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American Journal of Pathology, Vol 142, 1335-1338, Copyright © 1993 by American Society for Investigative Pathology

REGULAR ARTICLES

Intratracheal administration of endotoxin and cytokines. IV. The soluble tumor necrosis factor receptor type I inhibits acute inflammation

TR Ulich, S Yin, DG Remick, D Russell, SP Eisenberg and T Kohno
Department of Pathology, UC San Diego School of Medicine 921030.

Endotoxin lipopolysaccharide (LPS) administered intratracheally to rats causes pulmonary tumor necrosis factor alpha (TNF) and interleukin-1 (IL-1) production and results in acute broncho-alveolar neutrophilic inflammation. In the present study, the recombinant human TNF soluble receptor type I (sTNFrI) co-injected intratracheally with LPS is shown to inhibit significantly (P < 0.0001) the number of neutrophils in bronchoalveolar lavage specimens at 6 hours as compared to intratracheal injection of LPS alone. The sTNFrI was at least as effective as the recombinant human IL-1 receptor antagonist (IL-1ra) as an inhibitor of acute inflammation. Inhibition of LPS-induced acute inflammation by the combination of sTNFrI and IL-1ra was not significantly more than the inhibition afforded by sTNFrI alone. Intratracheal co-injection of sTNFrI with LPS unexpectedly increased TNF levels in BAL specimens, perhaps by changing the normal catabolism of TNF. On the other hand, co-injection of sTNFrI and LPS decreased IL- 6 levels in BAL fluid, most likely by interfering with the induction of IL-6 by TNF. The sTNFrI may prove to be an important pharmacological down-regulator of acute inflammation.

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