IL-8 is an essential mediator of the increased delayed-phase vascular permeability in LPS-induced rabbit pleurisy.
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 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.
Fukumoto
T
T
Department of Pathology, Kumamoto University School of Medicine, Honjo, Japan.
Matsukawa
A
A
Yoshimura
T
T
Edamitsu
S
S
Ohkawara
S
S
Takagi
K
K
Yoshinaga
M
M
D000818:Animals; D002199:Capillary Permeability; D005260:Female; D016209:Interleukin-8 / Q000502:physiology*; D008070:Lipopolysaccharides; D009504:Neutrophils / Q000502:physiology; D010998:Pleurisy / Q000276:immunology*; D011817:Rabbits; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology
D016209:Interleukin-8; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha