Journal ArticleDOI
Further observations on the fetal inflammatory response syndrome: A potential homeostatic role for the soluble receptors of tumor necrosis factor α
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TLDR
The fetal inflammatory response syndrome is associated with increased availability of the soluble receptors of tumor necrosis factor alpha in fetal plasma and these factors may attenuate the deleterious effects of tumor Necrosis factoralpha.About:
This article is published in American Journal of Obstetrics and Gynecology.The article was published on 2000-11-01. It has received 67 citations till now. The article focuses on the topics: Blood sampling & Tumor necrosis factor alpha.read more
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The preterm parturition syndrome
Roberto Romero,Jimmy Espinoza,Juan Pedro Kusanovic,Francesca Gotsch,Sonia S. Hassan,Offer Erez,Tinnakorn Chaiworapongsa,Moshe Mazor +7 more
TL;DR: The evidence indicating that the pathological processes implicated in the preterm parturition syndrome include: intrauterine infection/inflammation; uterine ischaemia; (3) uterine overdistension; (4) abnormal allograft reaction; (5) allergy; (6) cervical insufficiency; and (7) hormonal disorders (progesterone related and corticotrophin‐releasing factor related).
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Periventricular leukomalacia, inflammation and white matter lesions within the developing nervous system
Payam Rezaie,Andrew Dean +1 more
TL;DR: Current concepts on the pathogenesis of PVL are presented and the increasing evidence for an inflammatory pathogenic component to this disorder, either resulting from hypoxic‐ischemic injury or from infection is emphasized.
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Infection and prematurity and the role of preventive strategies
TL;DR: The evidence that infection is causally linked to premature birth is critically examined, as is the relationship between urogenital tract infection/colonization with microorganisms and the risk of preterm birth.
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Maternal infection: window on neuroimmune interactions in fetal brain development and mental illness
TL;DR: A recent mouse model has shown that respiratory infection in the pregnant mother leads to marked behavioral and pharmacological abnormalities in the offspring, some of which are relevant for schizophrenia and autism.
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Micronutrients and intrauterine infection, preterm birth and the fetal inflammatory response syndrome
TL;DR: The pathophysiology of the fetal inflammatory response syndrome is reviewed, as is its relationship to long-term handicap, such as cerebral palsy and bronchopulmonary dysplasia.
References
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HMG-1 as a Late Mediator of Endotoxin Lethality in Mice
Haichao Wang,Ona Bloom,Minghuang Zhang,Jaideep M. Vishnubhakat,Michael Ombrellino,Jiantu Che,Asia Frazier,Huan Yang,Svetlana Ivanova,Lyudmila V. Borovikova,Kirk R. Manogue,Eugen Faist,Edward Abraham,Jan Andersson,Ulf Andersson,Patricia E. Molina,Naji N. Abumrad,Andrew E. Sama,Kevin J. Tracey +18 more
TL;DR: High mobility group-1 (HMG-1) protein was found to be released by cultured macrophages more than 8 hours after stimulation with endotoxin, TNF, or IL-1, and showed increased serum levels after endotoxin exposure, suggesting that this protein warrants investigation as a therapeutic target.
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Anti-cachectin/TNF monoclonal antibodies prevent septic shock during lethal bacteraemia
Kevin J. Tracey,Kevin J. Tracey,Yuman Fong,David G. Hesse,Kirk R. Manogue,Annette T. Lee,George C. Kuo,Stephen F. Lowry,Anthony Cerami +8 more
TL;DR: Protection against shock, vital organ dysfunction, persistent stress hormone release and death was conferred by administration of antibodies 2 h before bacterial infusion, indicating that cachectin is a mediator of fatal bacteraemic shock and suggesting that antibodies against Cachectin offer a potential therapy of life-threatening infection.
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The pathophysiology of tumor necrosis factors.
TL;DR: It appears now that TNF rarely induces in vivo direct cytolysis of natural tumors, that it may not play a significant role in the cachexia most commonly observed in humans, that resulting from cancer, and that the critical role of TNF in shock is shared by other mediators, particularly interleukin 1 (ILl ), its frequent com-
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Mice lacking the tumour necrosis factor receptor 1 are resistant to TNF-mediated toxicity but highly susceptible to infection by Listeria monocytogenes
Joachim Rothe,Werner Lesslauer,Hansruedi Lötscher,Yolande Lang,Pascale Koebel,Frank Köntgen,Frank Köntgen,Alana Althage,Rolf M. Zinkernagel,Michael Steinmetz,Horst Bluethmann +10 more
TL;DR: It is reported here that mice homozygous for a disrupted Tnfr l allele (Tnfr1 0) are resistant to the lethal effect of low doses of lipopolysaccharide after sensitization with D-galactosamine, but remain sensitive to high doses oflipopoly Saccharide.
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The Tumor Necrosis Factor Ligand and Receptor Families
Flavia Bazzoni,Bruce Beutler +1 more
TL;DR: Tumor necrosis factor and lymphotoxin-α were isolated more than 10 years ago on the basis of their ability to kill tumor cells in vitro and to cause hemorrhagic necrosis of transplantable tumors in mice, and a factor known as cachectin was isolated from mouse macrophages, sequenced, and shown to be identical to TNF.