytokine (chemokine), is produced by various types of cells upon stimulation with inflammatory stimuli and exerts a variety of functions on leukocytes, particularly, neutrophils in vitro. However, no definitive evidence has been presented on its role in recruiting and activating neutrophils in the lesions of various types of inflammatory reactions. We administered a highly specific neutralizing antibody against IL-8 in several types of acute inflammatory reactions, including lipopolysaccharide (LPS)-induced dermatitis, LPS/IL-1-induced arthritis, lung reperfusion injury, and acute immune complex-type glomerulonephritis. Anti-IL-8 treatment prevented neutrophil-dependent tissue damage as well as neutrophil infiltration in these conditions. These results suggest that IL-8 plays a causative role in acute inflammation by recruiting and activating neutrophils. J. Leukoc. Biol. 56: 559–564; 1994.