Suppressive effect of <i>Escherichia coli</i> on adjuvant‐induced arthritis in germ‐free rats

Kohashi, Osamu; Kohashi, Yukiko; Takahashi, Tokutaro; Ozawa, Atsushi; Shigematsu, Nobuaki

doi:10.1002/art.1780290413

Cited by 77 publications

(45 citation statements)

References 26 publications

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“…Our findings are concordant with those described for adjuvant arthritis [21,22], a model with a pattern of susceptibility which is similar to that observed in SCW arthritis, Monoassociation of GF F344 rats with Gram-negative Escherichia coli resulted in resistance which equalled that in CV F344 rats whereas monoassociation with Gram-positive Lactobacillus casei did not really affect susceptibility, A combination of both bacteria suppressed susceptibility to a similar extent as E. coli alone. This suggests that Gram-negative bacterium-specific compounds, e.g, lipopolysaccharide (LPS; a known immunomodulator [23,24]), are responsible for decreased susceptibility.…”

Section: Discussionsupporting

confidence: 91%

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: Discussionsupporting

confidence: 91%

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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“…Furthermore, arthritis and severe inflammation can be induced in otherwise SCW arthritis-resistant F344/N rats, by interruption of the HPA axis at its effector end point, with the glucocorticoid receptor antagonist RU 486 (9). Taken together, these data indicate that LEW/N rats' pituitary and adrenal hyporesponsiveness to inflammatory and other stress mediators is a major factor contributing to their susceptibility to SCW arthritis, and possibly to other experimental inflammatory diseases (10)(11)(12)(13)(14)(15)(16)(17). This model is consistent with evidence that inflammatory-mediator activation of glucocorticoid secretion is one mechanism by which the immune response is appropriately regulated and restrained (18)(19)(20)(21).…”

mentioning

confidence: 68%

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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“…Literature data show that the exposure of mice/rats to certain bacteria can actually induce protection from, rather than development of a disease. It has been shown that E. coli can render germ-free rats resistant to subsequently induced AA [23]. Also, accumulating evidence suggests that resistance to AA was due to the protective effect of antibodies specifi c for some Hsps.…”

Section: Discussionmentioning

confidence: 99%

Immune response to gut Escherichia coli and susceptibility to adjuvant arthritis in the rats

Kovačević-Jovanović

Miletić

Stanojević

et al. 2015

Acta Microbiologica Et Immunologica Hungarica

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We have investigated the humoral immune response to antigens of predominant gut aerobic bacterial strains (i.e. Escherichia coli) over the course of adjuvant arthritis and oil-induced arthritis in two inbred rat strains: Dark Agouti (DA) and Albino Oxford (AO). We report the presence of antibodies specifi c to proteins of E. coli in molecular weight range between 20-30 kDa in sera of diseased DA rats, and the absence of these antibodies in the sera of AO rats. In DA rats, CFA and IFA provoked a stronger antibody response to E. coli, especially of the IgG2b antibody class. Intramuscular administration of E. coli preceding the adjuvant arthritis induction had no effect on the development and course of disease, as well as on the activation of T cells in the draining inguinal lymph nodes. Higher serum levels of natural and induced IgA antibodies, combined with a higher CD3 + CD26 + cell percentage were found in AO rats. The observed correlation between the serologic response to commensal fl ora and rats' genetic background as a defi ning factor for arthritis susceptibility may contribute to the process of creating a favorable (or less favorable) milieu for arthritis development.

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Suppressive effect of Escherichia coli on adjuvant‐induced arthritis in germ‐free rats

Cited by 77 publications

References 26 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

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

Immune response to gut Escherichia coli and susceptibility to adjuvant arthritis in the rats

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