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. Key points The causal relationship between gut microbiota and CAD development has yet to be confirmed. It is imperative to understand the potential direct and indirect causal roots between gut microbiota and CAD development via microbial metabolites and interaction with the immune system. Dynamic elements including our diet and demographic factors such as age, sex, and ethnicity can also affect our gut microbiota and CAD development and complicate this matter. Interdisciplinary approaches are required to shed light on the factors involved in the modulation of gut microbiota and its association with CAD development. Elucidating the system-level multifaceted web of factors involved in microbiome-mediated mechanisms and human health and disease can guide novel preventative and therapeutic interventions for CAD.

Colon mucus segregates the intestinal microbiota from host tissues, but how it organizes to function throughout the colon is unclear. In mice, we found that colon mucus consists of two distinct O-glycosylated entities of Muc2: a major form produced by the proximal colon, which encapsulates the fecal material including the microbiota, and a minor form derived from the distal colon, which adheres to the major form. The microbiota directs its own encapsulation by inducing Muc2 production from proximal colon goblet cells. In turn, O-glycans on proximal colon–derived Muc2 modulate the structure and function of the microbiota as well as transcription in the colon mucosa. Our work shows how proximal colon control of mucin production is an important element in the regulation of host-microbiota symbiosis.

The development and application of bio-sourced composites have been gaining wide attention, yet their deterioration due to the growth of ubiquitous microorganisms during storage/manufacturing/in-service phases is still not fully understood for optimum material selection and design purposes. In this study, samples of non-woven flax fibers, hemp fibers, and mats made of co-mingled randomly-oriented flax or hemp fiber (50%) and polypropylene fiber (50%) were subjected to 28 days of exposure to (i) no water-no fungi, (ii) water only and (iii) water along with the Chaetomium globosum fungus. Biocomposite samples were measured for weight loss over time, to observe the rate of fungal growth and the respiration of cellulose components in the fibers. Tensile testing was conducted to measure mechanical properties of the composite samples under different configurations. Scanning electron microscopy was employed to visualize fungal hyphal growth on the natural fibers, as well as to observe the fracture planes and failure modes of the biocomposite samples. Results showed that fungal growth significantly affects the dry mass as well as the tensile elastic modulus of the tested natural fiber mats and composites, and the effect depends on both the type and the length scale of fibers, as well as the exposure condition and time.