Systemic candidosis in silica-treated athymic and euthymic mice

Lee, K W; Balish, Edward

doi:10.1128/iai.41.3.902-907.1983

Cited by 23 publications

(10 citation statements)

References 16 publications

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“…and other as yet unknown mechanisms may be important as well (6,40). This condition may not be significantly different from that of laboratory animals in which innate resistance mechanisms (3,9,12,23,27,30) tend to prevent the spread of the organisms until T-dependent immunity has developed sufficiently to help with clearance of the fungus (2,8,15,20,34). In agreement with this notion, we have recently shown that systemic colonization of mice with low-virulence Candida cells leads to prolonged stimulation of T cells (10) and activation of microbicidal macrophages that confer protection against an otherwise lethal C. albicans challenge (4).…”

Section: Discussionmentioning

confidence: 98%

Th1 and Th2 cytokine secretion patterns in murine candidiasis: association of Th1 responses with acquired resistance

et al. 1991

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Two chemically mutagenized agerminative variants of Candida albicans were used to immunize mice against challenge with highly virulent cells of the parent strain. Although both mutants (Vir-3 and Vir-13) resulted in nonlethal infection and could be recovered from mouse organs for many days after the intravenous inoculation of 10' to 106 cells, significant protection to systemic challenge with virulent C. albicans was induced by only one (Vir-3) of the two variants. Anticandidal resistance in Vir-3-infected mice was associated with the occurrence in vivo of strong delayed-type hypersensitivity to Candida antigen, detection in vitro of highly fungicidal effector macrophages, and presence in the serum of a large proportion of Candida-reactive antibodies of the immunoglobulin G2a isotype. Bulk cultures of purified CD4+ lymphocytes from mice infected with either mutant were compared for their ability to produce gamma interferon (IFN-y), interleukin-2 (IL-2), IL-4, and IL-6 in vitro. After stimulation with specific antigen, CD4+ cells from Vir-3-immunized mice released large amounts of the Thl-specific cytokines, IFN-'y and IL-2, at a time when CD4+ cells from Vir-13-infected mice predominantly secreted the characteristic Th2 cytokines, IL-4 and IL-6. These results were confirmed by quantitative analysis of cytokine-producing Thl and Th2 cells. In addition, only mice infected with Vir-3 displayed a high frequency of CD8+ cells with the potential for in vitro lysis of yeast-primed bone marrow macrophages. Purified CD4+ cells from Vir-3-infected mice, but not a mixture of these cells with CD4+ lymphocytes from mice infected with Vir-13, could adoptively transfer delayed-type hypersensitivity reactivity onto naive mice. Taken together, these data suggest that both Thl and Th2 CD4+ lymphocytes may be activated during experimental C. albicans infection in mice.

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Section: Discussionmentioning

confidence: 98%

Th1 and Th2 cytokine secretion patterns in murine candidiasis: association of Th1 responses with acquired resistance

et al. 1991

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“…It has long been known that phagocytic cells, neutrophils (110,111) and macrophages (112,113) in particular, are crucial for recovery from initial infections with C. albicans, and that the adaptive immunity and the T cell response play only a minor role (114). This latter conclusion has been reinforced by repeated demonstrations that immunodeficient 'nude' (97,115,116) and SCID (117) mice are no more susceptible to systemic infection than euthymic controls.…”

Section: Cellular Responsesmentioning

confidence: 99%

Protective and pathologic immune responses against Candida albicans infection

Ashman

2008

Front Biosci

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Candida albicans is an important opportunistic fungal pathogen. Clinical observations have indicated that both innate and adaptive immune responses are involved in recovery from initial infection, but analysis in murine models has shown that the contribution of the two arms of the cellular immune response differ in oral, vaginal, and systemic infections. The relative contributions of T cells and phagocytic cells, and the cytokines that mediate their interactions are discussed for each of the different manifestations of the disease, and the consequences of infection, in terms of protection and pathology, are evaluated.

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“…A role for classical thymus-dependent cell-mediated immunity in protection against mucosal candidiasis is supported by enhanced susceptibility to this form of candidiasis in athymic mice (17,39), patients with chronic mucocutaneous candidiasis (23), and patients with acquired immunodeficiency syndrome (44). However, data on the effect of T-lymphocyte-mediated systems in protection against invasive candidiasis do not establish as clear a role (2,6,10,11,14,16,20,25,26,30,40,41). Similarly, a role for a protective effect for B-lymphocyte-mediated mechanisms is not clearly established (1,12,16,18,32,35,39).…”

mentioning

confidence: 99%

Inoculation candidiasis in a murine model of severe combined immunodeficiency syndrome

et al. 1988

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To further elucidate the importance of T-and B-lymphocyte-mediated responses in host defense against systemic infection with Candida albicans, we studied this infection in a murine model of severe combined immunodeficiency (SCID). The course of inoculation candidiasis in these mice, which lack functional T and B lymphocytes, was compared with that in immunologically normal BALB/c mice. Mice were inoculated intravenously with 105 yeast cells. Quantitative cultures of liver, spleen, and kidneys were performed with necropsy specimens obtained 1, 3, 7, 10, 14, and 21 days after this intravenous inoculation. The differences in the time courses of recovery of organisms from liver and spleen specimens were not significantly different in the SCID mice compared with the BALB/c mice. The recovery of C. albicans from the kidneys was significantly lower in the SCID mice, indicating less persistence of the organism in the kidneys of the SCID mice than in those of the BALB/c mice. These data indicate that defense mechanisms other than Tand B-lymphocyte-mediated mechanisms are primarily responsible for host defense against inoculation candidiasis.

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Systemic candidosis in silica-treated athymic and euthymic mice

Cited by 23 publications

References 16 publications

Th1 and Th2 cytokine secretion patterns in murine candidiasis: association of Th1 responses with acquired resistance

Th1 and Th2 cytokine secretion patterns in murine candidiasis: association of Th1 responses with acquired resistance

Protective and pathologic immune responses against Candida albicans infection

Inoculation candidiasis in a murine model of severe combined immunodeficiency syndrome

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