Dr. Domenico FIORE
V.le Madonna delle Grazie, 17
35028 Piove di Sacco (Padova)
AMYOTROPHIC LATERAL SCLEROSIS:
The amyotrophic lateral sclerosis and some other neuropathies without patches are caused by a re-infection (toxi-infection) from Bordetella Pertussis in subjects with astrocytes non-producers of II-class HLA-Antigens: fundamentally they all have the same pathogenesys.
In thirtyfour patients affected by amyotrophic lateral sclerosis (ALS)
and in seven patients affected by other neuropathies without patches (N-PN),
I have searched for anti Bordetella Pertussis (BP) antibodies by the same
methodology I used for Multiple Sclerosis (MS): all of them have come
out to be affected by a BP infection taking place (See
notes 1, 2). If the diseases under discussion have the same
etiology (a toxi-infection by Bordetella Pertussis), how can we explain
the considerable difference in the anatomic-pathologic damages?
From experimental pathology we know that (See notes 3, 4, 5) :
From immunology we know that (See note 6) "the capacity of immune complexes of modifying or modulating the immune response, both humoral and cellular, is well-known , even if the intimate mechanisms that rule such processes are still mostly unknown." "A suppression of the immune response and of the lymphocyte activation by immune complexes has been known for a long time.."..
The underlying mechanisms would be (See note 6) :
From microbiology we know that (See note 7) the characters of immunologic response distinguish endotoxins (Lipopolysaccharide) from other antigens: the response expresses an IgM prolonged synthesis, sometimes in total absence of IgG (contrary to what usually happens with other antigens); the rates of these macroglobulins (IgM) vary in a cyclic way due to a phenomenon of back-control, for which the antigen-antibody complexes that are formed inhibit the further immune response. If the antigen endures enough time in the host, a new cycle of antibody synthesis may be produced.
As a matter of fact, when the immune circulating complexes reach a sufficiently high level, they inhibit the antibody production; for a certain period no other immune complexes are formed . The ones already formed (circulating), caught by the Reticuloendothelial System, are little by little eliminated (the inhibitory effect ceases). In the chronic infections (protracted passage of toxins in circulation), once the inhibitory effect by ICC has ceased, the production of new antibodies and the formation of new ICC start again, we come to a new inhibition of antibody production.
These cycles go on recurring till the toxin production lasts (till the infection lasts). To the questions we were asked, we may answer that: The early pathogenic mechanisms (pertussis reinfection in subject with a muco-ciliar barrier defect, BP toxin passage in circulation, immune circulating complexes formation) are the same described for MS (See notes 1-2). In the two categories of neuropathies (with patches or without patches) it is the astrocytes' and ICC's roles (ICC form in all cases) that makes the difference:
For their pathogenesis they may be considered "natural models" of the chronic progressive Multiple Sclerosis treated with immunosuppressors.
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