Introduction to Candida

Domer, Judith E.; Lehrer, Robert I.

doi:10.1007/978-1-4899-2400-1_4

Cited by 14 publications

(2 citation statements)

References 418 publications

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“…Candida albicans , an ubiquitous fungal microorganism, forms part of the normal microflora in the gastrointestinal tract and vagina even in individuals who do not have an apparent immunological dysfunction [ 1, 2], suggesting the presence of certain mechanisms that evade the host defence system against this pathogen. It has been well documented that the host defence mechanism against mucosal infection with Candida albicans is mediated mainly by cellular immunity [ 3–6]. In experimental models, protection against candidiasis is closely associated with the synthesis of IL‐12 and induction of Th1 cells [ 7–10].…”

Section: Introductionmentioning

confidence: 99%

Candida albicanssuppresses nitric oxide (NO) production by interferon-gamma (IFN-γ) and lipopolysaccharide (LPS)-stimulated murine peritoneal macrophages

Chinen

Qureshi

Koguchi

et al. 1999

Clinical and Experimental Immunology

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We examined the in vitro effect of Candida albicans on NO production by macrophages. Candida albicans suppressed not only NO production but also expression of inducible NO synthase (iNOS) mRNA by murine IFN-gamma and bacterial LPS-stimulated peritoneal macrophages. The suppression was not associated with inhibition but rather stimulation of IL-1 beta production. This effect was observed when more than 1 x 10(3)/ml of Candida albicans were added to macrophage cultures (1 x 10(6) cells/ml) and reached a maximal level at 1 x 10(6)/ml. The NO inhibitory effect of Candida albicans was mediated predominantly by as yet unidentified soluble factor(s) and to a lesser extent by direct contact. In addition, heat- or paraformaldehyde-killed Candida albicans did not show this inhibitory activity. Culture supernatant of Candida albicans also inhibited NO production by activated macrophages in a dose-dependent manner, and increased IL-1 beta production. Finally, the inhibitory effect was not mediated by IL-10 and transforming growth factor-beta (TGF-beta), since neutralizing antibodies to these cytokines did not influence Candida albicans-induced reduction in macrophage NO production. Our results suggest that Candida albicans may evade host defence mechanism(s) through a soluble factor-mediated suppression of NO production by stimulated macrophages, and that the effect is independent of production of immunosuppressive cytokines such as IL-10 and TGF-beta.

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Section: Introductionmentioning

confidence: 99%

Candida albicanssuppresses nitric oxide (NO) production by interferon-gamma (IFN-γ) and lipopolysaccharide (LPS)-stimulated murine peritoneal macrophages

Chinen

Qureshi

Koguchi

et al. 1999

Clinical and Experimental Immunology

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“…Previous studies have demonstrated that innate immunity, mediated by granulocytes (polymorphonuclear leukocytes) and monocytes/ macrophages, is crucial to containment and resolution of systemic candidiasis caused by other Candida species, including C. albicans (5,13,18,55,66). Phagocytic cells kill C. albicans yeast, hyphae, and pseudohyphae, using both oxidative and nonoxidative mechanisms (20,28,41,81). Previous in vitro and in vivo studies have demonstrated that polymorphonuclear leukocytes and/or macrophage antifungal activities are modulated by cytokines (1,61,62).…”

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confidence: 99%

Comparison of Pathogenesis and Host Immune Responses toCandida glabrataandCandida albicansin Systemically Infected Immunocompetent Mice

et al. 2001

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Cytokine-mediated host defense against Candida glabrata infection was compared to that against C. albicans, using immunocompetent murine models of systemic candidiasis. The pathogenesis of infection was evaluated morphologically and by culture of target organs, while the kinetics of induction of cytokine mRNAs and corresponding proteins were determined in kidneys by real-time reverse transcription-PCR and cytokinespecific murine enzyme-linked immunosorbent assays, respectively. Systemic infection with C. glabrata resulted in a chronic, nonfatal infection with recovery of organisms from kidneys, while intravenous inoculation with C. albicans resulted in rapid mortality with logarithmic growth of organisms in kidneys and recovery of C. albicans from the spleen, liver, and lungs. Survival of C. glabrata-infected mice was associated with rapid induction of mRNAs and corresponding immunoreactive proteins for the proinflammatory cytokines tumor necrosis factor alpha (TNF-␣), interleukin-12 (IL-12), and gamma interferon (IFN-␥) and the lack of induction of protein for the anti-inflammatory cytokine IL-10. In contrast, mortality in C. albicans-infected mice was associated with induction of mRNA and corresponding protein for IL-10 but delayed (i.e., TNF-␣) or absent (i.e., IL-12 and IFN-␥) induction of immunoreactive proinflammatory cytokines. Mice were subsequently treated with cytokine-specific neutralizing monoclonal antibodies (MAbs) to TNF-␣, IL-12, or IFN-␥, and the effect on growth of C. glabrata in kidneys was assessed. Neutralization of endogenous TNF-␣ resulted in a significant increase in C. glabrata organisms compared to similarly infected mice administered an isotype-matched control MAb, while neutralization of endogenous IL-12 or IFN-␥ had no significant effect on C. glabrata replication. These results demonstrate that in response to intravenous inoculation of C. glabrata, immunocompetent mice develop chronic nonfatal renal infections which are associated with rapid induction of the proinflammatory cytokines TNF-␣, IL-12, and IFN-␥. Furthermore, TNF-␣ plays a key role in host defense against systemic candidiasis caused by either C. glabrata or C. albicans, as the absence of endogenous TNF-␣ activity was associated with enhanced tissue burden in both infection models.

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Candidiasis

Segal

Elad²

2010

Topley &Amp; Wilson's Microbiology and Microbial Infections

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Introduction to Candida

Cited by 14 publications

References 418 publications

Candida albicanssuppresses nitric oxide (NO) production by interferon-gamma (IFN-γ) and lipopolysaccharide (LPS)-stimulated murine peritoneal macrophages

Candida albicanssuppresses nitric oxide (NO) production by interferon-gamma (IFN-γ) and lipopolysaccharide (LPS)-stimulated murine peritoneal macrophages

Comparison of Pathogenesis and Host Immune Responses toCandida glabrataandCandida albicansin Systemically Infected Immunocompetent Mice

Candidiasis

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