Detoxification of Endotoxin by Perfusion of Liver and Spleen.

Rutenburg, Selma H.; Skarnes, Robert C.; Palmerio, C; Fine, Jacob

doi:10.3181/00379727-125-32118

Cited by 40 publications

(13 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These proteins and receptors are also present in intestinal epithelial cells and have been associated with the transport of luminal endotoxin into circulation (Homef et al, 2003;Neal et al, 2006). Once in the systemic circulation, endotoxin can be deactivated or detoxified by immune cells, such as macrophages, or Kupffer cells present in the liver or splenic cells or by binding with acute phase proteins (Rutenburg et al, 1967;Satoh et al, 2008;Buttenschoen et al, 2010). However, if there is failure of systemic detection and deactivation, increased circulating concentrations of endotoxin can lead to local and systemic inflammation and, if severe enough, endotoxemia and even death (Zweifach and Janoff, 1965;Rice et al, 2003).…”

Section: Introductionmentioning

confidence: 95%

GROWTH AND DEVELOPMENT SYMPOSIUM: Endotoxin, inflammation, and intestinal function in livestock1,2

Mani

Weber

Baumgard

et al. 2012

Journal of Animal Science

155

131

View full text Add to dashboard Cite

Endotoxin, also referred to as lipopolysaccharide (LPS), can stimulate localized or systemic inflammation via the activation of pattern recognition receptors. Additionally, endotoxin and inflammation can regulate intestinal epithelial function by altering integrity, nutrient transport, and utilization. The gastrointestinal tract is a large reservoir of both gram-positive and gram-negative bacteria, of which the gram-negative bacteria serve as a source of endotoxin. Luminal endotoxin can enter circulation via two routes: 1) nonspecific paracellular transport through epithelial cell tight junctions, and 2) transcellular transport through lipid raft membrane domains involving receptor-mediated endocytosis. Paracellular transport of endotoxin occurs through dissociation of tight junction protein complexes resulting in reduced intestinal barrier integrity, which can be a result of enteric disease, inflammation, or environmental and metabolic stress. Transcellular transport, via specialized membrane regions rich in glycolipids, sphingolipids, cholesterol, and saturated fatty acids, is a result of raft recruitment of endotoxin-related signaling proteins leading to endotoxin signaling and endocytosis. Both transport routes and sensitivity to endotoxin may be altered by diet and environmental and metabolic stresses. Intestinal-derived endotoxin and inflammation result in suppressed appetite, activation of the immune system, and partitioning of energy and nutrients away from growth toward supporting the immune system requirements. In livestock, this leads to the suppression of growth, particularly suppression of lean tissue accretion. In this paper, we summarize the evidence that intestinal transport of endotoxin and the subsequent inflammation leads to decrease in the production performance of agricultural animals and we present an overview of endotoxin detoxification mechanisms in livestock.

show abstract

Section: Introductionmentioning

confidence: 95%

GROWTH AND DEVELOPMENT SYMPOSIUM: Endotoxin, inflammation, and intestinal function in livestock1,2

Mani

Weber

Baumgard

et al. 2012

Journal of Animal Science

155

131

View full text Add to dashboard Cite

show abstract

“…The disappearance of this antigen from immunodiffusion patterns correlates fully with the loss of the lethal action of endotoxins as ascertained in 3 different biological assays (2,5,6 ) . This method is based on the destruction of a major precipitating antigen ("C antigen") associated with the lethal property of endotoxins.…”

mentioning

confidence: 55%

“…The rapid uptake and detoxification of bacterial endotoxin by dog spleen in situ has been effectively demonstrated ( 1,2). Furthermore, crude extracts of splenic tissue have been shown to possess a strong detoxifying action against endotoxins in vitro (2,3).…”

mentioning

confidence: 99%

Fractionation of an Esterase from Calf Spleen Implicated in the Detoxification of Bacterial Endotoxin

Skarnes

Rutenburg

Fine

1968

Experimental Biology and Medicine

Self Cite

View full text Add to dashboard Cite

13) to spare essential protein tissues rather than to mobilize substrate.Summary and Conclusions. A study of plasma growth hormone and glucose, and body temperature, was conducted in six infants undergoing deep hypothermic cardiovascular surgery. Pronounced hyperglycemia occurred during hypothennia when the infants received exogenous glucose, confirming earlier reports of diminished plasma glucose utilization at low body temperatures. Although growth hormone levels were high during ether anesthesia, they fell or changed little with cooling, and did not appear related to core temperature or to plasma glucose concentration. These findings indicate that changes in growth hormone levels in operated hypothermic infants did not relate to cold stress, alterations in plasma glucose concentration, or diminished glucose utilization.

show abstract

“…In deed, investigators have variously described the central nervous system [12], spleen [14], or a humoral compartment [15] as the primary site of endotoxin toxicity. In addition to this whole spectrum of biological reac tivity, efforts to determine the critical lesions and the primary site of action in endotoxicosis suffer from the drawback that almost all the effects of endotoxin are reversed by the corticoid hormone.…”

Section: Discussionmentioning

confidence: 99%

Liver Enzyme Induction and Endotoxicosis in Mice

Agarwal¹

1972

Pathobiology

View full text Add to dashboard Cite

Repeated injections of either celite or bentonite resulted in sustained induction of liver tryptophan oxygenase (TO) in mice, but the animals were at least as sensitive to the lethal effects of endotoxin as normal controls. Cortisone did not induce liver TO in celite or bentonite-pretreated mice but the hormone protected such animals against endotoxic lethality. Both the endogenous levels, and the cortisone-mediated deposition of liver glycogen progressed normally in mice pretreated with either bentonite or celite. Animals given repeated injections of cortisone were abnormally sensitive to the lethal effects of endotoxin but the toxin did not lower liver TO any more than in control mice. Furthermore, cortisone was highly effective in protecting the hormone-pretreated mice against endotoxic lethality but did not super or hyper-induce liver TO under these conditions. Thus, contrary to previous reports, liver TO activity showed no relationship with any phase of endotoxicosis in mice. Therefore, it becomes necessary to reassess the contribution of the process of enzyme induction in the survival of the stressed animal.

show abstract

Detoxification of Endotoxin by Perfusion of Liver and Spleen.

Cited by 40 publications

References 0 publications

GROWTH AND DEVELOPMENT SYMPOSIUM: Endotoxin, inflammation, and intestinal function in livestock1,2

GROWTH AND DEVELOPMENT SYMPOSIUM: Endotoxin, inflammation, and intestinal function in livestock1,2

Fractionation of an Esterase from Calf Spleen Implicated in the Detoxification of Bacterial Endotoxin

Liver Enzyme Induction and Endotoxicosis in Mice

Contact Info

Product

Resources

About