Biology subjects

Wood, A. K.

Publications and source records attributed to Wood, A. K..

3 recordsLinked to original sources

bioRxiv2026

Postbiotic Binding of Micro- and Nanoplastics: In Vitro Intestinal Epithelial Protection and Proof of Concept in the Human Mouth

Micro- and nanoplastics (MNPs) are now recognized as ubiquitous dietary and environmental contaminants, yet practical strategies to reduce gastrointestinal exposure remain limited. This study evaluated whether Qi601, a heat-inactivated Limosilactobacillus fermentum biofilm-derived postbiotic, could bind plastic particles and reduce intestinal epithelial plastic burden. Prior probiotic studies have demonstrated live bacterial adsorption of MNPs and mitigation of MNP-associated toxicity in vivo; here, we evaluate whether a nonviable postbiotic preparation can produce analogous MNP-binding and epithelial-protective effects. Qi601 durably bound polystyrene nanoplastics under in vitro simulated digestion conditions. In Caco-2 intestinal epithelial monolayers, Qi601 reduced surface-associated and intracellular nanoplastic burden in both protection and rescue models, indicating decreased epithelial particle interaction both before and after established nanoplastic exposure. Multimodal imaging, including confocal microscopy, atomic force microscopy, and scanning electron microscopy, confirmed close physical association between Qi601 and nanoplastics. Finally, a first-in-human proof-of-concept chewing-gum study showed Qi601 binding in the human mouth to heterogeneous gum-derived microplastic fragments released during mastication. Together, these findings support the concept of postbiotic intervention for gastrointestinal epithelial protection against ingested MNPs.

microbiology↗

bioRxiv2026

Contact dependent suppression of Clostridioides difficile sporulation by enterococci requires the endocarditis and biofilm pilus

Clostridioides difficile is a healthcare-associated infection that arises when broad-spectrum antibiotic treatment disrupts the gut microbiota and is transmitted by highly resistant spores. Vancomycin-resistant Enterococcus faecium (VRE) is an opportunistic pathogen frequently co-isolated from C. difficile patients. We found that C. difficile sporulation is significantly reduced in VRE-C. difficile co-culture. Physical separation of C. difficile and VRE in transwell co-culture restored sporulation. Mixed macrocolony culture assays on solid agar confirmed physical contact is necessary for sporulation inhibition. We screened a panel of enterococci and found that most strains reduce sporulation, except Enterococcus saccharolyticus, which lacks predicted surface displayed virulence factors in its genome. We performed a candidate gene screen using an Enterococcus faecalis OG1RF transposon library and found that an insertion in the major pilin ebpC partially restored C. difficile sporulation in co-culture. These data were confirmed with in-frame deletions in the ebpABC pilus operon and a clinical isolate of E. feacalis lacking ebpABC. These findings suggest enterococci modulate C. difficile sporulation through a contact-dependent mechanism involving the Ebp pilus. ImportanceA characteristic of C. difficile infection is multiple episodes of acute disease. Spores are the transmission vector of C. difficile and are necessary for recurrence in models of disease. Our research demonstrates that C. difficile spore production is significantly reduced in the presence of enterococci, a common group of beneficial and pathogenic bacteria present in the gut microbiota. Physical contact with enterococci reduces C. difficile spore production. We attribute this effect to a protein structure on the surface of enterococci. This finding suggests a potential role for enterococci and the gut microbiota in general to uncover regulators of C. difficile spore formation. This may provide an avenue for innovative treatment strategies that reduce spore formation.

microbiology↗

bioRxiv2023

Acidification-dependent suppression of C. difficile by enterococci in vitro

Clostridioides difficile and Vancomycin-resistant Enterococcus faecium (VRE) are commonly co-isolated from hospitalized patients. We sought to develop a co-culture biofilm model to characterize interactions between these two opportunistic pathogens. Upon growth in biofilm-promoting media containing added glucose, fructose or trehalose, VRE produces sufficient acid to lower the pH and inhibit growth of C. difficile. We found this effect depended on the carbon source, and that acidification by VRE was necessary and sufficient to suppress C. difficile growth in liquid medium and in cecal content extracts from germ free mice. VRE frequently dominates the intestine of patients administered antibiotics which can predispose to the development of C. difficile infection. We reasoned that it may be possible to suppress C. difficile growth during co-infection with VRE by supplementing the mouse diet with a fermentable sugar. A VRE-dominated gut microbiota may convert the sugar to acid, lower the pH and reestablish colonization resistance to C. difficile. Supplementation of the diet of VRE colonized mice with high levels of fructose neither resulted in a lower pH, nor did it prevent colonization by C. difficile. Taken together, these data suggest that VRE can suppress growth of C. difficile by organic acid production in a carbon source-dependent manner in vitro, however, the mammalian intestine may require sophisticated approaches to lower pH therapeutically.

microbiology↗