Cadmium tolerant microbial strains possess different mechanisms for cadmium biosorption and immobilization in rice seedlings.

Nonalcoholic fatty liver disease (NAFLD) is a condition characterized by hepatic accumulation of excess lipids. T cells are commonly classified into various subsets based on their surface markers including T cell receptors, type of antigen presentation and pathophysiological functions. Several studies have implicated various T cell subsets and natural killer (NK) cells in the progression of NAFLD. While NK cells are mainly components of the innate hepatic immune system, the majority of T cell subsets can be part of both the adaptive and innate systems. Several studies have reported that various stages of NAFLD are accompanied by the accumulation of distinct T cell subsets and NK cells with different functions and phenotypes observed usually resulting in proinflammatory effects. More importantly, the overall stimulation of the intrahepatic T cell subsets is directly influenced by the homeostasis of the gut microbiota. Similarly, NK cells have been found to accumulate in the liver in response to pathogens and tumors. In this review, we discussed the nature and pathophysiological roles of T cell subsets including γδ T cells, NKT cells, Mucosal-associated invariant T (MAIT) cells as well as NK cells in NAFLD.

T Cell Subsets and Natural Killer Cells in the Pathogenesis of Nonalcoholic Fatty Liver Disease

The ecotoxicology and human health risks of environmental pollutants are creating global concern, especially in the context of the prevalent and severe contamination of environmental abiotic and biotic compartments [...].

Gut Microbiota Manipulation to Mitigate the Detrimental Effects of Environmental Pollutants

Proteomics and metabolic phenotyping define principal roles for the aryl hydrocarbon receptor in mouse liver

Cadmium (Cd) contamination in soils and accumulation in cereal grains have posed food security risks and serious health concerns worldwide. Understanding the Cd transport process and its management for minimizing Cd accumulation in cereals may help to improve crop growth and grain quality. In this review, we summarize Cd uptake, translocation, and accumulation mechanisms in cereal crops and discuss efficient measures to reduce Cd uptake as well as potential remediation strategies, including the applications of plant growth regulators, microbes, nanoparticles, and cropping systems and developing low-Cd grain cultivars by CRISPR/Cas9. In addition, miRNAs modulate Cd translocation, and accumulation in crops through the regulation of their target genes was revealed. Combined use of multiple remediation methods may successfully decrease Cd concentrations in cereals. The findings in this review provide some insights into innovative and applicable approaches for reducing Cd accumulation in cereal grains and sustainable management of Cd-contaminated paddy fields.

Cadmium in Cereal Crops: Uptake and Transport Mechanisms and Minimizing Strategies.

Noncaloric artificial sweeteners (NAS) are extensively introduced into commonly consumed drinks and foods worldwide. However, data on the health effects of NAS consumption remain elusive. Saccharin and sucralose have been shown to pass through the human gastrointestinal tract without undergoing absorption and metabolism and directly encounter the gut microbiota community. Here, we aimed to identify a novel mechanism linking intestinal Akkermansia muciniphila and the aryl hydrocarbon receptor (AHR) to saccharin/sucralose-induced nonalcoholic fatty liver disease (NAFLD) in mice. Saccharin/sucralose consumption altered the gut microbial community structure, with significant depletion of A. muciniphila abundance in the cecal contents of mice, resulting in disruption of intestinal permeability and a high level of serum lipopolysaccharide, which likely contributed to systemic inflammation and caused NAFLD in mice. Saccharin/sucralose also markedly decreased microbiota-derived AHR ligands and colonic AHR expression, which are closely associated with many metabolic syndromes. Metformin or fructo-oligosaccharide supplementation significantly restored A. muciniphila and AHR ligands in sucralose-consuming mice, consequently ameliorating NAFLD.IMPORTANCE Our findings indicate that the gut-liver signaling axis contributes to saccharin/sucralose consumption-induced NAFLD. Supplementation with metformin or fructo-oligosaccharide is a potential therapeutic strategy for NAFLD treatment. In addition, we also developed a new nutritional strategy by using a natural sweetener (neohesperidin dihydrochalcone [NHDC]) as a substitute for NAS and free sugars.

Xin An Zeng

Papers

Impaired Intestinal Akkermansia muciniphila and Aryl Hydrocarbon Receptor Ligands Contribute to Nonalcoholic Fatty Liver Disease in Mice.

A newly isolated bacterium Comamonas sp. XL8 alleviates the toxicity of cadmium exposure in rice seedlings by accumulating cadmium.