astroman said...
As far as infections being responsible for molecular mimicry, like bacteria - I have wondered if this has just been assumed by the Functional and Natural Path area the last ten years or so, or if this has actually been proven? I always have wondered the original source, as now its just shared info.
No this is definitely proven and widely accepted. Guillaine-Barre syndrome as a byproduct of C jejuni infection and H pylori mediated anti-lewis antigen ab's are the best examples. There are two reasons for this. The first is obviously immune subversion. Having antigens that look like human antigens is a great way to dupe immune cells into self-tolerance. Tolerance can be broken however. Perhaps a sudden rise in the expression of antigen by proliferating bacteria could be one way. This reason is probably exploited more by parasites who prefer to lay low and only occasionally cause disease. Ie like most of our chronic conditions that are contingent on all sorts of life style factors that may lead to immune suppression and overexpression of certain natural microbiota that otherwise remain hidden without causing symptoms. Lyme fits this descript
ion when you consider that it doesn't normally cause much disease in its natural hosts
The other reason is that microorganisms infecting a certain tissue express self antigen for the purposes of adhesion to cell membranes which is often a first step to intracellularization. So for example gram-negative bacteria will often express sugar residues on the tips of their membrane lipopolysaccharides that resemble human antigen because in those tissues are lectins (sugar binding proteins) that bind those antigens. Remember self-antigens aren't just innocuous proteins that stick out from cell membranes. They are functional components of the human cell and cell-to-cell communication pathways. If a bacteria is mimicking it it's either because it's trying to avoid the immune system, or because it's trying to hijack the pathway that antigen is involved in.
As to the original question. It doesn't take molecular mimicry a long time to get a hold. Guillaine Barre syndrome is almost instantaneous (well there's the lag of antibody development). It's almost ridiculous, in my personal opinion, to consider autoimmunity and infectious disease as two separate issues. The former is just a part of the latter. There is no reason the autoimmunity wouldn't shut off with resolution of the infection (and importantly coinfections). The body has an amazingly redundant system of checks and balances to prevent injuring itself. It takes some serious wit to mess that up and maintain it. Most of the time, as we've seen with chronic lyme vs plds, the belief that autoimmunity is self-perpetuating is built out of logical fallacy. Ie absence of evidence for infection = evidence of absence. One day perhaps people will understand the difference between acute phase and chronic phase and why identifying pathogens in the chronic phase can be so darned difficult. Until then we keep treating infectious diseases with immune suppressants
DONT DO THAT. Yes it might hurt when you treat and raise immune function. That is the essence of a herxheimer. You are releasing inflammatory antigens from dead bacteria. Some of these might be promoting cross reactive antibodies to your own tissues. Your "autoimmune" disease might flare but at the expense of dead bacteria. Immunosuppressants might calm the symptoms but at the expense of facilitating disease progression.