Soil microbiomes underpin terrestrial ecosystem functioning and drive nutrient cycling, plant productivity and ecological resilience. However, diverse pollutants, ranging from heavy metals and pesticides to plastics, perfluoroalkyl and polyfluoroalkyl substances and nanomaterials, are reshaping microbial communities in ways that threaten soil health and broader ecological stability. Thus, soils are hotspots of microbial evolution under chemical mixtures. Pollution alters microbial diversity, composition and functional capacity through mechanisms such as direct toxicity, shifts in soil chemistry and selective evolutionary pressures. These disruptions impair nutrient cycling, destabilize plant-microorganism interactions and accelerate the spread of antimicrobial resistance, with cascading effects on food webs and human health under a One Health framework. At the same time, soil microbiomes can serve as indicators of ecosystem stress and as tools for bioremediation and ecological restoration. This Review synthesizes current understanding of terrestrial pollution-microbiome interactions, highlights functional and health implications, and explores how microbiome-informed approaches can guide sustainable soil management and environmental protection under global change, while identifying key knowledge gaps and outlining future research directions for predictive and integrative microbiome-based solutions.

In immunocompetent hosts, Salmonella enterica serovar Typhimurium typically causes transient intestinal blooms with acute diarrhoea, followed by asymptomatic systemic carriage with intermittent reactivation. Inflammation elicited by bistable expression of type III secretion systems and pathogen-associated signals shapes Salmonella pathogenesis in both the intestine and systemic tissues. Inflammation is a two-sided coin that, over time, can either benefit or harm the host, microbiota and Salmonella. The host deploys the inflammasome, hypoxia and reactive oxygen and nitrogen species in both intestinal and systemic tissues, but the effectors of these responses are cell-specific and tissue-specific. Salmonella fine-tunes its metabolism and virulence programmes in response to chemical and physical cues derived from the microbiota and from heterogeneous host cells that vary in embryonic origin, architecture and activation states. Similar to its host, Salmonella undergoes coordinated virulence, metabolic, redox and energetic reprogramming with outcomes tailored to specific host cells and tissues. Paradoxically, Salmonella often exploits common signalling and metabolic pathways to support rapid growth in the gut lumen and in the cytosol of enterocytes while sustaining an energy-conserving and metabolic-conserving survival strategy in viscera. In this Review, I discuss current perspectives of how the dynamic interplay between microbial competition, host defences and Salmonella countermeasures determines the outcome of infection ranging from acute gastroenteritis to quiescent chronic infection.

Despite a tremendous body of literature on environmental Actinomycetota, their role in the human gut remains poorly understood. In this Review, we highlight the representative species Eggerthella lenta, which has emerged as a major player in the gut microbiota and is increasingly amenable to mechanistic dissection. We discuss the unique metabolic niche of this asaccharolytic obligate anaerobe, including growth on amino acids and short-chain fatty acids, versatile anaerobic respiratory capacity, and the extensive biotransformation of endogenous, diet-derived and pharmaceutical small molecules. E. lenta is associated with a wide range of chronic diseases in humans and sufficient to exacerbate disease in preclinical models, prompting a renewed consideration of the pathogenic potential of this common member of the gut microbiota. Further mechanistic dissection coupled with the development of microbiome-editing tools is essential to understand E. lenta and its multifaceted contributions to gut microbial ecology and host pathophysiology.

Waterborne diseases are caused by pathogens that are transmitted via ingestion of contaminated water and remain a leading cause of death particularly in young children. Climate change threatens to undermine the progress that has been made in reducing waterborne diseases. In this Review, we explore how meteorological conditions that are influenced by climate change, including temperature, heavy rainfall and flooding, drought, and extreme weather, affect the biology and transmission of waterborne pathogens, with a focus on those that spread via the faecal-oral route. We discuss evidence that these impacts vary across pathogens and consider how such information is used to project disease risks under future climatic conditions, including incorporating social vulnerability and pathogen-specific outcomes to more accurately estimate future disease burden. We also review strategies to blunt climate-related increases in waterborne diseases, including vaccination; water, sanitation and hygiene interventions; and enhanced surveillance. As climate change continues to alter our global environment, understanding its impacts on waterborne diseases can improve our ability to reduce climate harms, identify and protect vulnerable populations, and develop evidence-based approaches to promote population health.