Preparation of Various Fractions from &lt;i&gt;Mycobacterium smegmati&lt;/i&gt;&lt;i&gt;s&lt;/i&gt;, Their Arthritogenicity and Their Preventive Effect on Adjuvant Disease

Kohashi, Osamu; Pearson, Carl M.; Shimono, Tomoyuki; Kotani, Shozo

doi:10.1159/000231619

Cited by 14 publications

(13 citation statements)

References 17 publications

(24 reference statements)

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“…The present results (table III) confirm our previous report [5] in which lysozyme-solubilized product was a very weak arthritogen rather than a nonarthritogen. The arthritis-inducing ability of this product tested here appeared to be remarkably potentiated by poly I:C and acetylated wax D, but not by cord factor, with respect to the incidence and severity of the disease.…”

Section: Discussionsupporting

confidence: 92%

“…It is also shown that poly I:C, acetylated wax D and cord factor by themselves did not produce the disease. In view of the fact that these three compounds are known to serve as an immunoadjuvant [1,6,7], it is probable that arthritogenicity requires a specific antigen responsi ble for the disease production in addition to adjuvanticity, as previously described [5,10].…”

Section: Discussionmentioning

confidence: 99%

“…The preparation of the delipidated cells, cell walls, cell envelope, cell membrane fraction and lysozyme-solubilized product was described in detail in a previous paper [5], Immunological adjuvants. A copolymer of poly I and poly C (poly I:C) was ob tained from P-L Biochemicals, Milwaukee, Wise.…”

Section: Methodsmentioning

confidence: 99%

“…This observation led us to investi gate whether various immunoadjuvants such as poly I:C, cord factor [1] and acetylated wax D can potentiate the arthritogenicity of lysozyme-so lubilized product of M. smegmatis which by itself produced very mild dis ease with very low incidence [5].…”

Section: Introductionmentioning

confidence: 99%

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Arthritogenicity of Mycobacterium smegmatis Subfractions, Related to Different Oil Vehicle and Different Composition

Kohashi¹,

Pearson²

1976

Int Arch Allergy Immunol

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Arthrigenicity of Mycobacterium smegmatis subfractions appeared to be remarkably potentiated in oil vehicles such as squalane or mineral oil, while water-in-oil emulsions containing Arlacel A appeared to decrease or suppress their arthritogenicity. It seems that Arlacel A can exert a suppressive effect on the arthritogenicity of the subfractions. Poly I:C and acetylated wax D potentiated the arthritogenicity of lysozyme-solubilized product, while cord factor was unable to do so. When given together with either cell membrane fraction or cell envelope, the lysozyme-solubilized product produced much more severe disease than that of lysozyme-solubilized product alone. Cell walls lost much of their arthritogenicity when mixed with lysozyme-solubilized product.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Arthritogenicity of Mycobacterium smegmatis Subfractions, Related to Different Oil Vehicle and Different Composition

Kohashi¹,

Pearson²

1976

Int Arch Allergy Immunol

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“…However, in chronic infections, when elevated levels of steroids persist, the continued stimulation of factor production could contribute to establishing autoimmunity due to the absence of regulation by suppressor T cells. This hypothesis may partially explain why potent MbF inducers such as peptidoglycan and other bacterial cell wall components that stimulate production of IL-1 also induce experimental (adjuvant) polyarthritis (39).…”

Section: Discussionmentioning

confidence: 99%

Differential effects of glucocorticosteroids on the functions of helper and suppressor T lymphocytes.

Bradley¹,

Mishell²

1981

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

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The effects of dexamethasone (Dex) on the functions ofantigen-primed helper and suppressor T cells were studied in humoral immune responses in vitro. In doses equivalent to elevated physiologic concentrations, the suppressor T cell activity was abolished. In contrast, the helper T cell function was resistant to even pharmacologic concentrations of Dex. The apparent steroid resistance of the helper T cells was found to be mediated by the products ofactivated macrophages. While macrophage factors protected helper T cells from steroid inhibition, they did not prevent the effects of Dex on suppressor T cells. Because bacterial cell wall and membrane components are potent inducers of the factors that mediate steroid resistance of helper T cells, the combination of physiologically elevated levels of steroids and macrophage factors during acute infections may function to facilitate the expression of host immunity. However, the persistance of these conditions, as in chronic inflammation, may also contribute to the pathogenesis of autoimmunity by perturbing the balance of immune regulation by helper and suppressor T cells.

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Adjuvant polyarthritis. vii. The role of type ii collagen in pathogenesis

Iizuka

Chang

1982

Arthritis & Rheumatism

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The development of immune response in rats directed toward EL4 cells, after the injection of EL4 cells suspended in a saline/oil emulsion, was enhanced by the incorporation of Mycobacterium into the saline/oil emulsion; the incorporation of type I1 collagen into the salineacetic acid/oil emulsion in concentrations ranging from 0.5-25 pg/ml had no apparent effect on the development of immune response. The incorporation of type I1 collagen into the saline-acetic acidloil emulsion at higher concentrations (100 pg and 1.0 mg/ml) significantly suppressed both the humoral and the cell-mediated immune response. Pretreatment of rats with the maximal subarthritogenic dose of complete Freund's adjuvant prevented the development of arthritis in response to a subsequent injection of an arthritogenic dose of the same adjuvant, but had no effect on the development of type I1 collagen-induced arthritis. These observations suggest that adjuvant arthritis and the type I1 collagen-induced arthritis are distinctly different diseases.Adjuvant arthritis in the rat is believed to arise from an aberrant immune response to antigen(s) whose identity remains elusive. The disease may be the result of a delayed hypersensitivity response to bacilli or The endogenous sensitizing immunogen responsible for the development of adjuvant arthritis has been suggested by Trentham and coworkers ( 3 ) to be type I1 collagen. This conclusion was based on their observations that chronic arthritis in the rat, similar to the classic adjuvant arthritis, can be induced by an oily preparation of type I1 collagen (43) and that rats with classic adjuvant arthritis exhibited cellular and humora1 immunity to homologous type I1 collagen (3). Conversely, Cremer et a1 (6) suggested that collageninduced arthritis is an entity distinct from adjuvant arthritis, dependent upon the unique immunogenicity of type I1 collagen in the rat. Our objective in this investigation was to ascertain whether an autoimmune response to type I1 collagen underlies the pathogenesis of both type I1 collagen-induced and adjuvant-induced polyarthritis in the rat. MATERIALS AND METHODSAnimals. Outbred male Sprague-Dawley rats, 4-8 weeks of age, weighing from 120-250 gm, were purchased from Simonsen Laboratory, Gilroy, CA. These rats were housed in metal cages and given water and standard rat chew ad libitum.

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Preparation of Various Fractions from <i>Mycobacterium smegmati</i><i>s</i>, Their Arthritogenicity and Their Preventive Effect on Adjuvant Disease

Cited by 14 publications

References 17 publications

Arthritogenicity of <i>Mycobacterium smegmati</i><i>s</i> Subfractions, Related to Different Oil Vehicle and Different Composition

Arthritogenicity of <i>Mycobacterium smegmati</i><i>s</i> Subfractions, Related to Different Oil Vehicle and Different Composition

Differential effects of glucocorticosteroids on the functions of helper and suppressor T lymphocytes.

Adjuvant polyarthritis. vii. The role of type ii collagen in pathogenesis

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