Endotoxin, interleukin-1, and tumor necrosis factor cause neutrophil-dependent microvascular leakage in postcapillary venules.
Acute inflammation is characterized mainly by the egress of neutrophils from postcapillary venules and by increased vascular permeability leading to the formation of edema. The microvascular site of increased vascular permeability in local acute inflammatory lesions was investigated after the injection of endotoxin (LPS), interleukin-1 (IL-1), and tumor necrosis factor (TNF) into the dermis overlying the cremasteric and rectus abdominis muscles of rats. LPS caused leakage of colloidal carbon peaking at 3 to 4 hours at the level of the postcapillary venules and capillary leak was variably observed at later time points. IL-1 and TNF also caused postcapillary venular leakage. IL-1 was as potent as LPS and more so than TNF. The microvascular leak caused by LPS, IL-1, and TNF was accompanied by the tissue accumulation of neutrophils, and was neutrophil-dependent because LPS, IL-1, and TNF did not cause vascular labelling in neutropenic rats.
Yi
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Department of Pathology, University of California, School of Medicine, Irvine.
Ulich
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D000818:Animals; D002199:Capillary Permeability; D004731:Endotoxins / Q000494:pharmacology*; D007375:Interleukin-1 / Q000494:pharmacology*; D008070:Lipopolysaccharides; D008297:Male; D009503:Neutropenia / Q000378:metabolism; D009504:Neutrophils / Q000502:physiology*; D051381:Rats; D011919:Rats, Inbred Strains; D012016:Reference Values; D012485:Salmonella typhi; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology*; D014699:Venules / Q000378:metabolism*
D004731:Endotoxins; D007375:Interleukin-1; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha