The intestinal flora serves as a crucial regulator of healthy aging. As individuals age, the composition and function of the intestinal flora undergo substantial alterations, which are closely linked to various aging-related diseases. This article summarizes the changes in intestinal flora associated with aging and explores the potential of natural foods to ameliorate aging-related diseases via intestinal flora intervention. Specifically, interventions from natural food sources such as probiotics, prebiotics, appropriate dietary supplements, and nutritional intake have shown beneficial effects on improving gut health and delaying the aging process. The article further discusses the impact of various dietary patterns and nutritional restrictions on the intestinal flora composition and lifespan extension. Finally, the article summarizes key findings of intestinal flora in nutritional intervention studies involving intestinal flora and aging, providing evidence and future guidance for further exploring the potential intestinal flora intervention in anti-aging strategies.

Micro/nanoplastics (MNPs) are detected in human liver, and pose significant risks to human health. Oral exposure to MNPs derived from non-biodegradable plastics can induce toxicity in mouse liver. Similarly, nasal exposure to non-biodegradable plastics can cause airway dysbiosis in mice. However, the hepatotoxicity induced by foodborne and airborne biodegradable MNPs remains poorly understood. Here we show the hepatotoxic effects of biodegradable polylactic acid (PLA) MNPs through multi-omics analysis of various biological samples from mice, including gut, fecal, nasal, lung, liver, and blood samples. Our results show that both foodborne and airborne PLA MNPs compromise liver function, disrupt serum antioxidant activity, and cause liver pathology. Specifically, foodborne MNPs lead to gut microbial dysbiosis, metabolic alterations in the gut and serum, and liver transcriptomic changes. Airborne MNPs affect nasal and lung microbiota, alter lung and serum metabolites, and disrupt liver transcriptomics. The gut Lachnospiraceae_NK4A136_group is a potential biomarker for foodborne PLA MNP exposure, while nasal unclassified_Muribaculaceae and lung Klebsiella are potential biomarkers for airborne PLA MNP exposure. The relevant results suggest that foodborne PLA MNPs could affect the “gut microbiota-gut-liver” axis and induce hepatoxicity, while airborne PLA MNPs could disrupt the “airway microbiota-lung-liver” axis and cause hepatoxicity. These findings have implications for diagnosing PLA MNPs-induced hepatotoxicity and managing biodegradable materials in the environment. Our current study could be a starting point for biodegradable MNPs-induced hepatotoxicity. More research is needed to verify and inhibit the pathways that are crucial to MNPs-induced hepatotoxicity.

The liver is an important metabolic and detoxification organ and hence demands a large amount of energy, which is mainly produced by the mitochondria. Liver tissues of patients with alcohol-related or non-alcohol-related liver diseases contain ultrastructural mitochondrial lesions, mitochondrial DNA damage, disturbed mitochondrial dynamics, and compromised ATP production. Overproduction of mitochondrial reactive oxygen species induces oxidative damage to mitochondrial proteins and mitochondrial DNA, decreases mitochondrial membrane potential, triggers hepatocyte inflammation, and promotes programmed cell death, all of which impair liver function. Mitochondrial DNA may be a potential novel non-invasive biomarker of the risk of progression to liver cirrhosis and hepatocellular carcinoma in patients infected with the hepatitis B virus. We herein present a review of the mechanisms of mitochondrial dysfunction in the development of acute liver injury and chronic liver diseases, such as hepatocellular carcinoma, viral hepatitis, drug-induced liver injury, alcoholic liver disease, and non-alcoholic fatty liver disease. This review also discusses mitochondrion-centric therapies for treating liver diseases.

Vaccine is the most effective method to prevent the spread of communicable diseases, but the immune response it induces varies significantly among individuals and populations in different regions. Recent studies have shown that the composition and function of the gut microbiota play a key role in the immune response following vaccination. This article aims to explain the differences in gut microbiota among different vaccinated populations and animals, discuss how the gut microbiota affects the immune efficacy of the vaccine, and summarize strategies for targeting the gut microbiota to improve vaccine efficacy.