Effect of oil composition on both adjuvant-induced arthritis and delayed hypersensitivity to purified protein derivative and peptidoglycans in various rat strains

Kohashi, Osamu; Pearson, Margot; Beck, Frances W.J.; Alexander, Matthew

doi:10.1128/iai.17.2.244-249.1977

Cited by 30 publications

(6 citation statements)

References 12 publications

(19 reference statements)

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“…There are several characteristics which distinguish the model of experimental arthritis described in this report from adjuvant arthritis (7); but in that disease Buffalo rats have also been shown to have low susceptibility, whereas the Lewis strain is highly susceptible and the Fischer 344 strain has intermediate susceptibility (9). Susceptibility to adjuvant arthritis was reported to be inherited as a dominant trait (9).…”

Section: Discussionmentioning

confidence: 71%

Modulation of the susceptibility of inbred and outbred rats to arthritis induced by cell walls of group A streptococci

Anderle¹,

Greenblatt²,

Cromartie³

et al. 1979

Infect Immun

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Inbred Buffalo rats were resistant to the induction of experimental arthritis induced by systemic injection of cell wall fragments in a crude whole-cell sonic extract of group A streptococci. This was in contrast to the susceptibility of outbred Sprague-Dawley and certain other inbred strains. Preliminary breeding studies indicated that genetic control of resistance of susceptibility is multigenic. When Buffalo rats were infected with a saline suspension of isolated cell wall fragments, chronic remittent arthritis developed. Suspension of isolated cell wall fragments, chronic remittent arthritis developed. Suspension of the isolated cell walls in the supernatant fraction of group A streptococci solubilized by sonication eliminated the arthropathogenicity in Buffalo rats. Thus, a component separable from the cell wall fraction can modulate the arthropathogenicity of cell walls in rats, but the effect depends upon the genetic background of the rat. The antibody response of Buffalo rats to the polysaccharide antigen of cell walls was also affected by the supernatant fraction of sonicated group A streptococci.

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Section: Discussionmentioning

confidence: 71%

Modulation of the susceptibility of inbred and outbred rats to arthritis induced by cell walls of group A streptococci

Anderle¹,

Greenblatt²,

Cromartie³

et al. 1979

Infect Immun

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“…At present, the pathways leading from adjuvant injection to arthritis remain elusive [30], although models induced by non‐immunogenic adjuvants were first described more than 20 years ago [6,31,32]. A possible delineation of disease pathways may come from genetic dissections of adjuvant arthritis models.…”

Section: Discussionmentioning

confidence: 99%

The arthritogenic adjuvant squalene does not accumulate in joints, but gives rise to pathogenic cells in both draining and non-draining lymph nodes

Holm

Svelander

Bucht

et al. 2002

Clinical and Experimental Immunology

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SUMMARYA single intradermal injection of the adjuvant-oil squalene induces T cell-mediated arthritis in DA rats. The chain of events leading from non-specific provocation of the immune system to arthritis, with clinical similarities to rheumatoid arthritis, is largely undetermined. Here, we combined in vivo tracking of tritium-labelled squalene with lymph node (LN) cell transfer experiments to determine where critical activation events may take place. The majority of squalene remained at the injection site (79%). The amounts recovered in peripheral joints (<1%) were equal to that recovered in other organs that can be targets in autoimmune diseases. This argues that arthritis does not develop as a consequence of adjuvant accumulation in joints. In contrast, substantial amounts of squalene were recovered in hyperplastic LN draining the injection site (1-13%). The adjuvant was deposited to a larger extent in cells than in extracellular matrix. The draining LN cells could transfer arthritis to naïve irradiated DA rats following in vitro stimulation with conA. Interestingly, non-draining LN were also hyperplastic and harboured arthritogenic cells, although they contained low amounts of squalene (<1%). Consequently, the amount of arthritogenic adjuvant in a particular LN is not closely linked to the development of pathogenic cells. The distribution pattern of squalene was similar in MHC-identical but arthritis-resistant PVG.1AV1 and LEW.1AV1 rats, and it was unaffected by T cell depletion with a monoclonal antibody (R73). Thus, T cells and non-MHC genes do not regulate dissemination of squalene, but rather determine arthritis development at the level of adjuvant response.

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“…In AA, the mycobacteria are administered in mineral oil suspension. The oil itself is poorly biodegradable and probably more than just an inactive vehicle for bacterial debris in induction of polyarthritis (Kohashi et al 1977). The mechanisms by which chronic inflammation is elicited in AA and SCWP may be similar.…”

Section: Overviewmentioning

confidence: 99%

Role of bacterial debris in inflammatory diseases of the joint and eye

Fox

1990

APMIS

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Fox, A. Role of bacterial debris in inflammatory diseases of the joint and eye. APMIS 98: 957-968,1990.Several distinct rheumatic conditions (including Lyme arthritis, Reiter's syndrome and rheumatic fever) as well as certain forms of the blinding disease, uveitis, may share a common etiology. In each instance specific bacterial pathogens may infect a distant site, which on interaction with the immune system, leads to a sterile inflammation in the joint or eye. These "reactive" conditions may result, in some cases, from prior localization of non-viable bacterial remnants (including the cell wall or peptidoglycan) or alternatively "dormant" fastidious bacteria in the affected joint or eye where they act as persisting antigens. Classical culture techniques, would not detect the presence of these putative microbial antigens. Alternative approaches for detection of ubiquitous components of bacteria in the host (using appropriate chemical, molecular and immunological techniques) are discussed.

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Effect of oil composition on both adjuvant-induced arthritis and delayed hypersensitivity to purified protein derivative and peptidoglycans in various rat strains

Cited by 30 publications

References 12 publications

Modulation of the susceptibility of inbred and outbred rats to arthritis induced by cell walls of group A streptococci

Modulation of the susceptibility of inbred and outbred rats to arthritis induced by cell walls of group A streptococci

The arthritogenic adjuvant squalene does not accumulate in joints, but gives rise to pathogenic cells in both draining and non-draining lymph nodes

Role of bacterial debris in inflammatory diseases of the joint and eye

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