Listeria monocytogenes, a major zoonotic food-borne intracellular pathogen, is ubiquitous in the natural environment and easily contaminates animal-derived food products. The consumption of the contaminated food can cause severe listeriosis in both humans and animals, with the mortality rate reaching up to 30%. The antimicrobial therapy is the only feasible approach for treating L. monocytogenes infection since L. monocytogenes is susceptible to multiple antimicrobials. However, the reports of multidrug-resistant strains are increasing due to the selective pressure exerted by the irrational use of antimicrobials or disinfectants. The antimicrobial resistance mechanisms of L. monocytogenes are complex. Efflux pump proteins are crucial in bacteria and participate in various biological processes. Specifically, they can influence bacterial sensitivity to antibiotics, facilitate the efflux of toxic compounds, and affect bacterial virulence. Over the last two decades, scholars have conducted research on the efflux pumps-mediated resistance of L. monocytogenes, identifying several efflux pump proteins associated with the efflux of antibiotics or toxic compounds. Additionally, some efflux pumps are involved in the virulence expression process of L. monocytogenes. This paper reviews the research advances in the functions and regulatory mechanisms of efflux pumps in multidrug-resistant L. monocytogenes. It provides a theoretical foundation for probing into the environmental adaption mechanisms of L. monocytogenes, curbing the spread of this pathogen, and identifying new drug targets for combating infections.

Persulfidation plays a role in protein functioning and signaling, maintaining the physiological and metabolic balance of cells, protecting cells from oxidative stress, and regulating sulfur homeostasis. This article summarized the internal relationship of hydrogen sulfide, reactive sulfur species, and cysteine metabolism, expounded the mechanism of sulfur homeostasis regulation, and introduced the role of persulfidation in microbial sulfur homeostasis, providing new thoughts for the future research.

The roles of gut microbiota and its metabolites in the pathogenesis and rehabilitation of neurodegenerative diseases, gastrointestinal diseases, and musculoskeletal systemic diseases in the elderly are receiving increasing attention. Gut microbiota and its metabolites can regulate the functions of the cranial nervous system and the musculoskeletal system through various pathways, involving the immune, endocrine, and nervous systems. Conversely, the gut, brain, and musculoskeletal system can act on the intestinal system via inflammatory, metabolic, and mitochondrial pathways to regulate the gut microbiota. Accordingly, bidirectional signaling mechanisms are formed via the gut-brain, gut-muscle, and gut-brain-muscle axes, which affect the organism health. This review summarizes that gut microbiota establishes gut-brain-muscle interconnections mainly through metabolites, intestinal permeability, and immune-neural pathways, providing new ideas for improving the brain neuroplasticity and muscle health.

Atopic dermatitis (AD) is a highly prevalent allergic skin disease characterised by recurrent attacks and severe itching. The pathogenesis of AD involves a variety of factors including genetic susceptibility, epidermal barrier dysfunction, microbiome dysbiosis, immune imbalance, and the environment, while the available therapeutic drugs have severe side effects and limited efficacy. Studies have demonstrated that gut microbiota, particularly probiotics, play a role in AD. Probiotics can alleviate AD symptoms by inhibiting pathogens, enhancing barriers, improving the intestinal environment, and balancing the Th1/Th2 immune response, among other mechanisms. In this review, we summarized the skin and intestinal microecological characteristics of AD patients and systematically elucidated the mechanisms of probiotics in alleviating AD from the pathogenesis and influencing factors of AD, aiming to provide theoretical support for probiotics in the treatment of AD and related allergic skin diseases.