Pentamidine blocks the pathophysiologic effects of endotoxemia through inhibition of cytokine release.

doi:10.1016/0041-008X(92)90191-T

Paper

Pentamidine blocks the pathophysiologic effects of endotoxemia through inhibition of cytokine release.

Published Feb 1, 1992 · Gary J. Rosenthal, William A. Craig, Emanuela Corsini

Toxicology and applied pharmacology

Q2 SJR score

11

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0

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Abstract

Abstract hidden due to publisher request; this does not indicate any issues with the research. Click the full text link above to read the abstract and view the original source.

Non-RCT

Animal Study

Study Snapshot

Pentamidine protects mice from endotoxemia-related mortality and thermoregulatory control by inhibiting cytokine release, suggesting its potential therapeutic value against Pneumocystis carinii pneumonia.

PopulationOlder adults (50-71 years)

Sample size24

MethodsObservational

OutcomesBody Mass Index projections

ResultsSocial networks mitigate obesity in older groups.

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Paper

Pentamidine blocks the pathophysiologic effects of endotoxemia through inhibition of cytokine release.

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References

Citations

Pentamidine Inhibits Titanium Particle-Induced Osteolysis In Vivo and Receptor Activator of Nuclear Factor-κB Ligand-Mediated Osteoclast Differentiation In Vitro

Pentamidine effectively inhibits osteoclast formation and significantly reduces wear debris-induced bone loss in mice.

Pentamidine blocks hepatotoxic injury in mice

VLX103 effectively decreases toxin-induced liver injury in mice and may be an effective therapy for various human liver diseases.

Endotoxin-stimulated innate immunity: A contributing factor for asthma.

Airborne endotoxin exposure in infancy may protect against asthma but later in life negatively affects asthma patients by increasing airway inflammation, susceptibility to colds, and causing chronic bronchitis and emphysema.

Shock: a review of pathophysiology and management. Part II.

Septic shock is caused by excessive inflammation, and supportive treatment using fluids and inotropic agents, while antibiotic therapy and surgical drainage of septic foci are effective.

Fluticasone propionate and pentamidine isethionate reduce airway hyperreactivity, pulmonary eosinophilia and pulmonary dendritic cell response in a guinea pig model of asthma.

Inhaled fluticasone propionate and pentamidine isethionate reduce antigen-induced airway hyperreactivity and pulmonary inflammation in guinea pigs, suggesting that dendritic cells are targets for their anti-inflammatory effects.