Freund's complete adjuvant (FCA)
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"Salk et al. (1953) applied Freund’s adjuvant to poliomyelitis vaccine, and later followed with extensive testing of killed crude as well as purified polio virus vaccine in animals and humans, where the reactions in humans were considered inconsequential."--Viera Scheibner

"Freund's adjuvant is a water-in-oil emulsion consisting of a mineral oil, an antibody stimulator such as tubercule bacilli, and an emulsifying agent such as lanolin or Arlacel A."--Jamie  Murphy p 49)

Theil DJ, Tsunoda I, Rodriguez F, Whitton JL, Fujinami RS.  Viruses can silently prime for and trigger central nervous system autoimmune disease.    J Neurovirol 2001 Jun;7(3):220-7 Related Articles, Books, LinkOut   Department of Neurology, University of Utah School of Medicine, Salt Lake City, Utah 84132, USA.
Although many viruses have been isolated from patients with multiple sclerosis (MS), as yet, no one agent has been demonstrated to cause MS. In contrast, epidemiological data indicate that viral infections are associated with exacerbations of MS. Here, we present data showing that virus infections can subclinically prime animals for central nervous system (CNS) autoimmune disease; long after the original infection has been eradicated, a nonspecific challenge/infection can trigger an exacerbation. The priming infectious agent must show molecular mimicry with self-CNS antigens such as glial fibrillary acidic protein (GFAP), myelin associated glycoprotein (MAG) or myelin proteolipid protein (PLP). The subsequent challenge, however, may be nonspecific; complete Freund's adjuvant (CFA), or infection with a recombinant vaccinia virus encoding an irrelevant protein, could trigger CNS disease. In the CNS, we could detect a mononuclear cell infiltration, but no demyelination was found. However, if the pathogenesis of MS is similar to that of this novel animal model for CNS autoimmune disease, our findings could help explain why exacerbations of MS are often associated with a variety of different viral infections. PMID: 11517396

Powell HC, Mizisin AP, Wiley CA, Morey MK, Hughes RA.   Relationship of adjuvants and swine influenza vaccine to experimental neuropathy in rabbits.  Acta Neuropathol (Berl). 1987;73(1):12-8.PMID: 3037840 [PubMed - indexed for MEDLINE]
Experimental neuropathy, characterized by endoneurial edema and demyelination, was induced by inoculating rabbits with a combination of Freund's complete adjuvant (FCA), gangliosides, lecithin and cholesterol. A less severe demyelinating neuropathy could be induced by treatment with FCA alone but no significant change could be elicited by injection of swine influenza vaccine (SFV) alone. When FCA was combined with gangliosides, lecithins, cholesterol and SFV, neuropathy occurred, but the changes were less severe than if these agents were used without SFV. Sera were tested for myelin basic protein (MBP) and galactocerebroside (GC) antibodies in each experimental group. Neither SFV alone nor SFV combined with Freund's complete adjuvant, gangliosides, cholesterol and lecithin evoked significant antibody titers to MBP or GC. However, rabbits inoculated with FCA, gangliosides, lecithin and cholesterol had rising titers of antibody to both MBP and GC over the 3-month experimental period. One rabbit inoculated with FCA alone had significant antibody to MBP. The findings suggest that Freund's complete adjuvant alone can induce demyelination in the peripheral nerves of rabbits and that SFV may modulate the immune response acting either as an adjuvant or suppressant in the experimental demyelinating disease.

Holmdahl R, Lorentzen JC, Lu S, Olofsson P, Wester L, Holmberg J, Pettersson U. Arthritis induced in rats with nonimmunogenic adjuvants as models for rheumatoid arthritis.   Immunol Rev. 2001 Dec;184:184-202. PMID: 12086312 [PubMed - in process]
Rat models are useful for studies of the pathogenesis of rheumatoid arthritis (RA) since rats are extraordinarily sensitive to induction of arthritis with adjuvants. Injection of not only the classical complete Freund's adjuvant but also mineral oil without mycobacteria and pure adjuvants such as pristane and squalene, induce severe arthritis in many rat strains. Models like pristane-induced arthritis in rats are optimal models for RA since they fulfill the RA criteria including a chronic relapsing disease course. Arthritogenic adjuvants like pristane, avridine, squalene and mineral oil are not immunogenic since they do not contain major histocompatibility complex (MHC) binding peptides. Nevertheless, the diseases are MHC-associated and dependent on the activation of alphabetaTCR (T-cell receptor)-expressing T cells. However, it has not been possible to link the immune response to joint antigens or other endogenous components although immunization with various cartilage proteins induce arthritis but with different pathogeneses. To unravel the mechanisms behind adjuvant-induced arthritis, a disease-oriented genetic approach is optimal. Several loci that control onset of arthritis, severity and chronicity of the disease have been identified in genetic crosses and most of these have been confirmed in congenic strains. In addition, many of these loci are found in other autoimmune models in the rat as well as associated with arthritis in mice and humans.