LEUKEMIA INHIBITORY FACTOR LEVELS ARE ELEVATED IN SEPTIC SHOCK AND VARIOUS INFLAMMATORY BODY-FLUIDS

Waring, P; Wycherley, K; Cary, D; Nicola, N; Metcalf, D

Author(s): Waring, P; Wycherley, K; Cary, D; Nicola, N; Metcalf, D;
Details: Publication Year 1992-11,Volume 90,Issue #5,Page 2031-2037
Journal Title: JOURNAL OF CLINICAL INVESTIGATION
Publication Type: Journal Article
Abstract: Leukemia inhibitory factor (LIF) has many biological actions which parallel those of IL-1, IL-6 and tumor necrosis factor-alpha, but its role in the pathogenesis of human disease is unknown. A specific radioreceptor competition assay capable of detecting LIF at concentrations above 1 ng/ml (45 pM) was developed. To identify disease states in which LIF might be involved, a cross-sectional survey of serum and body fluids from approximately 1,500 subjects with a variety of diseases was performed using the LIF radioreceptor competition assay. Serum LIF concentrations were transiently elevated (2-200 ng/ml) in six subjects with meningococcal or Gram-negative septic shock, and in a subject with idiopathic fulminant hepatic failure. Moderately elevated LIF concentrations (> 10 ng/ml) were detected in cerebrospinal fluid from subjects with bacterial meningitis, in effusions associated with pneumonia and peritonitis, and in amniotic fluid from a woman with chorioamnionitis. Low LIF concentrations (1-10 ng/ml) were present in synovial fluid from subjects with inflammatory arthritis, amniotic fluid from women in labor, and some reactive, chronic inflammatory and malignant effusions and cyst fluids, but rarely in transudates. These initial findings suggest that LIF might be involved in the pathogenesis of inflammation and septic shock.
Publisher: ROCKEFELLER UNIV PRESS
Keywords: TUMOR NECROSIS FACTOR; COLONY-STIMULATING FACTOR; CEREBROSPINAL-FLUID; FACTOR LIF; CONDITIONED MEDIUM; BONE-RESORPTION; CANCER CACHEXIA; AMNIOTIC-FLUID; PRETERM LABOR; CELLS
Publisher's Version: https://doi.org/10.1172/JCI116083
Terms of Use/Rights Notice: Refer to copyright notice on published article.

Creation Date: 1992-11-01 12:00:00