Endotoxin Antagonists Part V

Content Guide. Part I Part II Part III Part IV

A look at some pre and pro-biotics in endotoxemia or related inflammation.
Prebiotics:
Galacto-oligoaccharides (GOS):

A Mixture of trans-Galactooligosaccharides Reduces Markers of Metabolic Syndrome and Modulates the Fecal Microbiota and Immune Function of Overweight Adults
GOS can increase bifido bacteria, which is often correlated with lowering endotoxin. Some of the markers that were improved in this study are markers that are known to be associated with higher endotoxin transport into the plasma and liver.

A comparative in vitro evaluation of the fermentation properties of prebiotic oligosaccharides.
GOS increase bifido and decrease clostridia.

Galacto-oligosaccharides and bowel function
GOS can relieve constipation, which is associated with SIBO and increased liver and plasma endotoxin.

Fucosylated but Not Sialylated Milk Oligosaccharides Diminish Colon Motor Contractions
Human milk oligosaccharides promote positive changes in gut epithelium and immune system.

Galactooligosaccharide supplementation reduces stress-induced gastrointestinal dysfunction and days of cold or flu: a randomized, double-blind, controlled trial in healthy university students.
“Stress” increases permeability and therefore endotoxin transport and immune function. Some have commented that the effects of “flu” are similar to endotoxemia and may be treated in a similar manner, for example activated charcoal to bind endotoxin. In this paper exam stress was associated with higher occurrence of diarrhea, indigestion, reflux syndromes and with abdominal pain, cold and flu. GOS supplementation showed effect in reducing all these stress associated symptoms.

Effects of infant formula containing galacto-oligosaccharides on the intestinal microflora in infants.
GOS supplementation can improve markers of gastrointestinal function, including levels of bifidobacteria in formula fed infants.

Effects of orally administered galacto-oligosaccharides on immunological parameters in foals: a pilot study
Foals supplemented with GOS had lower markers of inflammatory response to endotoxin.

Variations in bovine milk oligosaccharides during early and middle lactation stages analyzed by high-performance liquid chromatography-chip/mass spectrometry
Bovine colostrum may be a significant source of GOS (I’m not sure how to interpret the papers relevance to be honest)
Bovine colostrum in oral treatment of enterogenic endotoxaemia in rats
…however the fact that colostrum can decrease endotoxemia in rodents might support that, though there are probably other mechanisms…

Oligofructose:
Selective increases of bifidobacteria in gut microflora improve high-fat-diet-induced diabetes in mice through a mechanism associated with endotoxaemia.
Oligofructose can protect against the damaging effects of a high fat diet in rodents, improving levels of bifidobacteria, decreasing endotoxin and some of the associated markers, glucose tolerance, glucose-induced insulin secretion and normalised inflammatory tone, plasma and adipose tissue proinflammatory cytokines. It improves body weight gain and reduces body fat mass development (in rodents).

Probiotics:
Lactobacillus farciminis:

Prevention of gut leakiness by a probiotic treatment leads to attenuated HPA response to an acute psychological stress in rats.
Stress activates the HPA axis, increases corticotropin releasing factor, and ACTH. L. Farciminis lowered the increased intestinal permeability and endotoxin transport from stress and prevented the HPA axis response and subsequent neuroinflammation.

Bifidobacterium:
In vivo effects of bifidobacteria and lactoferrin on gut endotoxin concentration and mucosal immunity in Balb/c mice.
Supplementation of bifidobacteria attenuated increase in endotoxin over controls.

Effects of specific lactic acid bacteria on the intestinal permeability to macromolecules and the inflammatory condition.
Lactofermented milk products of Bifidobacterium breve and Streptococcus thermophilus can decrease intestinal permeability and inhibit endotoxin induced increases in TNF-alpha.

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