Demyelination results from inflammation – and leads to more inflammation via release of sulfatide
Multiple sclerosis (MS) is generally regarded as an autoimmune disease – one in which the immune system mistakenly attacks a part of the body – in this case the covering of neurons in the central nervous system.
Without their insulating cover, the nerves do not function properly. MS can result in widely varying symptoms depending on which nerves are ‘attacked.’
The study abstract summarized below does not directly reference multiple sclerosis. But it does suggest one possible mechanism by which an initially small lesion could progress, and how the disease might be self-sustaining.
Damage to the nerve covering – the myelin sheath – releases sulfatide. Sulfatide then triggers inflammation via activation of NF-kB. The inflammation leads to further damage to the nerve sheath, further release of sulfatide, more NF-kB activation, more inflammation, etc.
It seems likely that those without multiple sclerosis suffer occasional damage to a myelin sheath, but that such damage does not become progressively worse, despite the release of sulfatide.
It may be that the immune system of those who do not suffer with multiple sclerosis is better able to shut down inflammation and prevent the vicious cycle from developing.
Perhaps by providing supplemental NF-kB inhibitors we could prevent self-perpetuating inflammation in multiple sclerosis, or at least reduce the severity of that inflammation – thereby lessening damage and speeding the onset of remission.
Sulfatide, a major lipid component of myelin sheath, activates inflammatory responses as an endogenous stimulator in brain-resident immune cells.
Summary of the absrtact
Sulfatide, a major lipid component of myelin sheath, participates in diverse cellular events of the CNS, and its cellular level has recently been implicated in many inflammation-associated neuronal diseases.
Sulfatide alone can trigger an inflammatory response in glia, brain-resident immune cells. Sulfatide activated the glia, and it significantly induced the production of various inflammatory mediators, activating NF-kB.
These results show that abnormally released sulfatide at demyelinated regions may further stimulate inflammation, leading to yet more demyelination.