The pathogenesis of group a streptococcal cell wall‐induced polyarthritis in the rat comparative studies in arthritis resistant and susceptible inbred rat strains

Wilder, Ronald L.; Allen, Julie K.; Wahl, Larry M.; Calandra, Gary B.; Wahl, Sharon M.

doi:10.1002/art.1780261205

Cited by 74 publications

(36 citation statements)

References 25 publications

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“…Chronic, erosive polyarthritis induced by i,p, administration of a single dose of SCW in an aqueous, sterile suspension develops easily in susceptible Lewis rats, whereas most other strains are resistant [1,2,7], The fact that F344 rats are resistant excludes that MHC class I and/or II antigens, and thus epitope selection, are of decisive importance. However, functional T lymphocytes have been shown to play a pivotal role in suseeptibility to SCWinduced, chronic joint inflammation; there even is evidence that SCW-specific T cells are required [3][4][5][6][8][9][10][11]17], Thus, an answer to the question why T cells from F344 rats do not respond to SCW after priming with cell walls might elucidate the mechanism of resistance to SCW arthritis.…”

Section: Discussionmentioning

confidence: 99%

“…Dependent on the SCW batch used, either biphasic disease or only the chronic phase may be seen, Thymectomized [3,4], cyclosporin A-treated [4,5] or nude Lewis rats [6], as well as F344 rats [7] are resistant to the second, destructive episode of inflammation, whereas they undergo the acute phase with comparable severity to the Lewis rat. Together, these data strongly suggest an absolute dependence on functional T lymphocytes of the ehronic phase of SCW-induced arthritis.…”

Section: Introductionmentioning

confidence: 99%

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Gut flora induces and maintains resistance against streptococcal cell wall-induced arthritis in F344 rats

Broek

Bruggen

Koopman

et al. 1992

Clinical and Experimental Immunology

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SUMMARYStreptococcal cell wall (SCW)-induced arthritis is a chronic, erosive polyarthritis that can be induced in susceptible Lewis rats by one i,p, injection of an aqueous, sterile suspension of SCW, F344 rats are resistant to chronic joint inflammation. Our previous studies showed a correlation between susceptibility to SCW-induced arthritis and the ability to mount SCW-specific T cell responses, suggesting tolerance to SCW as a putative mechanism. Here we prevented the induction of tolerance to bacterial epitopes in F344 rats by using them germ-free and analysed susceptibility to arthritis subsequently. In addition, we conventionalized germ-free F344 rats at different times before induction of arthritis. Our results show that germ-free F344 rats are susceptible to SCW-induced arthritis with a similar severity, chronicity, incidence and onset as Lewis rats. Moreover, T cells isolated from germ-free F344 rats were able to respond to SCW, Conventionalization dramatically moderates arthritis and makes T cells unresponsive to SCW again. Thus, in normal rats (F344) a state of tolerance to arthritogenic epitopes is induced (neonatally) and maintained through life by the bacterial flora, resulting in resistance to bacterium-induced artritides. In arthritis-prone (Lewis) rats, this tolerance is deficient and/or easily broken.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Gut flora induces and maintains resistance against streptococcal cell wall-induced arthritis in F344 rats

Broek

Bruggen

Koopman

et al. 1992

Clinical and Experimental Immunology

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“…STOP CSA eighth to the tenth day post-injection (8,14). Beginning between the second and third weeks, nearly 100% of the animals develop an exacerbation of peripheral joint swelling which results in a chronic proliferative and erosive synovitis that persists for months.…”

Section: Days After Injection Scwmentioning

confidence: 99%

Inhibition by cyclosporin A of streptococcal cell wall‐induced arthritis and hepatic granulomas in rats

Yocum

Allen

Wahl

et al. 1986

Arthritis & Rheumatism

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We investigated the effect of cyclosporin A, an inhibitor of T helperhnducer lymphocyte activation, on the dtwelopment of streptococcal cell wall-induced arm thritis and hepatic granulomas in female LEW/N rats. Continuous daily treatment with cyclosporin A, begun either 24 hours before or 7-12 days after streptococcal cell wall administration and continued for 6 weeks, resulted in significant inhibition of the chronic proliferative, erosive synovitis and total inhibition of hepatic granuloma formation. When cyclosporin A was stopped at 6 weeks, its effects continued for at least another 5 weeks, demonstrating long-term benefit without continued administration of the drug. In contrast, therapy given only during the acute phases of the experimental disease (days 1-12) did not inhibit the development of chronic disease. Cyclosporin A had no apparent effects on str'eptococcal cell wall antigen distribution or persistence in tissues. These data provide additional evidence of an important role for the T helperhnducer lymphocyte in the experimental model and suggest that cyFrom the Arthritis and Rheumatism Branch, National Institute (of Arthritis, Diabetes, and Digestive and Kidney Diseases,

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“…Histocompatible Fischer (F344/N) rats, on the other hand, do not develop arthritis in response to the same SCW stimulus (1)(2)(3)(4)(5)(6)(7)(8). We previously found that the susceptibility of LEW/N rats to SCW arthritis is related to their defective hypothalamic-pituitary-adrenal (HPA) axis responses to inflammatory and other stress mediators and that the relative SCW arthritis resistance of F344/N rats is related to their intact HPA responses to the same stimuli (9).…”

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confidence: 99%

A central nervous system defect in biosynthesis of corticotropin-releasing hormone is associated with susceptibility to streptococcal cell wall-induced arthritis in Lewis rats.

Sternberg

Young

Bernardini

et al. 1989

Proc. Natl. Acad. Sci. U.S.A.

503

244

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We have recently found that susceptibility to streptococcal cell wall (SCW)-induced arthritis in Lewis (LEW/N) rats is due, in part, to defective inflammatory and stress mediator-induced activation of the hypothalamic-pituitary-adrenal (HPA) axis. Conversely, the relative arthritis resistance of histocompatible Fischer (F344/N) rats is related to their intact responses to the same stimuli. Specifically, LEW/N rats, in contrast to F344/N rats, have markedly impaired plasma corticotropin and corticosterone responses to SCW, recombinant human interleukin lat, the serotonin agonist quipazine, or synthetic rat/human corticotropin-releasing hormone (CRH). To explore the mechanism of this defect, we examined the functional integrity of the hypothalamic CRH neuron in LEW/N rats compared to F344/N rats. LEW/N rats, in contrast to F344/N rats, showed profoundly deficient paraventricular nucleus CRH mRNA levels and hypothalamic CRH content in response to SCW. Compared to F344/N rats, there was no increase in LEW/N hypothalamic CRH content or CRH release from explanted LEW/N hypothalami in organ culture in response to recombinant interleukin ar. These data provide strong evidence that the defective LEW/N corticotropin and corticosterone responses to inflammatory and other stress mediators, and the LEW/N susceptibility to experimental arthritis, are due in part to a hypothalamic defect in the synthesis and secretion of CRH. The additional finding of deficient expression in LEW/N rats of the hypothalamic enkephalin gene, which is coordinately regulated with the CRH gene in response to stress, suggests that the primary defect is not in the CRH gene but is instead related to its inappropriate regulation.Inbred Lewis (LEW/N) female rats develop severe proliferative and erosive arthritis, which mimics human rheumatoid arthritis, in response to a single intraperitoneal injection of group A streptococcal cell wall peptidoglycan group-specific polysaccharide (SCW). Histocompatible Fischer (F344/N) rats, on the other hand, do not develop arthritis in response to the same SCW stimulus (1-8). We previously found that the susceptibility of LEW/N rats to SCW arthritis is related to their defective hypothalamic-pituitary-adrenal (HPA) axis responses to inflammatory and other stress mediators and that the relative SCW arthritis resistance of F344/N rats is related to their intact HPA responses to the same stimuli (9).Specifically, LEW/N rats, in contrast to F344/N rats, have markedly impaired plasma corticotropin (ACTH) and corticosterone responses to intraperitoneally injected SCW, to recombinant human interleukin la (rIL-la), to the serotonin agonist quipazine, and to synthetic rat/human corticotropinreleasing hormone (CRH). In addition, LEW/N rats, compared to F344/N rats, have smaller adrenal glands and larger thymuses, consistent with chronic lack of stimulation by ACTH and suppression by corticosterone, respectively (9). Furthermore, arthritis and severe inflammation can be induced in otherwise SCW arthritis-resistant F344/N ...

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The pathogenesis of group a streptococcal cell wall‐induced polyarthritis in the rat comparative studies in arthritis resistant and susceptible inbred rat strains

Cited by 74 publications

References 25 publications

Gut flora induces and maintains resistance against streptococcal cell wall-induced arthritis in F344 rats

Gut flora induces and maintains resistance against streptococcal cell wall-induced arthritis in F344 rats

Inhibition by cyclosporin A of streptococcal cell wall‐induced arthritis and hepatic granulomas in rats

A central nervous system defect in biosynthesis of corticotropin-releasing hormone is associated with susceptibility to streptococcal cell wall-induced arthritis in Lewis rats.

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