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Journals AJP - Lung Cellular and Molecular Physiology Volume 266: March

STEPHEN J. SMART AND THOMAS B. CASALE Department of Internal Medicine, University of Iowa College of Medicine and Veterans Affairs Medical Center, Iowa City, Iowa 52242 Smart, Stephen J., and Thomas B. Casale TNF-(xinduced is IL-8 dependent. Am. J. Physiol. 266 (Lung Cell. Mol. Physiol. 10): L238-L245, 1994.-The early phases of airway inflammation include complex interactions between leukocytes, vascular endothelium, and inflammatory cytokines. Therefore, we examined tumor necrosis factor-a (TNF-&induced through polycarbonate filters and human umbilical vein endothelial (HUVE) cells cultured as monolayers on these filters. TNF-a induced both dose- and time-dependent of s across both barriers. At 1O-11-1O-g M TNF-(x, across HUVE monolayers was more than twofold greater than that observed across naked filters. Modified checkerboard experiments indicated that s crossed naked filters as a chemokinetic rather than chemotactic response. Supernatants of TNF-ar (lOmg M)stimulated HUVE monolayers induced threefold greater of s across naked filters than 10mg M TNF-(x itself, suggesting release of soluble chemotactic factor(s). Pretreatment of HUVE monolayers with actinomycin D inhibited both TNF- 90%. Supernatants from TNF-a-treated HUVE cells contained significant concentrations of interleukin 8 (IL-@, and coincubation of these supernatants with anti-IL-8 decreased supernatant-induced chemotaxis. Finally, coincubation of TNF-(x with anti-IL-8 during trans

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TNF-alpha-induced transendothelial neutrophil migration is IL-8 dependent

S. J. Smart and T. B. Casale
AJP - Lung Cellular and Molecular Physiology , Volume 266: L238
The American Physiological Society – Mar 1, 1994

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