IL-8 is an essential mediator of the increased delayed-phase vascular permeability in LPS-induced rabbit pleurisy

• Published in: Journal of leukocyte biology Vol. 63; no. 5; pp. 584 - 590
• Main Authors: Fukumoto, Takumi, Matsukawa, Akihiro, Yoshimura, Teizo, Edamitsu, Sunao, Ohkawara, Susumu, Takagi, Katsumasa, Yoshinaga, Masaru
• Format: Journal Article
• Language: English
• Published: United States Society for Leukocyte Biology 01-05-1998
• Subjects: Animals; Capillary Permeability; Female; inflammation; Interleukin-8 - physiology; Lipopolysaccharides; neutrophil infiltration; Neutrophils - physiology; Pleurisy - immunology; Rabbits; Time Factors; tumor necrosis factor α; Tumor Necrosis Factor-alpha - physiology
• ISSN: 0741-5400; 1938-3673
• DOI: 10.1002/jlb.63.5.584

We investigated the involvement of IL‐8 in the delayed vascular permeability (VP) in rabbit lipopolysaccharide (LPS)‐pleurisy. Maximal level of interleukin‐8 (IL‐8) was detected in pleural fluid at 2 h after LPS injection and anti‐IL‐8 inhibited the delayed VP by 90%. Injection of homologous IL‐8 induced VP, the time‐course of which preceded that of LPS‐induced delayed VP. Production of IL‐8 in LPS‐pleurisy was inhibited with anti‐tumor necrosis factor α (TNF‐α), whereas the production of TNF‐α was not affected with anti‐IL‐8. Injection of IL‐8 did not induce TNF‐α production and anti‐TNF‐α had no effect on IL‐8‐induced VP. Injection of homologous TNF‐α induced IL‐8 production and VP, and TNF‐α‐induced delayed VP was blocked with anti‐IL‐8. These results indicate important roles of IL‐8 in LPS‐induced delayed VP and that TNF‐α causes the delayed VP through the production of IL‐8. J. Leukoc. Biol. 63: 584–590; 1998.