Nitric oxide has long been suspected as the possible damaging factor in multiple sclerosis. The logic goes like this: The body for some unknown reason starts attacking the brain as if it were a foreign protein (like a bacteria). The microglia (the cells in the brain which are responsible for immune responses that might be needed inside the blood brain barrier-the regular white blood cells are kept out by the BBB)produce large amounts of nitric oxide (NO) which damage the nearby nerves and support cells. If only we could get rid of the NO then we could control MS. An example of this kind of research can be found HERE. Also another one HERE. It is clear that the researchers consider the production of NO an abherrent and undesirable response and a contributor to autoimmunity. You might note that they also are very clearly believing the autoimmune model. Many physicians and researchers forget that this is just a model, not a proven fact.
Yet, as we are so abundantly aware here on this site, CPn has been implicated in the pathogenesis of MS. How might the NO angle play in to that? Jim recently found a paper which indicates NO is important to the body in it's fight against CPn. In other words, the body uses NO on purpose to fight CPn. What follows is that abstract printed from pubmed:
Can J Microbiol. 2005 Nov;51(11):941-947.
Effect of nitric oxide on the growth of Chlamydophila pneumoniae.
Carratelli CR, Rizzo A, Paolillo R, Catania MR, Catalanotti P, Rossano F.
Chlamydophila pneumoniae is an important human intracellular pathogen; however, the pathogenesis of C. pneumoniae infection is poorly understood and the immune control mechanism versus host cells is not completely known. The role of the nitric oxide (NO) synthase pathway in inhibiting the ability of C. pneumoniae to infect macrophage J774 cells and the ability of NO to damage isolated C. pneumoniae were investigated. Exposure of infected cultures to recombinant murine gamma interferon (MurIFN-γ) resulted in increased production of NO and reduced viability. Addition of 2-(N,N-diethylamino)-diazenolase-2-oxide before infection of J774 cells or during chlamydial cultivation released NO, both resulting in a reduction in the viability of C. pneumoniae in a dose-dependent way. These results indicate that immune control of chlamydial growth in murine macrophage cells may trigger a mechanism that includes NO release with effects on the multiplication of the microorganism, thus suggesting that NO may play a role in preventing the systemic spread of Chlamydia.
PMID: 16333333 [PubMed - as supplied by publisher]
Yet another important angle is highlighted in this work. Note that the gamma interferon plays a role in the NO production just as it does in the inhibition of tryptophan which also knocks back the infectoin. Gamma interferon is an important player in the reduction of CPn stores with this dual role in the fight! But also consider this important fact: It is well known that giving people with MS gamma interferon makes them worse. Symptoms increase dramatically. Could it be that the sudden ample stores of gamma interferon result in a sudden vigorous response to CPn causing both NO bystander damage (the nerves near the area with the NO get hurt by the NO) and also an endotoxin reaction? Interesting theory.
This will be even more incredible as you read THIS paper. It says clearly that lipopolysaccharide (LPS) causes demyelination. What is LPS? Endotoxin, the protein fragments left over when a gram negative bacteria like CPn dies.
Another smoking gun for CPn as the causitive agent in MS.