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Harold W. Clark, Ph.D.

®

Autoimmune Diseases Caused by Mycoplasmas

By Harold W. Clark, PhD,

Mycoplasma Research Institute, Florida

http:/homepage.hitter.net/hwcmri

From the book Why Arthritis?

Searching for the Cause and the Cure of Rheumatoid Disease

Submitted by The Arthritis Trust of America, 7376 Walker

Road, Fairview, TN 37062-8141; http://www.arthritistrust.org.The

primary function of the immune system is to distinguish foreign

invaders, such as microbes, from the components of host tissues

and facilitate in their elimination. Even though there are experi-

mental animal models of autoimmunity, reacting against their own

tissues, there is no general unifying theory to explain how the au-

toimmune processes like rheumatoid arthritis (RA) and Lupus (SLE)

get started in humans and progresses in chronic and cyclic pat-

terns. It would seem that autoimmunity and autoimmune diseases

have multiple origins including environmental factors such as mi-

crobial infections and genetics. Current investigations of autoim-

mune diseases have focused on the concept of molecular mimicry

by viral, bacterial, mycoplasma or other microbial antigens having

antigenic epitopes or structure similar to and reactive with both the

host proteins and the foreign proteins. In the laboratory mycoplas-

mas have been found to mimic their culture media contributing to

their variable physical and chemical properties. They also can de-

tach membrane components from erythrocytes and leukocytes re-

sulting in autoantibody production and disease.

Now for the first time a natural mechanism that could apply to

multiple Autoimmune (AI) Diseases has been demonstrated in

mycoplasma infected rabbits. Mycoplasma are ubiquitous with

unique properties, making them widely suspected as a potential

cause of hypersensitivity in the multifaceted AI diseases. Being the

smallest free-living microorganisms limits their metabolic action.

Mycoplasmas are highly pleomorphic with a lipoprotein membrane

controlling their permeability and adherence to vascular and neural

tissue membranes. Mycoplasma’s fastidious growth requirements

are provided by their saprophytic activity and available pre-formed

macro molecules in a cell-free tissue digest broth. These include

basic peptides, cholesterol and fatty acids (lipoglobulins), nucle-

otides (basic). Mycoplasma affinity for mucoproteins is indicated

by their frequent colonization of the nasopharyngeal (NP) and the

urogenital (UG) tracts, Finding mycoplasma and ureaplasma strains

in the central nervous system would indicate their potential role in

the neurologic disorders. Of special consideration is finding the

greatest mycoplasma infectivity in females (4:1) reflecting their

prevalence in most autoimmune (AI) diseases and thus the basis

for the Gender Gap. Also the organ and tissue preference of the

several human mycoplasma strains could contribute to a variety of

AI diseases.

Mycoplasmas cultured in serum enriched broth specifically

incorporate basic proteins such as IgG gamma globulin from the

serum. The molecular attachment alters the basic protein structure

making them foreign and autoantigenic to the host. When attached

to the mycoplasma lipoprotein membrane the cells act as both car-

rier and adjuvant for the altered basic tissue proteins now

autoantigenic to the host. The altered IgG causes the production of

autoantibodies characteristic of the so-called rheumatoid factor (RF)

and other autoantibodies. Rheumatoid arthritis developing after

M.pneumoniae infection is host dependent producing immune com-

plex (IC) with IgG autoantibodies.

To test this autoirnmune mechanism, in the absence of human

tissue, M. pneumoniae was cultured in a rabbit digest broth en-

riched with rabbit serum. The cultured and washed mycoplasma

cells were used to immunize rabbits. The resulting rabbit antisera

was positive to both M. pneumoniae and IgG a rabbit autoantibody

to its altered self. Although not required for growth the mycoplasma

incorporated various amounts of the basic IgG protein from the

serum enriched culture. Injections of rabbits with their own native

serum does not elicit autoantibodies to the native IgG unless con-

formed and/or given with an adjuvant carrier such as with the avail-

able mycoplasma lipoprotein membrane. The production of an ex-

perimental autoimmune disease requires the host antigen, such as

basic myelin protein, to be given with some adjuvant .

Rheumatoid Arthritis (RA), one of the more prevalent autoim-

mune diseases, has long-been suspected of being caused by some

microbial agent and immune complex. Investigators have directed

their research towards typical microbial infections and not the host’s

hypersensitivity response mechanism of immune complex (IC) dis-

eases as currently suspected. The microbial antigens in the immune

complex should be identified to determine and eliminate their al-