Contrasting effects of misoprostol on systemic and intrapulmonary lipopolysaccharide-induced tumor necrosis factor-alpha.

  title={Contrasting effects of misoprostol on systemic and intrapulmonary lipopolysaccharide-induced tumor necrosis factor-alpha.},
  author={C Nakamura and Steve Nelson and Howard L. Lippton and Gregory J. Bagby and W. Summer},
  journal={Life sciences},
  volume={50 24},
Misoprostol Inhibits Lipopolysaccharide-Induced Pro-inflammatory Cytokine Production by Equine Leukocytes
Results indicate that misoprostol exerts anti-inflammatory effects on equine leukocytes when applied before or after a pro-inflammatory stimulus, and these effects were cytokine-specific and sometimes differed at the mRNA and protein levels.
Effects of the Prostaglandin Analogue Misoprostol on TNF-alpha Release by Activated Equine Leukocytes.
The results presented in this study show that addition of LPS to equine leukocytes induced TNF-α secretion and misoprostol effectively blunted this response, suggesting misop frostol may be useful as an immunomodulator of inflammatory cytokine production in SIRS/sepsis.
Misoprostol Therapeutics Revisited
Misoprostol enhances glycosoaminoglycan synthesis in cartilage after injury and reduces intraocular pressure in glaucoma and ocular hypertension, and reduces chemotherapy‐induced hair loss and recovery time from burn injury.
Novel applications of misoprostol.
  • M. Shield
  • Medicine, Biology
    Pharmacology & therapeutics
  • 1995
Treatment of canine atopic dermatitis with misoprostol, a prostaglandin E1 analogue: an open study
The present study suggests that LPR inhibitors may be effective in canine AD, and this results need to be confirmed in future studies.


Compartmentalization of intraalveolar and systemic lipopolysaccharide-induced tumor necrosis factor and the pulmonary inflammatory response.
Levels of TNF both in bronchoalveolar lavage fluid and associated with alveolar macrophages increased significantly from near nondetectable levels in control animals, and increases in TNF levels were confined to the LPS-challenged compartment.
Differential regulation of tumor necrosis factor-alpha in human alveolar macrophages and peripheral blood monocytes: a cellular and molecular analysis.
Data demonstrating that alveolar macrophages and peripheral blood monocytes obtained from 10 normal volunteers display a significant difference in both the production of TNF and their susceptibility to TNF regulation by prostaglandin E2 and Dex support the notion that human MO derived from different compartments or stages of differentiation exhibit differential responsiveness to immunomodulators.
Pentoxifylline prevents tumor necrosis factor-induced lung injury.
This study measured the effects of pentoxifylline (PTX) on parameters of TNF-induced lung injury including: lung wet-to-dry weight ratio, the ratio of lung- to-plasma 125I-labeled albumin (albumin index), bronchoalveolar lavage and peripheral leukocyte counts, and serial measurements of mean arterial pressure (MAP).
Neutrophil-mediated pulmonary vascular injury. Synergistic effect of trace amounts of lipopolysaccharide and neutrophil stimuli on vascular permeability and neutrophil sequestration in the lung.
It is suggested that small amounts of intravascularly administered LPS enhance the sequestration of neutrophil within the lung and increase lung vascular permeability and endothelial injury caused by neutrophils stimulated by intrav vascularly administered chemotactic factors.
Passive immunization against cachectin/tumor necrosis factor protects mice from lethal effect of endotoxin.
The data suggest that cachectin/TNF is one of the principal mediators of the lethal effect of endotoxin, and this effect was dose-dependent and was most effective when the antiserum was administered prior to the injection of the endotoxin.
The pulmonary vascular sequestration of neutrophils in endotoxemia is initiated by an effect of endotoxin on the neutrophil in the rabbit.
Intravenously administered LPS caused a marked, dose-dependent sequestration of 111In-neutrophils in the pulmonary vasculature, and exhaustive ultrastructural autoradiography showed discretely radiolabeled neutrophils located within pulmonary capillaries.
Anti-cachectin/TNF monoclonal antibodies prevent septic shock during lethal bacteraemia
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.
Overview of misoprostol clinical experience
Evidence presented in this supplement suggests a further increase in healing-rate response at 300 μg misoprostol qid, which suggests that this prostaglandin E1 derivative may be an important addition to the treatment of peptic ulcer disease.
Cachectin: more than a tumor necrosis factor.
The metabolic impact of infectious and neoplastic disease states has long been known to clinicians and may provoke a severe wasting diathesis, in which negative calorie and nitrogen balance lead to death despite the absence of a large parasite or tumor burden.