Bone marrow colony-formation in vitro after infection of genetically defined inbred mice with Candida albicans

Wanasaengsakul, Siripen; Ashman, R. B.

doi:10.1016/j.micpath.2003.12.003

Cited by 5 publications

(5 citation statements)

References 24 publications

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“…In addition, in the functional tests, we found that dectin-1 activation inhibited bone resorption of RANKL-induced osteoclasts. These results are consistent with previous observations that intravenous injection with Candida albicans enhanced new bone formation in mice [ 24 ], and dectin-1 activation in osteoclast precursors inhibited RANKL-induced osteoclast differentiation in vitro [ 18 ]. Furthermore, curdlan treatment failed to suppress dectin-1 −/− osteoclast differentiation.…”

Section: Discussionsupporting

confidence: 93%

Dectin-1 signaling inhibits osteoclastogenesis via IL-33-induced inhibition of NFATc1

et al. 2017

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Abnormal osteoclast activation contributes to osteolytic bone diseases (OBDs). It was reported that curdlan, an agonist of dectin-1, inhibits osteoclastogenesis. However, the underlying mechanisms are not fully elucidated. In this study, we found that curdlan potently inhibited RANKL-induced osteoclast differentiation and the resultant bone resorption. Curdlan inhibited the expression of nuclear factor of activated T-cells, cytoplasmic 1 (NFATc1), the key transcriptional factor for osteoclastogenesis. Notably, dectin-1 activation increased the expression of MafB, an inhibitor of NFATc1, and IL-33 in osteoclast precursors. Mechanistic studies revealed that IL-33 enhanced the expression of MafB in osteoclast precursors and inhibited osteoclast precursors to differentiate into mature osteoclasts. Furthermore, blocking ST2, the IL-33 receptor, partially abrogated curdlan-induced inhibition of NFATc1 expression and osteoclast differentiation. Thus, our study has provided new insights into the mechanisms of dectin-1-induced inhibition of osteoclastogenesis and may provide new targets for the therapy of OBDs.

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Section: Discussionsupporting

confidence: 93%

Dectin-1 signaling inhibits osteoclastogenesis via IL-33-induced inhibition of NFATc1

et al. 2017

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“…Neutrophils are known to be an important effector cell in Candida infection and CBA/CaH nude mice with chronic oral infections have a depleted colony‐forming response in vitro when compared with BALB/c 17 . As this suggested that neutrophil precursors might be a limiting factor in the susceptibility of this strain, the quantitative production of neutrophils in vitro by bone marrow derived from the two mouse strains was compared in a double‐cross‐over experiment.…”

Section: Resultsmentioning

confidence: 99%

“…Neutrophils are known to be an important effector cell in Candida infection and CBA/CaH nude mice with chronic oral infections have a depleted colony-forming response in vitro when compared with BALB/c. 17 As this suggested that neutrophil precursors might be a limiting factor in the susceptibility of this strain, the quantitative production of neutrophils in vitro by bone marrow derived from the two mouse strains was compared in a double-cross-over experiment. Generation of neutrophils by differentiation of BALB/c bone marrow cells on a BALB/c stromal cell layer produced the greatest yield (mean ± SD: 97.0 ± 7.6´10 5 cells/culture), whereas neutrophil production by BALB/c bone marrow cells on a CBA/CaH stromal cell layer was significantly less (44.6 ± 5.5, P < 0.001).…”

Section: Neutrophil Production From Bone Marrow Culturementioning

confidence: 99%

Effector function of leucocytes from susceptible and resistant mice against distinct isolates of Candida albicans

Farah

Ashman

2006

Immunol Cell Biol

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Summary Neutrophils and macrophages were generated in vitro from mice that display either high or low tissue susceptibilities to Candida albicans infection and their ability to phagocytose and kill three isolates of the yeast with different virulence characteristics was evaluated. In the absence of opsonization, phagocytosis by BALB/c and CBA/CaH neutrophils was comparable, but the killing was very poor. Opsonization with normal serum slightly decreased phagocytosis, but it had markedly different effects on killing, either enhancing or inhibiting candidacidal activity, depending on the combination of yeast isolate and mouse strain. In contrast, BALB/c macrophages showed high levels of phagocytosis and killing of both unopsonized yeasts and opsonized yeasts; whereas killing of unopsonized yeasts by CBA/CaH macrophages was poor, it was markedly enhanced by opsonization.Key words: killing, macrophage, neutrophil, opsonization, phagocytosis. IntroductionPhagocytic cells are the first line of defence against Candida infections. 1-6 These cells are primarily responsible for the elimination of fungi from infected tissues and organs and quantitative or qualitative differences in their function may be responsible, at least in part, for the variations in susceptibility or resistance that have been documented in inbred strains of mice.Few studies have correlated the functional activity of phagocytic cells to the virulence characteristics of various isolates of Candida albicans. Candida strains derived from environmental sampling were more resistant to killing by human neutrophils than those isolated from humans or birds, but the properties of the yeasts that were associated with susceptibility and resistance were not identified. 7 A comparison of two Candida strains differing in cell surface hydrophobicity and in fibronectin (Fn) binding showed that the strain expressing a low hydrophobicity and low binding of soluble Fn was more resistant to neutrophil killing and persisted longer in i.p.-infected mice than the strain with a higher hydrophobicity and higher binding of soluble Fn, 8 and differences in other properties, such as proteinase production, are also associated with differential susceptibility to killing by phagocytic cells. 9 However, little is known about the relative efficiency of phagocytosis and killing of various Candida isolates by neutrophils and macrophages from different inbred strains of mice and its correlation to susceptibility and resistance.We have previously shown that three distinct isolates of C. albicans differ in their ability to establish both systemic and oral infections and in the specificity and protective effects of antibodies raised against them; 10 hence, the aims of this study were to compare phagocytosis and killing of these strains of C. albicans by neutrophils and macrophages from mice that showed mild (BALB/c) or severe (CBA/CaH) tissue damage 11 and to evaluate the effects of serum opsonins on these responses. Materials and methods MiceInbred female mice were purchased from the Anim...

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“…A possibility for which there is some evidence is that T cells act to enhance production of phagocytic cells by the bone marrow. Studies in chronically orally-infected nude mice have demonstrated that bone marrow colony formation in vitro is significantly depressed in the CBA/CaH mice compared to BALB/c (26). Reconstitution with T cells significantly increased the colony-forming response in BALB/c, but not in CBA/CaH mice.…”

Section: Oral Candidiasismentioning

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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Bone marrow colony-formation in vitro after infection of genetically defined inbred mice with Candida albicans

Cited by 5 publications

References 24 publications

Dectin-1 signaling inhibits osteoclastogenesis via IL-33-induced inhibition of NFATc1

Dectin-1 signaling inhibits osteoclastogenesis via IL-33-induced inhibition of NFATc1

Effector function of leucocytes from susceptible and resistant mice against distinct isolates of Candida albicans

Protective and pathologic immune responses against Candida albicans infection

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