Bacteria-induced susceptibility to<i>Candida albicans</i>super-infection in mice via monocyte methyltransferase Setdb2

Chen, Xiaoping; Zheng, Hui; Li, Wenge; Chen, Guodong; Lu, Jinxing

doi:10.1111/cmi.12860

Cited by 4 publications

(4 citation statements)

References 47 publications

(85 reference statements)

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“…The mice were more susceptible shortly after CLP rather than later on when the immune system was partially reconstituted [333]. In line with this, it was shown that monocytes from CLP-treated mice expressed less antifungal effector genes upon secondary intravenous C. albicans challenge, had less inflammatory monocytes in circulation, and less neutrophil influx into the kidneys [334]. In mice that received C. albicans via oral gavage a few hours after CLP, mortality was also increased as compared with CLP-treated animals [335].…”

Section: Fungal-bacterial Interactions—niche By Nichementioning

confidence: 96%

Fungal-Bacterial Interactions in Health and Disease

et al. 2019

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Fungi and bacteria encounter each other in various niches of the human body. There, they interact directly with one another or indirectly via the host response. In both cases, interactions can affect host health and disease. In the present review, we summarized current knowledge on fungal-bacterial interactions during their commensal and pathogenic lifestyle. We focus on distinct mucosal niches: the oral cavity, lung, gut, and vagina. In addition, we describe interactions during bloodstream and wound infections and the possible consequences for the human host.

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Section: Fungal-bacterial Interactions—niche By Nichementioning

confidence: 96%

Fungal-Bacterial Interactions in Health and Disease

et al. 2019

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“…The study showed that the weight of the mice in the TA combined with the FLC treatment group recovered, and the survival rate was significantly improved compared with the weight and survival rate of mice in the FLC group (P < 0.05). In addition, a comprehensive analysis of the kidney, the main target organ of invasive C. albicans, infection was also conducted (Chen et al, 2018). The results showed that the TA combined with the FLC treatment group had a significantly lower kidney fungal burden (P < 0.05), reduced number of lesions, and inflammatory cell infiltration.…”

Section: Discussionmentioning

confidence: 99%

Antifungal Activity and Potential Mechanism of 6,7, 4′-O-Triacetylscutellarein Combined With Fluconazole Against Drug-Resistant C. albicans

Liao

et al. 2021

Front. Microbiol.

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The increased resistance of Candida albicans to conventional antifungal drugs poses a huge challenge to the clinical treatment of this infection. In recent years, combination therapy, a potential treatment method to overcome C. albicans resistance, has gained traction. This study assessed the effect of 6,7,4′-O-triacetylscutellarein (TA) combined with fluconazole (FLC) on C. albicans in vitro and in vivo. TA combined with FLC showed good synergistic antifungal activity against drug-resistant C. albicans in vitro, with a partial inhibitory concentration index (FICI) of 0.0188–0.1800. In addition, the time-kill curve confirmed the synergistic effect of TA and FLC. TA combined with FLC showed a strong synergistic inhibitory effect on the biofilm formation of resistant C. albicans. The combined antifungal efficacy of TA and FLC was evaluated in vivo in a mouse systemic fungal infection model. TA combined with FLC prolonged the survival rate of mice infected with drug-resistant C. albicans and reduced tissue invasion. TA combined with FLC also significantly inhibited the yeast-hypha conversion of C. albicans and significantly reduced the expression of RAS-cAMP-PKA signaling pathway-related genes (RAS1 and EFG1) and hyphal-related genes (HWP1 and ECE1). Furthermore, the mycelium growth on TA combined with the FLC group recovered after adding exogenous db-cAMP. Collectively, these results show that TA combined with FLC inhibits the formation of hyphae and biofilms through the RAS-cAMP-PKA signaling pathway, resulting in reduced infectivity and resistance of C. albicans. Therefore, this study provides a basis for the treatment of drug-resistant C. albicans infections.

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“…SETDB2 (CLLD8 or KMT1F) is a member of the histone H3K9 methyltransferase family-KMT1 sub-family, which includes SUV39H1, SUV39H2, G9a and SETDB1 [13][14][15]. SETDB2 plays important roles in immune system [15][16][17] and embryonic development [18,19]. In cancer research, SETDB2 has been found to be involved in cell cycle dysregulation in acute leukemia [20], associated with the prognosis and metastasis of renal tumors [21], and plays an oncogenic role in gastric cancer [22].…”

Section: Ivyspringmentioning

confidence: 99%

SETDB2 promoted breast cancer stem cell maintenance by interaction with and stabilization of ΔNp63α protein

Liu¹,

Xie²,

Jialun³

et al. 2020

Int. J. Biol. Sci.

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The histone H3K9 methyltransferase SETDB2 is involved in cell cycle dysregulation in acute leukemia and has oncogenic roles in gastric cancer. In our study, we found that SETDB2 plays essential roles in breast cancer stem cell maintenance. Depleted SETDB2 significantly decreased the breast cancer stem cell population and mammosphere formation in vitro and also inhibited breast tumor initiation and growth in vivo. Restoring SETDB2 expression rescued the defect in breast cancer stem cell maintenance. A mechanistic analysis showed that SETDB2 upregulated the transcription of the ΔNp63α downstream Hedgehog pathway gene. SETDB2 also interacted with and methylated ΔNp63α, and stabilized ΔNp63α protein. Restoring ΔNp63α expression rescued the breast cancer stem cell maintenance defect which mediated by SETDB2 knockdown. In conclusion, our study reveals a novel function of SETDB2 in cancer stem cell maintenance in breast cancer.

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Bacteria-induced susceptibility toCandida albicanssuper-infection in mice via monocyte methyltransferase Setdb2

Cited by 4 publications

References 47 publications

Fungal-Bacterial Interactions in Health and Disease

Fungal-Bacterial Interactions in Health and Disease

Antifungal Activity and Potential Mechanism of 6,7, 4′-O-Triacetylscutellarein Combined With Fluconazole Against Drug-Resistant C. albicans

SETDB2 promoted breast cancer stem cell maintenance by interaction with and stabilization of ΔNp63α protein

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