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Biology subjects

Best, T.

Publications and source records attributed to Best, T..

4 recordsLinked to original sources

Nanofitin-Engineered Affinity Chromatography for Marker-Defined Extracellular Vesicle Enrichment in Scalable Downstream Processing

Extracellular vesicles (EVs) are lipid bilayer-enclosed particles that mediate intercellular communication through the transfer of bioactive molecules. Their growing relevance in translational applications demands downstream purification workflows that are selective, scalable, and compatible with robust impurity control. Conventional EV isolation methods primarily rely on physicochemical properties such as size, density, or charge and therefore co-enrich overlapping EV fractions together with non-vesicular impurities. Here, we establish a Nanofitin(R)-based affinity chromatography workflow for selective enrichment of a CD81-positive EV fraction under EV-compatible elution conditions. Nanofitin(R) candidate NF06 was identified by ribosome display against the large extracellular loop of CD81 and combined nanomolar affinity with favorable release behavior while retaining binding after repeated regeneration cycles. Static screening with recombinant CD81 and HEK293-derived EVs identified 1 M arginine at pH 10 as the most suitable elution condition. Dynamic chromatography on a 1 mL column using tangential flow filtration-concentrated HEK293 conditioned medium achieved 66.9% overall recovery with an elution step yield of 57.7%. In parallel, dsDNA, host cell protein, and total protein were reduced by 2 to 3 log relative to conditioned medium. Nano flow cytometry showed enrichment of the CD81-positive EV fraction from 40% in conditioned medium to more than 90% in the eluates, together with a smaller and narrower particle size distribution. These results demonstrate that Nanofitin(R)-based affinity chromatography provides a practical route toward marker-defined EV enrichment that combines selective capture, EV-compatible release, and substantial impurity clearance in a chromatography-compatible process format.

bioengineering↗

FAK inhibitor treatment systemically regulates the glioblastoma immune environment via blocking monocyte trafficking

Glioblastoma (GBM) is the most common primary malignant brain tumour in adults with dismal survival rates, and current therapies, including most immunotherapies, are not efficacious due to the highly immunosuppressive microenvironment. Studies in other solid cancers report that impairment of the integrin effector pathway involving focal adhesion kinase (FAK) can promote anti-tumour immune responses. Therefore, we set out to address whether, and if so how, suppressing FAK function may influence GBM by using both tumour cell-specific FAK gene deletion and systemic delivery of a clinically relevant FAK kinase inhibitor (FAKi) VS-4718 in an orthotopic murine stem cell model of GBM. We found that treatment with the FAKi, but not tumour cell-specific FAK gene deletion, resulted in GBM clearance and improved survival. This was dependent on adaptive immunity, and tumour-infiltrating T cells in FAKi-treated tumours displayed increased cytotoxic potential and reduced exhaustion. We also found a significant reduction in immuno-suppressive peripherally-derived macrophages and FAKi treatment caused sequestration of inflammatory monocytes within the bone marrow, resulting in impaired monocyte trafficking to tumours as judged by adoptive transfer. This is due to suppression of key adhesion and migration signalling through 4{beta}1 integrin and CX3CR1 in peripheral monocytes. Our work here describes a previously unidentified role for FAK in trafficking of peripheral suppressive macrophages to GBM tumours, reducing T cell exhaustion and promoting anti-tumour immunity. This highlights a new way in which systemic FAK inhibitors can be used to provide a beneficial immune modulatory strategy for the treatment of GBM.

immunology↗

Cerebellar and subcortical atrophy contribute to psychiatric symptoms in frontotemporal dementia

Recent studies have suggested that cerebellar and subcortical structures are impacted early in the disease progression of genetic frontotemporal dementia (FTD) due to microtubule-associated protein tau (MAPT), progranulin (GRN) and chromosome 9 open reading frame 72 (C9orf72). However, the clinical contribution of the structures involved in the cerebello-subcortical circuitry has been understudied in FTD given their potentially central role in cognition and behaviour processes. The present study aims to investigate whether there is an association between the atrophy of the cerebellar and subcortical structures, and neuropsychiatric symptoms (using the revised version of the Cambridge Behavioral Inventory, CBI-R) across genetic mutations and whether this association starts during the preclinical phase of the disease. Our study included 983 participants from the Genetic Frontotemporal dementia Initiative (GENFI) including mutation carriers (n=608) and non-carrier first-degree relatives of known symptomatic carriers (n= 375). Voxel-wise analysis of the thalamus, striatum, globus pallidus, amygdala, and the cerebellum was performed using deformation based morphometry (DBM) and partial least squares analyses (PLS) were used to link morphometry and behavioural symptoms. Our univariate results suggest that in this group of primarily presymptomatic subjects, volume loss in subcortical and cerebellar structure was primarily a function of aging, with only the C9orf72 group showing more pronounced volume loss in the thalamus compared to the non-carrier individuals. PLS analyses demonstrated that the cerebello-subcortical circuitry is related to all neuropsychiatric symptoms from the CBI-R, with significant overlap in brain/behaviour patterns, but also specificity for each genetic group. The biggest differences were in the extent of the cerebellar involvement (larger extent in C9orf72 group) and more prominent amygdalar contribution in the MAPT group. Finally, our findings demonstrated that C9orf72 and MAPT brain scores were related to estimated years before the age of symptom onset (EYO) in a second order relationship highlighting a steeper brain score decline 20 years before expected symptom onset, while GRN brain scores were related to age and not EYO. Overall, these results demonstrated the important role of the subcortical structures and especially of the cerebellum in genetic FTD symptom expression.

neuroscience↗

Cannabidiol Inhibits SARS-CoV-2 Replication and Promotes the Host Innate Immune Response

The rapid spread of COVID-19 underscores the need for new treatments. Here we report that cannabidiol (CBD), a compound produced by the cannabis plant, inhibits SARS-CoV-2 infection. CBD and its metabolite, 7-OH-CBD, but not congeneric cannabinoids, potently block SARS-CoV-2 replication in lung epithelial cells. CBD acts after cellular infection, inhibiting viral gene expression and reversing many effects of SARS-CoV-2 on host gene transcription. CBD induces interferon expression and up-regulates its antiviral signaling pathway. A cohort of human patients previously taking CBD had significantly lower SARS-CoV-2 infection incidence of up to an order of magnitude relative to matched pairs or the general population. This study highlights CBD, and its active metabolite, 7-OH-CBD, as potential preventative agents and therapeutic treatments for SARS-CoV-2 at early stages of infection.

microbiology↗