In-vitro killing of<i>Candida</i>species by murine immunoeffectors and its relationship to the experimental pathogenicity

Vecchiarelli, Anna; Bistoni, Francesco; Cenci, Elio; Perito, Stefano; Cassone, Antonio

doi:10.1080/00362178585380541

Cited by 40 publications

(27 citation statements)

References 28 publications

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“…NK cells have not been shown to kill C. albicans in vitro [28][29][30] and depletion of NK cells with MAb did not enhance the susceptibility of mice to candidiasis [4,31,32]. Beige mice which have defective NK cells and phagocytic cells are more susceptible to acute systemic candidiasis than immunocompetent controls but they do not die from oroesophageal candidiasis after their alimentary tracts are colonized with C. albicans [15].…”

Section: Discussionmentioning

confidence: 99%

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Oroesophageal candidiasis is lethal for transgenic mice with combined natural killer and T-cell defects

Balish¹,

Warner²,

Pierson³

et al. 2001

Med Mycol

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Germfree transgenic epsilon 26 (Tgepsilon26) mice, which express the full-length human CD3epsilon gene, have combined defects in natural killer (NK) cells and T cells were found to be extremely susceptible to oroesophageal (palate, tongue, esophagus) and gastric (cardia-antrum section) candidiasis. The gnotobiotic Tgepsilon26 mice die, apparently from severe oroesophageal candidiasis, within 2-4 weeks after their alimentary tracts are colonized with Candida albicans. The Tgepsilon26 mice manifest resistance to acute systemic candidiasis (intravenous injection) and to systemic candidiasis of endogenous origin for the first 2 weeks after their alimentary tracts are colonized with C. albicans. Granulocyte depletion data suggest that granulocytes, in the absence of functional NK cells and T cells, can protect Tgepsilon26 mice from acute systemic candidiasis and from systemic candidiasis of endogenous origin, for at least 14 days after alimentary tract colonization. Granulocytes and macrophages, in the absence of NK cells and T cells, are unable to protect Tgepsilon26 mice from lethal oroesophageal candidiasis and systemic candidiasis of endogenous origin which was evident in moribund Tgepsilon26 mice 2-4 weeks after colonization. Thus, non-T cells (i.e., NK cells) and T cells play important roles in resistance to oroesophageal and systemic (acute and of endogenous origin) candidiasis.

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Section: Discussionmentioning

confidence: 99%

“…NK cells are apparently unable to kill C. albicans directly [28][29][30]. In addition, depletion of NK cells with monoclonal antibody (MAb) does not appear to enhance murine susceptibility to candidiasis [4,31,32].…”

Section: Introductionmentioning

confidence: 99%

Oroesophageal candidiasis is lethal for transgenic mice with combined natural killer and T-cell defects

Balish¹,

Warner²,

Pierson³

et al. 2001

Med Mycol

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“…Accordingly, C. guilliermondii displayed a limited capacity to stimulate tumor necrosis factor α (TNFα) when co-incubated with peritoneal macrophages (Aybay and Imir, 1996). However, it is readily phagocytosed by murine polymorphonuclear cells, bone marrow cells, peritoneal macrophages and spleen cells, when compared to the phagocytic index of C. albicans cells (Vecchiarelli et al, 1985). …”

Section: Introductionmentioning

confidence: 99%

Disruption of Protein Mannosylation Affects Candida guilliermondii Cell Wall, Immune Sensing, and Virulence

et al. 2016

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The fungal cell wall contains glycoproteins that interact with the host immune system. In the prominent pathogenic yeast Candida albicans, Pmr1 acts as a Golgi-resident ion pump that provides cofactors to mannosyltransferases, regulating the synthesis of mannans attached to glycoproteins. To gain insight into a putative conservation of such a crucial process within opportunistic yeasts, we were particularly interested in studying the role of the PMR1 homolog in a low-virulent species that rarely causes candidiasis, Candida guilliermondii. We disrupted C. guilliermondii PMR1 and found that loss of Pmr1 affected cell growth and morphology, biofilm formation, susceptibility to cell wall perturbing agents, mannan levels, and the wall composition and organization. Despite the significant increment in the amount of β1,3-glucan exposed at the wall surface, this positively influenced only the ability of the mutant to stimulate IL-10 production by human monocytes, suggesting that recognition of both mannan and β1,3-glucan, is required to stimulate strong levels of pro-inflammatory cytokines. Accordingly, our results indicate C. guilliermondii sensing by monocytes was critically dependent on the recognition of N-linked mannans and β1,3-glucan, as reported in other Candida species. In addition, chemical remotion of cell wall O-linked mannans was found to positively influence the recognition of C. guilliermondii by human monocytes, suggesting that O-linked mannans mask other cell wall components from immune cells. This observation contrasts with that reported in C. albicans. Finally, mice infected with C. guilliermondii pmr1Δ null mutant cells had significantly lower fungal burdens compared to animals challenged with the parental strain. Accordingly, the null mutant showed inability to kill larvae in the Galleria mellonella infection model. This study thus demonstrates that mannans are relevant for the C. guilliermondii-host interaction, with an atypical role for O-linked mannans.

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“…Production of PMNattracting chemokines, such as MIP-1␣ and -1␤, monocyte chemoattractant protein 1, and IL-8, by human monocytes in vitro is induced well by yeast forms of C. albicans and is induced much less by hyphal forms (34,136). Notably, the observation that activated leukocytes may kill hyphae extracellularly (139) suggests that hypha formation may be instrumental in keeping these candidacidal cells away from a very sensitive target. An anti-Sap immunoevasion mechanism is also suggested by the observation that some anti-Sap Abs do not inhibit enzyme activity (103).…”

Section: Experimental Candidal Vaginitismentioning

confidence: 99%

Anticandidal Immunity and Vaginitis: Novel Opportunities for Immune Intervention

2007

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The majority of human Candida infections occur at a mucosal surface. One of these infections, vulvovaginal candidiasis (VVC), is a widespread, common disease affecting a large proportion of otherwise healthy women. Some women undergo recurrent forms of VVC (RVVC); in these cases the quality of life is devastated, the associated cost of medical visits is high, there is substantial use of unprescribed therapy, and there is a possible increase in drug resistance. However, relatively little is known about the pathogenic and immunoregulatory mechanisms underlying VVC and RVVC. While there is consensus that local rather than systemic factors play a decisive role in controlling the infection, there is no consensus about the nature of the local factors. The results obtained with animal models and human investigations have not provided an overall consistent picture; rather, they have generated divergent interpretations about the role of innate and adaptive immunity against vaginal infection. Nonetheless, recent experimental evidence has resulted in some optimism concerning the challenge of clarifying the immunological basis of susceptibility to, and protection from, vaginal candidiasis through the development of appropriate immune interventions to integrate with or even replace antifungal chemotherapy.The aim of this review is to provide a short update of the evidence mentioned above and the resulting optimism. Here, we critically consider the linkage between the virulence traits of the fungus and the host responses to these traits, two interrelated aspects which have rarely been treated together in other reviews of the topic (36, 39-41, 48, 54, 56, 57, 65, 66, 74, 94, 102). On this basis, we suggest that despite substantial belief to the contrary, novel tools derived from adaptive immunity, in particular virulence-neutralizing antibodies (Abs), may become part of the anti-Candida armamentarium to fight vaginal infection.

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In-vitro killing ofCandidaspecies by murine immunoeffectors and its relationship to the experimental pathogenicity

Cited by 40 publications

References 28 publications

Oroesophageal candidiasis is lethal for transgenic mice with combined natural killer and T-cell defects

Oroesophageal candidiasis is lethal for transgenic mice with combined natural killer and T-cell defects

Disruption of Protein Mannosylation Affects Candida guilliermondii Cell Wall, Immune Sensing, and Virulence

Anticandidal Immunity and Vaginitis: Novel Opportunities for Immune Intervention

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