A major contributory cause of arthritis in adjuvant-inoculated rats: Granulocytes

Abstract

AbstraetThe predominant white ceil-type in circulating blood of normal rats is the lymphocyte. Granuloeytes increase in the circulating blood of adjuvant-inoculated rats; lymphocytes remain the same or increase slightly. Some drugs, like Cytosar | (cytarabine), inhibit granuioeyte increases primarily and inhibit arthritis development completely. Pretreatment of normal rats with cytarbine also inhibits the local inflammation caused by direct injections of M. butyrieum into hindpaws of rats. Pre-treatment of rats with M.butyrieum, causing granulocytes to increase in circulating blood, produces an exaggerated response to the subsequent inoculation ofM. butyricum directly into rats' paws.Injection of M. butyrieum in non-arthrltogenic vehicles (saline) does not produce the exaggerated response of granulocytes that occurs in response to injection in effective arthritogenic vehicles (mineral oil). Granulocytes are not increased greatly using the ineffective vehicle. Finally, lysates of either rat white cells (granulocytes) or platelets, both of which increase in adjuvant-inoculated rats, produce striking inflammatory reactions when inoculated locally into rats' hindpaws. The addition of non opsonized M. butyricum to granulocytes obtained from adjuvant-inoculated rats causes a significant increase in the release oflysosomal enzymes.From all these and other indirectly derived data, it is surmised that adjuvant inoculation produces a marked increase in granulocytes of circulating blood; as these increase with time, the 114. butyricum molecules or some constituent derived from them (as determined by the distribution of tritiated M. butyricum) arrive in joints and many other tissues, there reacting with granulocytes causing release of lysosomal constituents that produce the histopathology of adjuvant-disease. These results are discussed. IntroductionThe pathways and mechanisms for development of adjuvant-arthritis in the rat are unknown. Following inoculation of certain adjuvants (organism + appropriate vehicle)intradermally, rats develop a widespread disseminated disease, involving many organs -the appendages being only one manifestation of this

Rat Model for Poly-Autoimmunity

“…In all AA rats there was a strong involvement of polymorph nuclear cells (Fig. 1E) that is typical for inflammatory cartilage destruction in rat adjuvant arthritis and was also reported for patients with rheumatoid arthritis (Glenn et al, 1977;Mohr et al, 1981;Eden et al, 2001;Ribbhammar et al, 2003;Hutsona and Hasthorpe, 2005).…”

Antioxidant potential ofGaultheria fragrantissimaagainst adjuvant induced arthritis in Wistar rats

“…Hence, the present study was investigated on the antioxidant profile of Gaultheria fragrantissima in CFA induced arthritis in male Wistar rats. When CFA is injected in the right hind paw of rat, a non-infectious subacute polyarthritis, known as adjuvant arthritis, is induced (Geiler et al, 1974(Geiler et al, -1975Glenn et al, 1977). As a result, periarticular tissue edema is formed which causes increased paw swelling in the arthritic animal with a change in ankle diameter .…”

Adjuvant polyarthritis in rats: is this a satisfactory model for screening anti-arthritic drugs?

“…(4) increases in the plasma levels of haptoglobin, seromucoid, liver enzymes (SGOT, SGPT), collagenase, proteases, lysozyme, orosomucoid, alkaline and acid phosphatases, or-, fl-, and ~-globulins, gastrin and fibrinogen (the so-called inflammation units) [4,40,47,[49][50][51][52][53][54][55][56]. (5) decreased serum albumin content [4,55]. (6) increases in the content of all leucocytes [55].…”