Coronary artery disease (CAD) is the most common health problem worldwide and remains the leading cause of morbidity and mortality. Over the past decade, it has become clear that the inhabitants of our gut, the gut microbiota, play a vital role in human metabolism, immunity, and reactions to diseases, including CAD. Although correlations have been shown between CAD and the gut microbiota, demonstration of potential causal relationships is much more complex and challenging. In this review, we will discuss the potential direct and indirect causal roots between gut microbiota and CAD development via microbial metabolites and interaction with the immune system. Uncovering the causal relationship of gut microbiota and CAD development can lead to novel microbiome-based preventative and therapeutic interventions. However, an interdisciplinary approach is required to shed light on gut bacterial-mediated mechanisms (e.g., using advanced nanomedicine technologies and incorporation of demographic factors such as age, sex, and ethnicity) to enable efficacious and high-precision preventative and therapeutic strategies for CAD.

So much more to mucus: Mammals accommodate a dense community of metabolically active microorganisms in their gut. This is not a passive relationship, and host and microbe have antagonistic as well as mutualistic responses to each other. Using a whole-colon imaging method in mice, Bergstrom et al. looked at the role of colonic mucus in segregating the microbiota from host cells during elimination of feces (see the Perspective by Birchenough and Johansson). Host goblet cells synthesize two forms of mucin that differ in branched chain O-glycosylation and the site of production in the colon. A “thick” mucus in the proximal, ascending colon wraps the microbiota to form fecal pellets. Transit along the distal, descending colon is lubricated by “thin” mucus that transiently links with the thick mucus. Normal mucus encapsulation prevents inflammation and hyperplasia and thus is important for maintenance of a healthy gut. Science , this issue p. 467 ; see also p. 402

Fundamental restoration ecology and community ecology theories can help us better understand the underlying mechanisms of fecal microbiota transplantation (FMT) and to better design future microbial therapeutics for recurrent Clostridioides difficile infections (rCDI) and other dysbiosis-related conditions. In this study, stool samples were collected from donors and rCDI patients one week prior to FMT (pre-FMT), as well as from patients one week following FMT (post-FMT). Using metagenomic sequencing and machine learning, our results suggested that FMT outcome is not only dependent on the ecological structure of the recipients, but also the interactions between the donor and recipient microbiomes at the taxonomical and functional levels. We observed that the presence of specific bacteria in donors (Clostridioides spp., Desulfovibrio spp., Odoribacter spp. and Oscillibacter spp.) and the absence of fungi (Yarrowia spp.) and bacteria (Wigglesworthia spp.) in recipients prior to FMT could predict FMT success. Our results also suggested a series of interlocked mechanisms for FMT success, including the repair of the disturbed gut ecosystem by transient colonization of nexus species followed by secondary succession of bile acid metabolizers, sporulators, and short chain fatty acid producers.

Background: The escalating accumulation of micro- and nanoplastics (MNPs) in the environment has raised significant concerns regarding their neurotoxic potential in vertebrates. This critical review synthesizes evidence from 234 original research articles across aquatic and terrestrial models, as well as in vitro systems, to evaluate the impacts of MNPs on the brain. Main body: Emerging data suggest that MNPs may reach the brain via olfactory translocation or by penetrating the blood–brain barrier, potentially facilitated by biomolecular corona formation. However, distribution kinetics, long-term retention, and true internal exposure levels remain unresolved. We highlight that neurotoxic outcomes, such as oxidative stress, cholinergic dysfunction, neurotransmitter imbalances, and neuronal apoptosis, vary widely depending on particle size, shape, polymer type, exposure concentration, and host species. Nevertheless, inconsistencies across models and experimental conditions, such as mismatches between oxidative stress markers and behavioral effects or lack of dose-response relationships, hinder mechanistic clarity and translational relevance to human health. Notably, most current studies employ spherical polystyrene particles at supraphysiological concentrations, limiting ecological and clinical extrapolation. Interactions with microbial biofilms and host microbiota are largely unexplored, despite their probable role in modulating neurotoxicity via the gut–brain axis. Moreover, most studies rely on analytical methods validated only for microplastic detection, while robust, standardized approaches for identifying nanoplastics in environmental and biological matrices remain lacking. These gaps hinder accurate exposure quantification, obscure tissue-specific accumulation patterns, and complicate human health risk estimation. Conclusion: To advance the field, we recommend comprehensive physicochemical characterization of MNPs, adoption of environmentally relevant exposure scenarios, inclusion of diverse polymer types and shapes, and mechanistic integration through multi-omics and adverse outcome pathway frameworks. Addressing these challenges through harmonized methodologies and interdisciplinary collaboration is essential for developing predictive models of MNP-induced neurotoxicity and informing human health risk assessments. Graphical

Our study explores the pressing issue of micro- and nanoplastics (MNPs) inhalation and their subsequent penetration into the brain, highlighting a significant environmental health concern. We demonstrate that MNPs can indeed penetrate murine brain, warranting further investigation into their neurotoxic effects in humans. We then proceed to test the impact of MNPs at environmentally relevant concentrations, with focusing on variations in size and shape. Our findings reveal that these MNPs induce oxidative stress, cytotoxicity, and neurodegeneration in human neurons, with cortical neurons being more susceptible than nociceptors. Furthermore, we examine the role of biofilms on MNPs, demonstrating that MNPs can serve as a vehicle for pathogenic biofilms that significantly exacerbate these neurotoxic effects. This sequence of investigations reveals that minimal MNPs accumulation can cause oxidative stress and neurodegeneration in human neurons, significantly risking brain health and highlights the need to understand the neurological consequences of inhaling MNPs. Overall, our developed in vitro testing battery has significance in elucidating the effects of environmental factors and their associated pathological mechanisms in human neurons.

COVID-19 is a major pandemic facing the world today, which has implications on current microbiome-based treatments such as fecal microbiota transplantation (FMT) used for recurrent Clostridioides difficile infections. The bidirectional relationship between the inhabitants of our gut, the gut microbiota, and COVID-19 pathogenesis, as well as the underlying mechanism involved, must be elucidated in order to increase FMT safety and efficacy. In this perspective, we discuss the crucial cross-talk between the gut microbiota and the lungs, known as the gut–lung axis, during COVID-19 infection, as well as the putative effect of these microorganisms and their functional activity (i.e., short chain fatty acids and bile acids) on FMT treatment. In addition, we highlight the urgent need to investigate the possible impact of COVID-19 on FMT safety and efficacy, as well as instilling stringent screening protocols of donors and recipients during COVID-19 and post-COVID-19 pandemic to produce a cohesive and optimized FMT treatment plan across all centers and in all countries across the globe.