Monday, 23 December 2013

Bacterial Toxins a cause of MS?

Gay-F Staphylococcal immune complexes and myelinolytic toxin in early acute multiple sclerosis lesions—An immunohistological study supported by multifactorial cluster analysis and antigen-imprint isoelectric focusing. Mult Scler Rel Dis 2013; 3; 213-232

Highly significant clinical, epidemiological and pathogenetic similarities between multiple sclerosis (MS) and nasopharyngeal sinusitis has led to the hypothesis that MS is caused by the inadvertent incorporation of the lymphatic drainage of the nasopharynx into the extracellular fluid circulation of the CNS. It has been postulated that, in response to antigenic and toxic products generated by the mucosal nasopharygeal flora, the leptomeninges and CNS parenchyma acquire the characteristics of a persistently stimulated lymphoid organ. Using an extensive panel of bacterial antibodies, tissues from exceptionally early cases, identified and classified using multifactorial cluster analysis, were screened for bacterial antigens using immunohistological methods. Anti-staphylococcal antibodies detected antigen co-locating with IgG/C3d immune complexes in pre-demyelinating and in primary lesions. The distribution of the antigen in relation to the morphogenesis of early acute MS lesions is detailed. Evidence for the intrathecal processing of staphylococcal antigen was obtained using isoelectric focusing and antigen imprinting to identify antigen-specific oligoclonal bands. Employing a combination of isoelectric focusing, western blotting and mass spectrometric analysis, evidence for the intrathecal processing of staphylococcal β-haemolysin (sphingomyelinase) was obtained using CSF from MS cases. While a myelinolytic transportable toxin may be an important component in the pathogenesis of demyelination, in oligodendrocyte apoptosis, and in deviant immune responses within the CNS, the detection of other as yet unidentified staphylococcal-positive and negative oligoclonal bands points to the involvement of a cocktail of transportable antigens leaking in a similar manner into the CNS from the paranasal sinus mucosal tissues where these molecules are conserved by the resident flora to manipulate and subvert the normal processes of local and systemic immunity. Evidence for the access of other bacterial transportables to the CNS in MS should now be sought. The presence of ‘high-output’ toxigenic bacterial strains within the nasopharyngeal flora of MS patients should also be explored. The use of tracer molecules to detect and quantify nose-to-brain transport in MS patients is clearly apposite.

Whilst it has been suggested that I had to wake up to new ideas of MS and reported on the bacterial toxin up the nasal superhighway hypothesis  and suggested as ever that armchair scientists need to put meat on their stories, it has been pointed out that I may have been abit harsh and only half awake and missed this one.....which is hardly surprising because this rag called MSARDS, of which ProfG is an editor, is not on pubmed (for the forseeable future if I am not mistaken) so most people don't know the work exists. Maybe they (MSARDS) need to start putting their old articles out open source....yes go "green" especially as the first year was free to registered readers anyway to limit the strangle hold pubmed appears to be aiming Elsevier's (Publishing house of MSARDS) way. It would help their (MSARDS) impact factor as people would read then cite the work and this will then stimulate more submissions, which will help subscriptions...surely a win win 

Anyway I digress and back to this paper this paper suggests that bacterial toxins moving up the nose are a trigger for MS. So rather than the Charcot project for Viruses it should be anti-biotics, so maybe the armchair scientist needs to do a proper trial and put someones money where their mouth is. 

What do you think? Its a long way off block valves


  1. I just Googled " nasopharyngeal sinusitis and multiple sclerosis" and saw this link: - it appears to be the full article, so I don't understand what this means regarding the publishing comments you have written above. To be honest I don't really understand much of what you've written above: do you think the paper is rubbish? I'm concerned about the fact that this paper is going on 7 years old and what I gather from what you've written, there has been no investigation of this hypothesis. Is there a reason that research has not been pursued down this line?

  2. What was written above was a note to the ediors of MSARDS e..g. ProfG to gt ther journal seen properly in the internet othetwose noone pays attntion to the work. This article is a pont in case yes some f the work was done a few years ago and ignored. Just one more hyothesis and most go nowhere as the authrs spend more time thinkng and less time doing :-)
    Armchair science needd meat on t and pertition or. Endd up in the bin


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