Biology subjects

Arthur, L.

Publications and source records attributed to Arthur, L..

3 recordsLinked to original sources

bioRxiv2026

Engineered living materials suppress uropathogenic E. coli growth and invasion of urothelial cells through sustained probiotic release

Recurrent urinary tract infection (rUTI) is a significant public health problem. The most common cause of rUTI is uropathogenic Escherichia coli (UPEC). Antimicrobial prophylactic and therapeutic regimens for rUTI disrupts the microbiome and leads to infection with antimicrobial resistant organisms. Therefore, there is an urgent need to develop microbiome-sparing alternative approaches for preventing rUTI. Asymptomatic bacteriuria (ABU) E. coli strain 83972 (ABEC) outcompetes UPEC in the urinary tract without causing UTI symptoms, but its limited persistence in the bladder restricts its efficacy. Here, we investigate a device made from an engineered living material (ELM) that releases ABEC in a sustained manner as an antibiotic-free platform against UTIs and rUTIs. Using physiologically relevant in vitro models incorporating human urothelial cells, human urine, and periodic urine exchange, we show that ABEC-releasing ELMs suppress UPEC proliferation and inhibit UPEC attachment to and invasion into urothelial cells, particularly when ABEC is maintained at equal or higher levels than UPEC. Because ELMs continuously release ABEC, they sustain competitive pressure even as planktonic bacteria are cleared during voiding, outperforming a single dose of free-floating ABEC. In a rUTI model, sustained ABEC release from ELMs reduces the proliferation and re-invasion of UPEC expelled from infected urothelial cells, while UPEC infiltration into fractured ELMs remains negligible. Finally, we design a first-generation ELM device that can be transurethrally delivered and retained within the mouse urinary bladder, achieving sustained ABEC release in vivo, with ABEC persisting in the bladder, kidneys, and urine for at least 4 days. In summary, we report the development of an ELM device that continuously releases ABEC to suppress UPEC proliferation and urothelial cell invasion in in vitro models of rUTI, and demonstrate sustained ABEC release in vivo in a mouse bladder.

bioengineering↗

bioRxiv2025

Preventing unintentional bat captures in canopy traps used for insect surveys

There is growing interest in deploying insect traps in forest canopies for ecological research, invasive species surveillance, and biodiversity monitoring. However, forest canopies also harbor a diverse and abundant bat community, which may be incidentally trapped and killed by these devices. In this study, we investigated the impact of flight interception traps and multi-funnel traps deployed in oak canopies on incidental bat captures, and evaluated whether trap modifications could reduce this bycatch. We also examined how these modifications influenced the species richness, abundance, and mean body size of several beetle taxa, including Buprestidae, Cerambycidae, Cetoniinae, and Scolytinae. Both trap types captured bats. Flight interception traps accidentally caught seven species - Myotis bechsteinii, Myotis daubentonii, Myotis mystacinus, Nyctalus noctula, Nyctalus leisleri, Plecotus auritus, and Pipistrellus pipistrellus - with an average of 0.42 bats per trap. Multi-funnel traps primarily caught males of P. pipistrellus, with an average of 0.29 bats per trap. Adding a 13-mm mesh above the collection container significantly reduced bat bycatch to 0.02 and 0.05 bats per trap in flight interception traps and multi-funnel traps, respectively. This modification had no significant effect on insect species richness or mean body size, although it did reduce Cerambycidae and Scolytinae abundance in black multi-funnel and flight interception traps, respectively. This was likely due to more frequent clogging by twigs and leaves. We recommend modifying flight interception and multi-funnel traps deployed in forest canopies to prevent unintentional harm to protected bat species.

ecology↗

bioRxiv2020

Epigenetic aging of classical monocytes from healthy individuals

The impact of healthy aging on molecular programming of immune cells is poorly understood. Here, we report comprehensive characterization of healthy aging in human classical monocytes, with a focus on epigenomic, transcriptomic, and proteomic alterations, as well as the corresponding proteomic and metabolomic data for plasma, using healthy cohorts of 20 young and 20 older individuals (~27 and ~64 years old on average). For each individual, we performed eRRBS-based DNA methylation profiling, which allowed us to identify a set of age-associated differentially methylated regions (DMRs) - a novel, cell-type specific signature of aging in DNA methylome. Optimized ultra-low-input ChIP-seq (ULI-ChIP-seq) data acquisition and analysis pipelines applied to 5 chromatin marks for each individual revealed lack of large-scale age-associated changes in chromatin modifications and allowed us to link hypo- and hypermethylated DMRs to distinct chromatin modification patterns. Specifically, hypermethylation events were associated with H3K27me3 in the CpG islands near promoters of lowly-expressed genes, while hypomethylated DMRs were enriched in H3K4me1 marked regions and associated with normal pattern of expression. Furthermore, hypo- and hypermethylated DMRs followed distinct functional and genetic association patterns. Hypomethylation events were associated with age-related increase of expression of the corresponding genes, providing a link between DNA methylation and age-associated transcriptional changes in primary human cells. Furthermore, these locations were also enriched in genetic regions associated by GWAS with asthma, total blood protein, hemoglobin levels and MS. On the other side, acceleration of epigenetic age in HIV and asthma stems only from changes in hypermethylated DMRs but not from hypomethylated loci.

systems biology↗