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

Takumi Fukumoto, Akihiro Matsukawa, Teizo Yoshimura, Sunao Edamitsu, Susumu Ohkawara, Katsumasa Takagi, Masaru Yoshinaga

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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 antitumor necrosis factor at (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.

Original languageEnglish
Pages (from-to)584-590
Number of pages7
JournalJournal of Leukocyte Biology
Issue number5
Publication statusPublished - May 1998
Externally publishedYes



  • Inflammation
  • Neutrophil infiltration
  • Tumor necrosis factor α

ASJC Scopus subject areas

  • Cell Biology

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