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Comparison of the quality of protection elicited by toxoid and peptide liposomal vaccine formulations against ricin as assessed by markers of inflammation.

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Ricin is a very toxic substance which inhibits protein synthesis and produces severe tissue damage and inflammation. It is very potent when inhaled as an aerosol and protection has been examined in a series of studies using vaccine candidates including a formaldehyde inactivated ricin toxoid and the

An Intranasally Administered Monoclonal Antibody Cocktail Abrogates Ricin Toxin-Induced Pulmonary Tissue Damage and Inflammation.

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Ricin toxin, a plant-derived, mannosylated glycoprotein, elicits an incapacitating and potentially lethal inflammatory response in the airways following inhalation. Uptake of ricin by alveolar macrophages (AM) and other pulmonary cell types occurs via two parallel pathways: one mediated by ricin's B

Effect of anti-inflammatory agents on ricin-induced macrophage toxicity.

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The toxicity of ricin in susceptible cells is well characterized biochemically, but the pathophysiological implications of its toxicity and the immune response to ricin challenge in the lung are unknown. Incubating macrophage cell line with ricin (1 pM-10 nM) for 4 hours markedly inhibited

Intrapulmonary delivery of ricin at high dosage triggers a systemic inflammatory response and glomerular damage.

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In view of the possibility that ricin may be used as a bioweapon against human populations, we examined the pathological consequences that occur in mice after introduction of ricin into the pulmonary system. Intratracheal instillation of a lethal dose of ricin (20 microg/100 g body weight) resulted

Ricin increases IgE levels and airway inflammation but not hyperresponsiveness in the rat.

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The effect of ricin treatment on IgE levels and airway inflammation has been examined in ovalbumin (OA)-sensitized rats. Ricin augmented the total IgE titre and caused about a 10-fold increase in the antigen-specific IgE titre. Repeat antigen challenges (every second day) with an OA aerosol

IgE production, antigen-induced airway inflammation and airway hyperreactivity in the brown Norway rat: the effects of ricin.

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Ricin has been shown to enhance IgE production in the rat, probably through inhibition of suppressor T lymphocytes. We have studied further the effects of ricin on IgE titre and have determined its effects on antigen-induced airway inflammation and hyperreactivity in the Brown Norway rat.

Total Body Irradiation Mitigates Inflammation and Extends the Therapeutic Time Window for Anti-Ricin Antibody Treatment against Pulmonary Ricinosis in Mice.

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Ricin, a highly toxic plant-derived toxin, is considered a potential weapon in biowarfare and bioterrorism due to its pronounced toxicity, high availability, and ease of preparation. Pulmonary exposure to ricin results in the generation of an acute edematous inflammation followed by respiratory

Antibody/doxycycline combined therapy for pulmonary ricinosis: Attenuation of inflammation improves survival of ricin-intoxicated mice.

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Ricin, a highly toxic plant-derived toxin, is considered a potential weapon in biological warfare due to its high availability and ease of preparation. Pulmonary exposure to ricin results in the generation of an acute edematous inflammation followed by respiratory insufficiency and death. Passive

Inflammatory gene expression in response to sub-lethal ricin exposure in Balb/c mice.

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The toxin ricin has been shown to cause inflammatory lung damage, leading to pulmonary oedema and, at higher doses, mortality. In order to understand the genetic basis of this inflammatory cascade a custom microarray platform (1509 genes) directed towards immune and inflammatory markers was used to

Pulmonary inflammation triggered by ricin toxin requires macrophages and IL-1 signaling.

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Ricin is a potent ribotoxin considered to be a potentially dangerous bioterrorist agent due to its wide availability and the possibility of aerosol delivery to human populations. Studies in rodents and nonhuman primates have demonstrated that ricin delivered to the pulmonary system leads to acute

Role of apoptotic signaling pathways in regulation of inflammatory responses to ricin in primary murine macrophages.

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Because of its lethal effects, ease of preparation, and ability to be delivered by aerosolization, ricin has been developed as a lethal weapon by various terrorist groups. When introduced into the pulmonary system of rodents, ricin causes pathological changes in the lung that are known to occur in

Administration of ricin induces a severe inflammatory response via nonredundant stimulation of ERK, JNK, and P38 MAPK and provides a mouse model of hemolytic uremic syndrome.

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Recent interest in the health consequences of ricin as a weapon of terrorism has led us to investigate the effects of ricin on cells in vitro and in mice. Our previous studies showed that depurination of the 28S rRNA by ricin results in the inhibition of translation and the coordinate activation of

Critical role of Toll-Like Receptor 4 (TLR4) in Ricin toxin-induced inflammatory responses in macrophages.

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Ricin toxin (RT) is a natural plant-derived protein toxin from the seed of castor beans that belongs to a family of type II ribosome-inactivating proteins (RIPs). In addition to its main toxic mechanism of inhibiting the synthesis of cellular proteins, RT can induce the production of inflammatory

Examination of the inflammatory effect of ricin with special reference to the endogenous corticosteroid mobilisation.

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Lethal ricin intoxication in two adult dogs: toxicologic and histopathologic findings.

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Two adult dogs with the same owner were intoxicated by ingestion of fertilizer composed of residual plant material of the castor bean plant (Ricinus communis L.). Both dogs died within 2 and 3 days, respectively, after the first signs of vomiting and abundant hemorrhagic diarrhea. Toxicologic and

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