Tryptophan metabolites relieve intestinal Candida albicans infection by altering the gut microbiota to reduce IL-22 release from group 3 innate lymphoid cells of the colon lamina propria.

Invasive candidiasis may be caused by Candida albicans (C. albicans) colonization of the intestinal tract. Preventing intestinal damage caused by Candida albicans infection and protecting intestinal barrier function have become a critical issue. Integrated analyses of the microbiome with metabolome revealed a remarkable shift of the gut microbiota and tryptophan metabolites, kynurenic acid (KynA), and indolacrylic acid (IA) in mice infected with C. albicans. The transcriptome sequencing indicated that differentially expressed genes were significantly associated with innate immune responses and inflammatory responses. The results of this study suggest that KynA and IA (KI) can alleviate intestinal damage caused by Candida albicans infection in mice by reducing intestinal permeability, increasing intestinal firmness, alleviating intestinal inflammation, and reducing the secretion of interleukin-22 (IL-22) in the 3 groups of colon innate lymphoid cells (ILC3). We performed a fecal microbiota transplantation (FMT) experiment and found that the intestinal barrier function, inflammation, and IL-22 secretion of ILC3 in the colon lamina propria of the recipient mice subjected to C. albicans infection and KI treatment were consistent with the trends of the donor mice. Our results suggest that tryptophan metabolites may directly regulate colon lamina ILC3 to promote intestinal resistance to C. albicans invasion, or indirectly regulate the ILC3 secretion of IL-22 to play a protective role in the intestinal barrier by affecting intestinal microorganisms, which may become a potential target for alleviating intestine borne C. albicans infection.

Intestinal Infection of Candida albicans: Preventing the Formation of Biofilm by C. albicans and Protecting the Intestinal Epithelial Barrier.

The large mortality and morbidity rate of C. albicans infections is a crucial problem in medical mycology. Because the generation of biofilms and drug resistance are growing concerns, the growth of novel antifungal agents and the looking for newer objectives are necessary. In this review, inhibitors of C. albicans biofilm generation and molecular mechanisms of intestinal epithelial barrier protection are elucidated. Recent studies on various transcription elements; quorum-sensing molecules; host responses to adherence; and changes in efflux pumps, enzymes, bud to hyphal transition, and lipid profiles have increased the knowledge of the intricate mechanisms underlying biofilm resistance. In addition, the growth of novel biomaterials with anti-adhesive nature, natural products, drugs, bioactive compounds, proteins, lipids, and carbohydrates are being researched. Recently, more and more attention has been given to various metal nanoparticles that have also appeared as antibiofilm agents in C. albicans. The intestinal epithelial obstacle exerts an crucial effect on keeping intestinal homeostasis and is increasingly associated with various disorders associated with the intestine such as inflammatory bowel disease (IBD), irritable bowel syndrome, metabolic syndrome, allergies, hepatic inflammation, septic shock, etc. However, whether their involvement in the prevention of other intestinal disorders like IBD are useful in C. albicans remains unknown. Further studies must be carried out in order to validate their inhibition functions in intestinal C. albicans. This provides innovates ideas for intestinal C. albicans treatment.

The impact of ultrasonic treatment on blueberry wine anthocyanin color and its In-vitro anti-oxidant capacity.

Ultrasound (US) has been recognized as a non-thermal technology for accelerating blueberry wine aging for flavor development. However, influence of US on anthocyanin and color characteristics is uncertain. In this study, US was applied to new blueberry wine, and changes in color characteristics, anthocyanin content and anti-oxidant capacity were evaluated at early stage of aging period. Low-frequency power US resulted in an improvement in color characteristics and lower chromatic aberration as compared to untreated samples, specially at condition of 180 W, 20 min and 2 cycles. Furthermore, this contribution was attributed to unattenuated anthocyanins protected from US stress. Importantly, the structural polarity dependence was mediated by the impact of US on anthocyanins. Additionally, anti-oxidant activity of blueberry wine was not adversely affected under a moderate US condition. US treatment of blueberry wine was therefore considered to significantly enhance the color presentation, hinting at the possibility of promoting blueberry wine aging.

Toxic effects of zearalenone on gametogenesis and embryonic development: A molecular point of review.

Zearalenone is commonly generated from moldy cereal grain, which is toxic to the development of gametogenesis and embryo in human and animals. The zearalenone-induced reproductive damage is mainly attributed to four mechanisms. Firstly, zearalenone as an oestrogen-like compound binds to estrogen receptor and causes damage to germ cells and testicular structure. Secondly, zearalenone disrupts the blood-testis barrier, and causes the damage to germ cells. Thirdly, zearalenone elevates oxidative stress, which increases the production of lipid peroxides, and results in the damage to the antioxidant defense system. Fourth, zearalenone increases DNA damage and promotes cells apoptosis. In addition, Zearalenone induces inflammatory reactions and leads to the disorders of reproductive hormones. In this study, we systematically introduced the toxic effects of zearalenone on gametogenesis and embryonic development in animals, and focused on the molecular pathways, which providing a basis for further prevention of zearalenone-induced injury.