<i>Candida albicans</i>suppresses nitric oxide (NO) production by interferon-gamma (IFN-γ) and lipopolysaccharide (LPS)-stimulated murine peritoneal macrophages

Chinen, T.; Qureshi, Mahboob; Koguchi, Yoshinobu; Kawakami, Kazuyoshi

doi:10.1046/j.1365-2249.1999.00822.x

Cited by 61 publications

(66 citation statements)

References 49 publications

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“…Candida spp. have been shown to have immunomodulatory activity mediated by fungal factors, including mannan and glycoproteins, mannoprotein constituents of the cell wall, and surface antigens (5,9,40,47). Although interactions occurring between the host immune system and Candida have been investigated in some detail for planktonically grown Candida cultures (reviewed in references 31, 33, 34, 35, and 38), no information is currently available for such interactions in a biofilm environment.…”

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confidence: 99%

Interaction ofCandida albicanswith Adherent Human Peripheral Blood Mononuclear Cells IncreasesC. albicansBiofilm Formation and Results in Differential Expression of Pro- and Anti-Inflammatory Cytokines

et al. 2007

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Monocytes and macrophages are the cell types most commonly associated with the innate immune response against Candida albicans infection. Interactions between the host immune system and Candida organisms have been investigated for planktonic Candida cells, but no studies have addressed these interactions in a biofilm environment. In this study, for the first time, we evaluated the ability of C. albicans to form biofilms in the presence or absence of adherent peripheral blood mononuclear cells (PBMCs; enriched for monocytes and macrophages by adherence). Our analyses using scanning electron and confocal scanning laser microscopy showed that the presence of PBMCs enhanced the ability of C. albicans to form biofilms and that the majority of PBMCs were localized to the basal and middle layers of the biofilm. In contrast to the interactions of PBMCs with planktonic C. albicans, where PBMCs phagocytose fungal cells, PBMCs did not appear to phagocytose fungal cells in biofilms. Furthermore, time-lapse laser microscopy revealed dynamic interactions between C. albicans and PBMCs in a biofilm. Additionally, we found that (i) only viable PBMCs influence Candida biofilm formation, (ii) cell surface components of PBMCs did not contribute to the enhancement of C. albicans biofilm, (iii) the biofilm-enhancing effect of PBMCs is mediated by a soluble factor released into the coculture medium of PBMCs with C. albicans, and (iv) supernatant collected from this coculture contained differential levels of pro-and anti-inflammatory cytokines. Our studies provide new insight into the interaction between Candida biofilm and host immune cells and demonstrate that immunocytes may influence the ability of C. albicans to form biofilms.

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Interaction ofCandida albicanswith Adherent Human Peripheral Blood Mononuclear Cells IncreasesC. albicansBiofilm Formation and Results in Differential Expression of Pro- and Anti-Inflammatory Cytokines

et al. 2007

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“…Recognition of C. albicans by macrophages is followed by the induction of a variety of immunological mechanisms, whose function is to limit the damage caused by the organism (3,13). However, C. albicans also suppresses aspects of macrophage response to evade host defenses (3,4,14), and glycolipid-phospholipomannan of the fungus can induce macrophage apoptosis (15,16). Recognition of C. albicans by macrophages and subsequent modulation of macrophage function may therefore be an important early event in determining the subsequent course of disease and/or clearance of C. albicans in the infected host.…”

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Loss of Cell Wall Mannosylphosphate in Candida albicans Does Not Influence Macrophage Recognition

Hobson

Munro

Bates

et al. 2004

Journal of Biological Chemistry

126

139

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The outer layer of the cell wall of the human pathogenic fungus Candida albicans is enriched with heavily mannosylated glycoproteins that are the immediate point of contact between the fungus and cells of the host, including phagocytes. Previous work had identified components of the acid-labile fraction of N-linked mannan, comprising ␤-1,2-linked mannose residues attached via a phosphodiester bond, as potential ligands for macrophage receptors and modulators of macrophage function. We therefore isolated and disrupted the CaMNN4 gene, which is required for mannosyl phosphate transfer and hence the attachment of ␤-1,2 mannose oligosaccharides to the acid-labile N-mannan side chains. With the mannosylphosphate eliminated, the mnn4⌬ null mutant was unable to bind the charged cationic dye Alcian Blue and was devoid of acid-labile ␤-1,2-linked oligomannosaccharides. The mnn4⌬ mutant was unaffected in cell growth and morphogenesis in vitro and in virulence in a murine model of systemic C. albicans infection. The null mutant was also not affected in its interaction with macrophages. Mannosylphosphate is therefore not required for macrophage interactions or for virulence of C. albicans.

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“…Nitric oxide synthase 2 (NOS2) knockout mice have not yet been assessed for their susceptibility to mucosal or systemic candidiasis of endogenous origin; however, mice with chemically induced deficiencies in RNI demonstrated an increased susceptibility to invasive and mucosal candidiasis (37), and RNI has been shown to be important for the candidacidal activity of macrophages (34)(35)(36). Intriguingly, recent studies indicate Candida albicans can suppress the production of RNI metabolites produced by murine phagocytic cells in vitro (9,30). Thus, defects in both ROI and RNI could exist in Candida-infected ROI-defective hosts; however, murine susceptibility to mucosal and systemic candidiasis in animals defective in both ROI and RNI has not been assessed.…”

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Susceptibility of Germfree Phagocyte Oxidase- and Nitric Oxide Synthase 2-Deficient Mice, Defective in the Production of Reactive Metabolites of Both Oxygen and Nitrogen, to Mucosal and Systemic Candidiasis of Endogenous Origin

Balish¹,

Warner

Nicholas³

et al. 2005

Infect Immun

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defective in the production of both reactive oxygen intermediates (ROI) and reactive nitrogen intermediates (RNI), were used to investigate the role of phagocytic cells during mucosal and systemic candidiasis of endogenous origin. The alimentary tracts of germfree mice were colonized with Candida albicans wild type or each of two hyphal signaling-defective mutants (efg1/efg1 and efg1/efg1 cph1/cph1). All Candida-colonized gp91 phox؊/؊ /NOS2 ؊/؊ mice were moribund within 12 to 15 days after oral inoculation. C. albicans wild-type and mutant strains colonized the alimentary tracts equally well and were able to translocate, most likely via Peyer's patches and mesenteric lymph nodes, to the internal organs and trigger the formation of abscesses; however, the wild-type and mutant strains did not survive in the abscessed murine tissues. Surprisingly, there was no significant difference in the ability of peritoneal exudate cells from gp91 phox؊/؊ /NOS2 ؊/؊ , NOS2 ؊/؊ , gp91 phox؊/؊ , or immunocompetent C57BL/6 mice to kill C. albicans in vitro. This suggests that anti-Candida factors other than ROI and RNI can control the growth of C. albicans and that gp91 phox؊/؊ /NOS2 ؊/؊ mice die due to the inability of the host to control its inflammatory response to Candida. Correspondingly, reverse transcription-PCR analysis showed increased expression of the cytokines gamma interferon, tumor necrosis factor alpha, and the chemokines MIP-2 and KC at the site of infection, while interleukin-15 expression remained relatively unchanged between germfree and infected tissues. These studies indicate that defects in ROI and RNI enabled C. albicans to translocate and disseminate to the internal organs, resulting in an uncontrolled immune response, severe pathology, and death; however, ROI and RNI were not required for the killing of phagocytized C. albicans, indicating that other anti-Candida factors either compensate or are sufficient for the killing of phagocytized Candida.

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

Cited by 61 publications

References 49 publications

Interaction ofCandida albicanswith Adherent Human Peripheral Blood Mononuclear Cells IncreasesC. albicansBiofilm Formation and Results in Differential Expression of Pro- and Anti-Inflammatory Cytokines

Interaction ofCandida albicanswith Adherent Human Peripheral Blood Mononuclear Cells IncreasesC. albicansBiofilm Formation and Results in Differential Expression of Pro- and Anti-Inflammatory Cytokines

Loss of Cell Wall Mannosylphosphate in Candida albicans Does Not Influence Macrophage Recognition

Susceptibility of Germfree Phagocyte Oxidase- and Nitric Oxide Synthase 2-Deficient Mice, Defective in the Production of Reactive Metabolites of Both Oxygen and Nitrogen, to Mucosal and Systemic Candidiasis of Endogenous Origin

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