Cellular Immunology

1985

DOI: 10.1016/0008-8749(85)90354-5

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Streptococcal cell wall arthritis: Studies with nude (athymic) inbred Lewis rats

Susan C. Ridge¹,

John B. Zabriske

²

,

Arnold L. Oronsky³

et al.

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1987

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Cited by 39 publications

(16 citation statements)

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“…Our finding that inflammation induced in nude (athymic) rats by intraarticular injection of PG-APS is less prolonged than that in euthymic rats is consistent with the less severe chronic arthritis seen in nude rats after a systemic PG-APS injection (44,45). However, this did not influence the capacity of LPS to induce a recurrence of arthritis, indicating that T lymphocytes are not required for the transient acute reaction .…”

Section: Resultssupporting

confidence: 80%

Lipopolysaccharide induces recurrence of arthritis in rat joints previously injured by peptidoglycan-polysaccharide.

et al. 1987

The Journal of Experimental Medicine

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LPS and peptidoglycan or covalent peptidoglycan-polysaccharide (PG-PS)' complexes are the major toxic components of bacterial cell walls. Lipid A and PG possess many of the biologic activities that LPS and PG-PS, respectively, have in common, such as pyrogenicity, polyclonal activation of lymphoid cells, complement activation, mitogenicity, macrophage activation, and adjuvanticity (1-3). Both also induce arthritis after injection into laboratory animals. Systemic injection of rats with a sterile, aqueous suspension of PG-PS from the group A streptococcus (PG-APS) induces a chronic erosive relapsing arthritis that has many features of rheumatoid arthritis (4-6). Distinct PG-PS structures from a number of other bacteria, including human indigenous intestinal species, induce arthritis of varying chronicity (7-10) . LPS induces primarily an acute arthritis of relatively short duration after intraarticular (i.a.) injection (7, 11-15), but there have been few reports of its arthropathic activity after systemic administration (16, 17, 17a) .In spite of the shared biologic properties and ubiquitous distribution of LPS and PG-PS, the interaction of their phlogistic activities in an inflammatory process has received little attention. During investigations of mechanisms of recurrent arthritis induced by PG-APS, we noted that a systemic injection of 100 Ag of Salmonella typhimurium LPS induced a transient recurrence of arthritis in rat joints previously inflamed by exposure to PG-APS (7,18) . We now report that the systemic injection of a much lower dose of LPS will induce a recurrence of arthritis injoints inflamed 3 wk previously by the intraarticular injection of PG-APS and describe this reaction in detail . We show that LPS from many bacteria, including Yersinia enterocolitica and Neisseria gonorrhoeae, are active ; that lipid A

“…Our finding that inflammation induced in nude (athymic) rats by intraarticular injection of PG-APS is less prolonged than that in euthymic rats is consistent with the less severe chronic arthritis seen in nude rats after a systemic PG-APS injection (44,45). However, this did not influence the capacity of LPS to induce a recurrence of arthritis, indicating that T lymphocytes are not required for the transient acute reaction .…”

Section: Resultssupporting

confidence: 80%

Lipopolysaccharide induces recurrence of arthritis in rat joints previously injured by peptidoglycan-polysaccharide.

et al. 1987

The Journal of Experimental Medicine

View full text Add to dashboard Cite

LPS and peptidoglycan or covalent peptidoglycan-polysaccharide (PG-PS)' complexes are the major toxic components of bacterial cell walls. Lipid A and PG possess many of the biologic activities that LPS and PG-PS, respectively, have in common, such as pyrogenicity, polyclonal activation of lymphoid cells, complement activation, mitogenicity, macrophage activation, and adjuvanticity (1-3). Both also induce arthritis after injection into laboratory animals. Systemic injection of rats with a sterile, aqueous suspension of PG-PS from the group A streptococcus (PG-APS) induces a chronic erosive relapsing arthritis that has many features of rheumatoid arthritis (4-6). Distinct PG-PS structures from a number of other bacteria, including human indigenous intestinal species, induce arthritis of varying chronicity (7-10) . LPS induces primarily an acute arthritis of relatively short duration after intraarticular (i.a.) injection (7, 11-15), but there have been few reports of its arthropathic activity after systemic administration (16, 17, 17a) .In spite of the shared biologic properties and ubiquitous distribution of LPS and PG-PS, the interaction of their phlogistic activities in an inflammatory process has received little attention. During investigations of mechanisms of recurrent arthritis induced by PG-APS, we noted that a systemic injection of 100 Ag of Salmonella typhimurium LPS induced a transient recurrence of arthritis in rat joints previously inflamed by exposure to PG-APS (7,18) . We now report that the systemic injection of a much lower dose of LPS will induce a recurrence of arthritis injoints inflamed 3 wk previously by the intraarticular injection of PG-APS and describe this reaction in detail . We show that LPS from many bacteria, including Yersinia enterocolitica and Neisseria gonorrhoeae, are active ; that lipid A

“…Evaluation of lymphocyte function at various time points after SCW administration revealed that within 18 h the proliferative response was suppressed . This immune-deficient state continued through the development of acute arthritic symptoms (days [3][4][5] and persisted during the evolution of the chronic erosive joint lesions (>3 wk) (Fig. 2).…”

Section: Resultsmentioning

confidence: 93%

Bacterial cell wall-induced immunosuppression. Role of transforming growth factor beta.

¹

,

²

,

³

et al. 1988

The Journal of Experimental Medicine

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Group A streptococcal cell wall (SCW)-injected rats exhibit a profound immunosuppression that persists for months after the initial intraperitoneal injection of SCW. The goal of this study was to determine the mechanisms for the suppressed T lymphocyte proliferative responses in this experimental model of chronic inflammation. When spleen cell preparations were depleted of adherent cells, restoration of T cell proliferative responses to Con A and PHA occurred, implicating adherent macrophages in the regulation of immunosuppression. Furthermore, macrophages from SCW-treated animals, when cocultured with normal spleen cells in the presence of Con A or PHA, effectively inhibited the proliferative response. Supernatants from suppressed spleen cell cultures were found to inhibit normal T cell mitogenesis. Taken together, these results implicated a soluble macrophage-derived suppressor factor in the down regulation of T cell proliferation after exposure to SCW in vivo. Subsequent in vitro studies to identify this suppressor molecule(s) revealed the activity to be indistinguishable from the polypeptide transforming growth factor beta (TGF-beta). Furthermore, TGF-beta was identified by immunolocalization within the spleens of SCW-injected animals. The cells within the spleen that stained positively for TGF-beta were phagocytic cells that had ingested, and were presumably activated by, the SCW. These studies document that TGF-beta, previously shown to be a potent immunosuppressive agent in vitro, also effectively inhibits immune function in chronic inflammatory lesions in vivo.

“…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%

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

¹

,

²

,

³

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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