Fumihiko Namba1, Mikiko Kobayashi-Miura2, Taro Goda3, Yukiko Nakura1, Fumiko Nishiumi1, Aoi Son2, Akio Kubota4, Junji Yodoi2, Itaru Yanagihara1. 1. Department of Developmental Medicine, Osaka Medical Center and Research Institute for Maternal and Child Health, Osaka, Japan. 2. Department of Biological Responses, Infection and Prevention, Institute for Virus Research, Kyoto University, Kyoto, Japan. 3. Department of Surgery, Izumiotsu Municipal Hospital, Osaka, Japan. 4. Second Department of Surgery, Wakayama Medical University, Wakayama, Japan.
Abstract
BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSION: Thioredoxin-1 may thus represent a novel effective treatment to delay inflammation-induced preterm delivery.
BACKGROUND: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. METHODS: 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 humanthioredoxin-1, ovalbumin, or vehicle, with a 3-h interval between injections. RESULTS: 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 humanthioredoxin-1, and the rate of inflammation-induced preterm delivery was attenuated. CONCLUSION:Thioredoxin-1 may thus represent a novel effective treatment to delay inflammation-induced preterm delivery.
Authors: H Nakamura; L A Herzenberg; J Bai; S Araya; N Kondo; Y Nishinaka; L A Herzenberg; J Yodoi Journal: Proc Natl Acad Sci U S A Date: 2001-12-11 Impact factor: 11.205
Authors: Hannah H Chang; Jim Larson; Hannah Blencowe; Catherine Y Spong; Christopher P Howson; Sarah Cairns-Smith; Eve M Lackritz; Shoo K Lee; Elizabeth Mason; Andrew C Serazin; Salimah Walani; Joe Leigh Simpson; Joy E Lawn Journal: Lancet Date: 2012-11-16 Impact factor: 79.321
Authors: Y Tagaya; Y Maeda; A Mitsui; N Kondo; H Matsui; J Hamuro; N Brown; K Arai; T Yokota; H Wakasugi Journal: EMBO J Date: 1989-03 Impact factor: 11.598