TY - JOUR
T1 - Intratracheal administration of endotoxin and cytokines
T2 - VII. The soluble interleukin-1 receptor and the soluble tumor necrosis factor receptor II (p80) Inhibit acute inflammation
AU - Ulich, Thomas R.
AU - Yi, Eunhee S.
AU - Yin, Songmei
AU - Smith, Craig
AU - Remick, Daniel
PY - 1994/7
Y1 - 1994/7
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=0028364361&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0028364361&partnerID=8YFLogxK
U2 - 10.1006/clin.1994.1117
DO - 10.1006/clin.1994.1117
M3 - Article
C2 - 8020186
AN - SCOPUS:0028364361
SN - 0090-1229
VL - 72
SP - 137
EP - 140
JO - Clinical Immunology and Immunopathology
JF - Clinical Immunology and Immunopathology
IS - 1
ER -