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The American Journal of Pathology logoLink to The American Journal of Pathology
. 1993 May;142(5):1335–1338.

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

T R Ulich 1, S Yin 1, D G Remick 1, D Russell 1, S P Eisenberg 1, T Kohno 1
PMCID: PMC1886915  PMID: 8388171

Abstract

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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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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