Nature of the Skin-reactive Principle in Culture Filtrates Prepared from
            <i>Paracoccidioides brasiliensis</i>

Restrepo-Moreno, Angela; Schneidau, John D.

doi:10.1128/jb.93.6.1741-1748.1967

Cited by 86 publications

(29 citation statements)

References 5 publications

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“…Viable blastoconidia from which antigens were to be prepared were harvested from 10-liter fermentor (New Brunswick Scientific Co., Edison, N.J.) cultures grown in Trypticase (BBL Microbiology Systems, Cockeysville, Md.) soy dialysate broth (44), that had been incubated for 18 h at 37°C with constant aeration and agitation, and were washed with 0.15 M phosphate-buffered saline (pH 7.2) containing 0.001 M phenylmethylsulfonyl fluoride. Blastoconidia were stored frozen in phosphatebuffered saline containing the inhibitor before fractionation.…”

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confidence: 99%

Characterization of Candida albicans mannan-induced, mannan-specific delayed hypersensitivity suppressor cells

et al. 1990

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We have shown previously that CBA/J mice immunized with Candida albicans developed delayed hypersensitivity (DH) demonstrable with mannan (MAN) extracted from the same organism and that the intravenous (i.v.) injection of MAN prior to or during the immunization phase resulted in the suppression of the MAN-specific DH response. In this study, we demonstrate that MAN-induced suppression of DH is a T-lymphocyte-mediated phenomenon. Suppressor cells induced in vivo by the i.v. injection of MAN into naive mice 1 to 7 days prior to harvest were passaged through nylon wool, treated with various surface-specific antibodies and complement, and then injected i.v. into immunized syngeneic recipients. Enrichment of splenic T cells by passage over nylon wool and transfer of the nylon-wool-nonadherent populations to immunized recipient mice suppressed DH in a dose-dependent manner. Depletion of Thy' or Lyt-2+ cells from nylon-wool-nonadherent populations regularly ablated the ability of such suspensions to transfer suppression. Treatment of the same transfer suspensions with anti-Lyt-1 had variable effects, suggesting that the surface density of the Lyt-1 antigen was not as constant from population to population as was the Lyt-2 antigen. In addition, C. albicans MAN-induced suppressor cells were able to suppress DH demonstrable with Candida tropicalis MAN in animals immunized with C. tropicalis. Suppression of DH by MAN in this model, therefore, is mediated by Thy' Lyt-2+ lymphocytes.

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confidence: 99%

Characterization of Candida albicans mannan-induced, mannan-specific delayed hypersensitivity suppressor cells

et al. 1990

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“…Viable blastospores either for inoculation into mice or for preparation of subcellular fractions were grown in soy dialysate broth (31) for 18 h at 370C on a gyratory shaker. To obtain subcellular fractions, washed blastospores were disrupted in a Braun model MSK homogenizer (Bronwill Scientific Inc., Roches-ter, N.Y.), and fractions rich in cell walls, membranes and mitochondria, or soluble cytoplasmic substances were obtained after a series of three differential centrifugations, beginning with 400 x g and ending with 144,000 x g. The cell wall fraction was extracted with ethylenediamine to obtain water-soluble glycoproteins (9).…”

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confidence: 99%

Effects of cyclophosphamide on murine candidiasis

Moser¹,

Domer²

1980

Infect Immun

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Male CBA/J mice were given a single dose of 200 mg of cyclophosphamide (CY) per kg 3 days before a first or second cutaneous inoculation with viable Candida albicans in an attempt to suppress antibody formation and determine the effects of such suppression on the development of acquired immunity. After cutaneous inoculation, mice not treated with CY developed acquired immunity to intravenous challenge, which was accompanied by the development of circulating antibodies, delayed hypersensitivity, and in vitro responsiveness of lymph node cells to Candida antigens. CY treatment resulted in an immediate depression of peripheral blood leukocytes, with polymorphonuclear leukocytes and monocytes rebounding quickly to normal or above normal levels while lymphocytes remained depressed throughout the 4-week observation period. In vitro stimulation of lymph node cells from CY-treated mice was depressed shortly after treatment; however, responses to phytohemagglutinin and three Candida antigens (a cell wall preparation, a membrane preparation, and soluble cytoplasmic substances) recovered, whereas the responses to lipopolysaccharide did not. CY effects on the cutaneous lesion were twofold; first, the number of viable Candida cells in the lesions was much higher in animals receiving CY 3 days before Candida inoculation, and second, the size of the dermal lesion was either greatly enhanced or reduced depending upon the time of CY treatment relative to the number of cutaneous Candida inoculations. CY-treated animals developed higher levels of delayed hypersensitivity to the membrane preparation when infected once cutaneously than did corresponding untreated animals. The number of mice responding with circulating antibodies to soluble cytoplasmic substances after cutaneous inoculation was greatly reduced in CY-treated groups, and this impaired ability to produce antibodies correlated with the poor survival of these mice after intravenous challenge. Our results suggest that the ability to produce antibody at the time of challenge is crucial to successful defense against systemic candidiasis in this murine model.

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“…Since specific cultural and fractionation techniques have been reported in detail elsewhere (13,14), they are described only briefly here. Viable blastospores for inoculation into mice were grown in a soy dialysate broth (27). The antigen used for footpad testing, designated crude HEX, was extracted from a membrane fraction of C. albicans by using phosphate-buffered saline (pH 7.4) at 500C.…”

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Experimental Murine Candidiasis: Pathological and Immune Responses in T-Lymphocyte-Depleted Mice

et al. 1978

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Mice depleted of T-lymphocytes by thymectomy and irradiation (TXB) and immunologically competent mice were compared for gross and histological pathology as well as immune responses after cutaneous and/or intravenous challenge with Candida albicans. In response to a first cutaneous inoculation with viable Candida, TXB, sham-operated (SXB), and unmanipulated (normal) mice, all developed lesions of comparable size, duration, and histopathology. When challenged a second time cutaneously, normal and SXB mice developed lesions which were greatly increased in size when compared with those produced by a first cutaneous infection, whereas TXB mice developed lesions comparable in size to those initiated by the first infection. Histologically, the first and second lesions in all animals were acute abscesses predominantly comprised of polymorphonuclear leukocytes. The larger second lesions in SXB and normal mice were accompanied by detectable circulating antibody and by delayed hypersensitivity. Neither circulating antibody nor delayed hypersensitivity were stimulated in the TXB mice. When challenged intravenously, all previously uninfected mice, regardless of T-cell status, were equally susceptible to C. albicans. Contrary to SXB or normal mice, however, TXB mice which had been infected cutaneously were not more resistant to a subsequent intravenous challenge as judged by 6-week survival. The results suggest that T-cells do not play a significant role in innate resistance of mice to systemic candidiasis, but that such cells are important in the development of acquired resistance.Candida albicans (Robin) Berkhout is a fungus which does not usually invade the normal host, although it is a member of the normal human microbial flora. The mechanism by which healthy individuals resist invasion is unclear, but it is generally believed that cell-mediated immunity, and thus the T-lymphocyte, is an important factor in acquired resistance. The latter statement is based primarily on clinical evidence, in that individuals with immunodeficiency diseases (3,18,22,32,35) or with diseases for which the treatment itself is immunosuppressive (1, 17, 20, 24, 28, 37) are particularly susceptible. Experimental evidence to corroborate the clinical evidence is somewhat meager.Recently, however, a natural model of immunological modification, viz., the nude or athymic mouse, has been used to investigate innate resistance to C. albicans. Cutler (10) inoculated nude mice with large doses of C. albicans intravenously and observed that such mice were more t Present address: Mt. Sinai Hospital, Department of Microbiology, New York, NY 10029.

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Nature of the Skin-reactive Principle in Culture Filtrates Prepared from Paracoccidioides brasiliensis

Cited by 86 publications

References 5 publications

Characterization of Candida albicans mannan-induced, mannan-specific delayed hypersensitivity suppressor cells

Characterization of Candida albicans mannan-induced, mannan-specific delayed hypersensitivity suppressor cells

Effects of cyclophosphamide on murine candidiasis

Experimental Murine Candidiasis: Pathological and Immune Responses in T-Lymphocyte-Depleted Mice

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