Intratracheal administration of endotoxin and cytokines: VII. The soluble interleukin-1 receptor and the soluble tumor necrosis factor receptor II (p80) Inhibit acute inflammation

Thomas R. Ulich, Eunhee S. Yi, Songmei Yin, Craig Smith, Daniel Remick

Research output: Contribution to journalArticle

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Abstract

Intratracheal administration of endotoxin (LPS) causes acute neutrophilic inflammation via induction of pulmonary tumor necrosis factor α (TNF) and interleukin-1 (IL-1) expression. In the present study, the anti-inflammatory activity of soluble IL-1 receptor (sIL-1r) and soluble TNF receptor p80 (sTNFr-p80) in LPS-induced acute pulmonary inflammation was investigated. The sIL-1r coinjected intratracheally with LPS in rats significantly inhibits neutrophilic exudation into bronchoalveolar lavage (BAL) fluid by 47% after 6 hr compared to injection of LPS alone. TNF and IL-6 in the same BAL fluids were both lowered by approximately 50% after intratracheal coinjection of sIL-1r and LPS as compared to LPS alone. In the same model, the sTNFr-p80 inhibited acute inflammation. Paradoxically, TNF levels in BAL fluids were generally elevated after the intratracheal coinjectiun of LPS and monomeric sTNFr-p80 compared to injection of LPS injection alone. The combined anti-inflammatory effect of sIL-1r and sTNFr-p80 at the maximally effective individual doses is not significantly greater than the effect of either soluble receptor alone.

Original languageEnglish (US)
Pages (from-to)137-140
Number of pages4
JournalClinical Immunology and Immunopathology
Volume72
Issue number1
DOIs
StatePublished - Jul 1994

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ASJC Scopus subject areas

  • Immunology and Allergy
  • Pathology and Forensic Medicine
  • Immunology

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