Enterococci are ubiquitous members of the gut microbiota in human beings and animals and are among the most important nosocomial organisms. Due to their opportunistic pathogenicity, enterococci are referred to as pathobionts and play decisive roles in a diverse array of polymicrobial infections. Enterococci can promote the colonization, pathogenesis, and persistence of various pathogens, compromise the efficacy of drugs, and pose a severe threat to public health. Most current treatments tend to focus on the sole pathogenic bacteria, with insufficient attention to the driving role of enterococci. In this review, we summarize the characteristics of enterococci in infections, the factors facilitating their outgrowth, as well as the sites and types of enterococci-associated polymicrobial infections. We present an overview of the underlying mechanisms of enterococci-mediated pathogenesis in polymicrobial infections. Furthermore, we discuss alternative strategies and potential intervention approaches to restrict such infections, shedding light on the discovery and development of new therapies against polymicrobial infections.

Microbes are widely recognized to be vital to host health. This new consensus rests, in part, on experiments showing how hosts malfunction when microbes are removed. More and more microbial dependencies are being discovered, even in fundamental processes such as development, immunity, physiology, and behavior. But why do they exist? The default explanation is that microbes are beneficial; when hosts lose microbes, they also lose benefits. Here I call attention to evolutionary addiction, whereby a host trait evolves a need for microbes without having been improved by them. Evolutionary addiction should be considered when interpreting microbe-removal experiments, as it is a distinct and potentially common process. Further, it may have unique implications for the evolution and stability of host-microbe interactions.

International governments defined antimicrobial stewardship (AS) as an essential ally against antimicrobial resistance (AMR). Patient and public engagement (PPE) in AS was pointed out as an imperative requirement to be embraced. We discuss PPE state of the art in AS and methodological reflections on how to achieve its effective implementation.

Biological nitrogen (N2) fixation is critical in global biogeochemical cycles and in sustaining the productivity of the oceans. There remain many unanswered questions, unresolved hypotheses, and unchallenged paradigms. The fundamental balance of N input and losses has not been fully resolved. One of the major N2-fixers, Trichodesmium, remains an enigma with intriguing biological and ecological secrets. Cyanobacterial N2 fixation, once thought to be primarily due to free-living cyanobacteria, now also appears to be dependent on microbial interactions, from microbiomes to unicellular symbioses, which remain poorly characterized. Nitrogenase genes associated with diverse non-cyanobacterial diazotrophs (NCDs) are prevalent, but their significance remains a huge knowledge gap. Answering questions, new and old, such as those discussed here, is needed to understand the ocean's N and C cycles and their responses to environmental change.

In silico and experimental approaches have allowed an ever-growing understanding of the interactions within the microbiota. For instance, recently acquired data have increased knowledge of the mechanisms that support, in the gut and vaginal microbiota, the resistance to colonization by Candida albicans, an opportunistic fungal pathogen whose overgrowth can initiate severe infections in immunocompromised patients. Here, we review how bacteria from the microbiota interact with C. albicans. We show how recent OMICs-based pipelines, using metagenomics and/or metabolomics, have identified bacterial species and metabolites modulating C. albicans growth. We finally discuss how the combined use of cutting-edge OMICs-based and experimental approaches could provide new means to control C. albicans overgrowth within the microbiota and prevent its consequences.

While the fungus Candida albicans is a common colonizer of healthy humans, it is also responsible for mucosal infections and severe invasive disease. Understanding the mechanisms that allow C. albicans to exist as both a benign commensal and as an invasive pathogen have been the focus of numerous studies, and recent findings indicate an important role for cross-kingdom interactions on C. albicans biology. This review highlights how C. albicans-bacteria interactions influence healthy polymicrobial community structure, host immune responses, microbial pathogenesis, and how dysbiosis may lead to C. albicans infection. Finally, we discuss how cross-kingdom interactions represent an opportunity to identify new antivirulence compounds that target fungal infections.

Marine species, such as corals and kelp, are responding to climate change by altering their distributions. Microbial biofilms underpin key processes that affect the establishment, maintenance, and function of these dominant habitat-formers. Climate-mediated changes to microbial biofilms can therefore strongly influence species' range shifts. Here, we review emerging research on the interactions between benthic biofilms and habitat-formers and identify two key areas of interaction where climate change can impact this dynamic: (i) via direct effects on biofilm composition, and (ii) via impacts on the complex feedback loops which exist between the biofilm microbes and habitat-forming organisms. We propose that these key interactions will be fundamental in driving the speed and extent of tropicalisation of coastal ecosystems under climate change.

Probiotics can be programmed to sense and respond to intracellular disease signals to deliver the desired therapeutic effectors. The sense-and-respond genetic circuits, especially self-tunable ones, hold promise in improving the precision, effectiveness, and intelligence of therapeutic activities. Here, we present notable advances in the creation of engineered probiotics that harbour sense-and-respond genetic circuits.

The retransmissions of SARS-CoV-2 from several mammals - primarily mink and white-tailed deer - to humans have raised concerns for the emergence of a new animal-derived SARS-CoV-2 variant to worsen the pandemic. Here, we discuss animal species that are susceptible to natural or experimental infection with SARS-CoV-2 and can transmit the virus to mates or humans. We describe cutting-edge techniques to assess the impact of a mutation in the viral spike (S) protein on its receptor and on antibody binding. Our review of spike sequences of animal-derived viruses identified nine unique amino acid exchanges in the receptor-binding domain (RBD) that are not present in any variant of concern (VOC). These mutations are present in SARS-CoV-2 found in companion animals such as dogs and cats, and they exhibit a higher frequency in SARS-CoV-2 found in mink and white-tailed deer, suggesting that sustained transmissions may contribute to maintaining novel mutations. Four of these exchanges, such as Leu452Met, could undermine acquired immune protection in humans while maintaining high affinity for the human angiotensin-converting enzyme 2 (ACE2) receptor. Finally, we discuss important avenues of future research into animal-derived viruses with public health risks.

Ongoing climate change will both profoundly impact land-use (e.g., changes in crop species or cultivar and cropping practices) and abiotic factors (e.g., moisture and temperature), which will in turn alter plant-microorganism interactions in soils, including soil-borne pathogens (i.e., plant pathogenic bacteria, fungi, oomycetes, viruses, and nematodes). These pathogens often cause soil-borne disease complexes, which, due to their complexity, frequently remain undiagnosed and unmanaged, leading to chronic yield and quality losses. Root exudates are a complex group of organic substances released in the rhizosphere with potential to recruit, repel, stimulate, inhibit, or kill other organisms, including the detrimental ones. An improved understanding of how root exudates affect interspecies and/or interkingdom interactions in the rhizosphere under ongoing climate change is a prerequisite to effectively manage plant-associated microbes, including those causing diseases.

Human gut bacteria produce metabolites that support energy and carbon metabolism of colonic epithelial cells. While butyrate is commonly considered the primary fuel, it alone cannot meet all the carbon requirements for cellular synthetic functions. Glucose, delivered via circulation or microbial metabolism, serves as a universal carbon source for synthetic processes like DNA, RNA, protein, and lipid production. Detailed knowledge of epithelial carbon and energy metabolism is particularly relevant for epithelial regeneration in digestive and metabolic diseases, such as inflammatory bowel disease and type 2 diabetes. Here, we review the production and role of different colonic microbial metabolites in energy and carbon metabolism of colonocytes, also critically evaluating the common perception that butyrate is the preferred fuel.

Interferon (IFN)-stimulated gene 15 (ISG15), a ubiquitin-like pleiotropic protein and one of the most abundant ISGs, has been studied extensively; however, its roles in SARS-CoV-2 and other viral infections have just begun to be elucidated. Emerging evidence suggests that ISG15 - either in its conjugated or unconjugated 'free' form - acts both intracellularly and extracellularly, and exerts anti- or pro-viral effects. To counteract ISG15's antiviral roles, viruses have evolved sophisticated tactics. Here, we discuss recent advances in ISG15's physiological functions as a post-translational modifier or 'cytokine-like' molecule during SARS-CoV-2 and other viral infections. Furthermore, we highlight the detailed mechanisms viruses use to block ISG15-dependent antiviral defenses. A comprehensive understanding of ISG15 biology in the context of virus infection may spur new therapeutic approaches for a range of viral infectious diseases.