These data suggested that the killing capability of neutrophils to C. albicans was monitored by β-1,3-glucan via CR3/SYK pathway-dependent LC3B-II accumulation and provided an explanation for the variable killing capability of neutrophils to different strains of C. albicans, which would be beneficial in improving infection control and therapeutic strategies for invasive candidiasis.
NOS3/eNOS is expressed by endothelial cells in the kidney, and colonization of this organ was decreased during the sub-acute stage of disseminated candidiasis.
In addition, virulence of C. glabrata Δvph2 mutant in a mouse model of disseminated candidiasis was reduced in comparison with that of the wild-type and VPH2-reconstituted strains.
To investigate the role of IL-13 during a severe systemic Candida albicans infection, BALB/c control and IL-13<sup>-/-</sup> mice were examined for colony forming units (CFU) in the kidneys and survival days after intravenous infection.
Here, we investigated the role of the mTOR pathway in CD4<sup>+</sup> T-cell survival in a mouse model of rapidly progressive lethal sepsis induced by severe invasive candidiasis and explored the possible mechanism.
Interferons (IFNs) are critical mediators of the innate defense to infection, and in this study we evaluated the contribution of a specific gene coding for IFIT2 induced by type I IFNs in a murine model of disseminated <i>Candida albicans</i> Invasive candidiasis is a frequent challenge during immunosuppression or surgical medical interventions, and <i>C. albicans</i> is a common culprit that leads to high rates of mortality.
Furthermore, LMIR3-KO mice were significantly more resistant to Pseudomonas peritonitis and systemic candidiasis, although this may not be entirely due to the enhanced activity of neutrophils.
Mice lacking expression of the homologous phosphatases Sts-1 and Sts-2 (Sts<sup>-/-</sup> mice) are resistant to disseminated candidiasis caused by the fungal pathogen <i>Candida albicans</i> To better understand the immunological mechanisms underlying the enhanced resistance of Sts<sup>-/-</sup> mice, we examined the kinetics of fungal clearance at early time points.In contrast to the rapid <i>C. albicans</i> growth seen in normal kidneys during the first 24 h postinfection, we observed a reduction in kidney fungal CFU within Sts<sup>-/-</sup> mice beginning at 12 to 18 h postinfection.
Mice lacking expression of the homologous phosphatases Sts-1 and Sts-2 (Sts<sup>-/-</sup> mice) are resistant to disseminated candidiasis caused by the fungal pathogen <i>Candida albicans</i> To better understand the immunological mechanisms underlying the enhanced resistance of Sts<sup>-/-</sup> mice, we examined the kinetics of fungal clearance at early time points.In contrast to the rapid <i>C. albicans</i> growth seen in normal kidneys during the first 24 h postinfection, we observed a reduction in kidney fungal CFU within Sts<sup>-/-</sup> mice beginning at 12 to 18 h postinfection.
Our findings unveil a role for IL-15 as a critical mediator in defense against systemic candidiasis and hold promise for the design of IL-15-based antifungal immunotherapies.
Azole antifungals are potent inhibitors of fungal lanosterol 14α demethylase (CYP51) and have been used for eradication of systemic candidiasis clinically.
Phagocytosis of Candida by the macrophages lacking the Dectin-2 receptor was moderately decreased, while production of most of the macrophage-derived cytokines from Dectin-2(-/-) mice with systemic candidiasis was decreased.
Together, our data demonstrate a biological function for mouse Cxcr1 in vivo and indicate that CXCR1-dependent neutrophil effector function is a critical innate protective mechanism of fungal clearance and host survival in systemic candidiasis.
The products of SAP genes are considered to be virulent factors of C. albicans that participated in causing mucocutaneous and systemic candidiasis in humans.