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Il-8 Is an Essential Mediator of the Increased Delayed-Phase Vascular Permeability in Lps-Induced Rabbit Pleurisy

  1. Author:
    Fukumoto, T.
    Matsukawa, A.
    Yoshimura, T.
    Edamitsu, S.
    Ohkawara, S.
    Takagi, K.
    Yoshinaga, M.
    1. Year: 1998
  2. Journal: Journal of Leukocyte Biology
    1. 63
    2. 5
    3. Pages: 584-590
  4. Type of Article: Article
  1. Abstract:

    We investigated use 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 alpha (TNF-alpha), whereas the production of TNF-alpha was not affected with anti-IL-8. Injection of IL-8 did not induce TNF-alpha production and anti-TNF-alpha had no effect on IL-8-induced VP. injection of homologous TNF-alpha induced IL-8 production and VP, and TNF-alpha 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-alpha causes the delayed VP through the production of IL-8. [References: 38]

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