The Inflammatory Conspiracy in Multiple Sclerosis: A Crossroads of Clues and Insights through Mast Cells, Platelets, Inflammation, Gut Microbiota, Mood Disorders and Stem Cells

Abstract

Multiple Sclerosis is a chronic neurological disease characterized by demyelination and axonal loss. This pathology, still largely of unknown etiology, carries within it a complex series of etiopathogenetic components of which it is difficult to trace the origin. An inflammatory state is likely to be the basis of the pathology. Crucial elements of the inflammatory process are the interactions between platelets and mast cells as well as the bacterial component of the intestinal microbiota. In addition, the involvement of mast cells in autoimmune demyelinating diseases has been shown. The present work tries to hang up on that Ariadne’s thread which, in the molecular complexity of the interactions between mast cells, platelets, microbiota and inflammation, characterizes Multiple Sclerosis and attempts to bring the pathology back to the causal determinism of psychopathological phenomenology. Therefore, we consider the possibility that the original error of Multiple Sclerosis can be investigated in the genetic origin of the depressive pathology.

Mast Cells in Human Health and Diseases 2.0

“…MCs are an important component of the gastrointestinal tract, influencing immune and pathological processes affecting the digestive tract [ 3 , 7 ]. It is known that the physiological functioning of the intestinal epithelial barrier is crucial for maintaining the homeostasis of the internal medium, while uncontrolled barrier mechanisms could lead to an increase in mucosal permeability and the passage of luminal antigens, toxins, and/or microorganisms through the intestinal epithelium, potentially induce disturbances in epithelial–neuro–immune interactions, and facilitate and exacerbate inflammatory states [ 29 , 30 ].…”

Targeting gut microbiota: new therapeutic opportunities in multiple sclerosis

“…The key points of this investigation included: i) imbalance between pro-inflammatory and anti-inflammatory/regulatory components of the immune response involved in the MS background and ii) ability of commensal bacteria to promote either the pro- or anti-inflammatory pathway via different mechanisms. 74 …”