Circulating endotoxin and systemic immune activation in sporadic amyotrophic lateral sclerosis (sALS)

Abstract

The present study reports elevated levels of endotoxin/lipopolysaccharide (LPS) concentrations in plasma from patients with sporadic amyotrophic lateral sclerosis (sALS) and Alzheimer's (AD) as compared to healthy controls. Levels of plasma LPS showed a significant positive correlation with degree of blood monocyte/macrophage activation in disease groups and was most elevated in patients with advanced sALS disease. There was a significant negative relationship between plasma LPS and levels of monocyte/macrophage IL-10 expression in sALS blood. These data suggest that systemic LPS levels and activated monocyte/macrophages may play significant roles in the pathogenesis of sALS.

Rhamnolipids, Microbial Virulence Factors, in Alzheimer’s Disease

“…Overall, many diseases of chronic inflammation may be attributed to the presence of microbial components such as LPSs [1,15,70]. The continuous generation of bacterial components, considered as potent inflammatory agents, as well as their feedback from the pool of the dormant bacteria, may well justify the persistent, but mild-manifested inflammation, followed by inflammatory cytokine production, which is characteristic of many diseases [20].…”

“…The concentration of endotoxin LPSs in plasma from AD patients increased compared to controls. This increase was reflected in a proportionally-dependent degree of blood monocytes activation, which was positively associated with the genesis of AD [15]. Bacterial cells in the blood of AD patients in dormancy were visualized with ultrastructural microscopy: when iron deficiency has been overcome, it leads to their revivification [16].…”

Alzheimer’s disease and gut microbiota

“…So the levels of LPS in the blood represent not only inflammation but also leaky gut. Studies found that the plasma levels of LPS in patients with AD were three times higher than healthy controls (Zhang et al, 2009). LPS is usually used to create inflammation in laboratory animals.…”

The Neuroinflammation in the Physiopathology of Amyotrophic Lateral Sclerosis

“…Whether neuroinflammation is a cause or a consequence of motoneuron death is still debated. It is interesting to note that inflammation is not limited to the CNS but systemic with increased levels of plasma LPS associated with increased numbers of activated circulating monocytes and T lymphocytes that correlate with disease evolution [142,157]. A thymic dysfunction is also observed in parallel to the neurodegenerative process in mutant SOD1 mice and ALS patient [158].…”