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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, METHODS, RESULTS. Meshes: Animals, Animals, Newborn, Anti-Inflammatory Agents, Chemokine CCL2, Cytokines, Female, Humans, Inflammation, Interferon-gamma, Interleukin-6, Lipopolysaccharides, Macrophages, Male, Mice, Mice, Inbred C3H, Obstetric Labor, Premature, Placenta, Pregnancy, Reactive Oxygen Species, Recombinant Proteins, Thioredoxins, Tumor Necrosis Factor-alpha.
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Does human thioredoxin-1 attenuate the rate of lipopolysaccharide-induced preterm delivery in mice in association with its anti-inflammatory effect? Context: Maternal intrauterine infection/inflammation represents the major etiology of preterm delivery and the leading cause of neonatal mortality and morbidity. The aim of this study was to investigate the anti-inflammatory properties of thioredoxin-1 in vivo and its potential ability to attenuate the rate of inflammation-induced preterm delivery. Two intraperitoneal injections of lipopolysaccharide from Escherichia coli were administered in pregnant mice on gestational day 15, with a 3-h interval between the injections. From either 1 h before or 1 h after the first lipopolysaccharide injection, mice received three intravenous injections of either recombinant human thioredoxin-1, ovalbumin, or vehicle, with a 3-h interval between injections. Intraperitoneal injection of lipopolysaccharide induced a rise of tumor necrosis factor-α, interferon-γ, monocyte chemotactic protein 1, and interleukin-6 in maternal serum levels and provoked preterm delivery. Recombinant human thoredoxin-1 prevented the rise in these proinflammatory cytokine levels. After the inflammatory challenge, placentas exhibited severe maternal vascular dilatation and congestion and a marked decidual neutrophil activation. These placental pathological findings were ameliorated by recombinant human thioredoxin-1, and the rate of inflammation-induced preterm delivery was attenuated.
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Thioredoxin-1 may thus represent a novel effective treatment to delay inflammation-induced preterm delivery. Final Decision: yes