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Fortmann, S. D.

Publications and source records attributed to Fortmann, S. D..

3 recordsLinked to original sources

Fixation Before Dissociation Using a Deep Eutectic Solvent Preserves In Vivo States and Phospho-Signaling in Single-Cell Sequencing

Single-cell RNA-sequencing (scRNA-seq) presents an opportunity to deconstruct cellular networks but is limited by the loss of biological information, including in vivo cellular states and phospho-signaling. Herein, we present fixation before dissociation using a deep eutectic solvent (DES), which preserves multiple domains of in vivo biological data, including morphology, RNA, proteins, and post-translational modifications. In scRNA-seq of viable versus DES bone marrow, dissociation induced global stress responses, immune and stromal cell activation, and loss of highly sensitive cell populations, which were prevented with DES. Further, we introduce a validated and flexible method for performing intracellular CITE-seq in DES-fixed cells. Leveraging this approach during Th17 T cell stimulation allowed the simultaneous quantification of transcriptomes and four phosphorylated proteins, leading to the identification of a hyperactivated state in p-ERK/p-FOS double positive cells, which we experimentally validated. We anticipate that DES-based fixatives will allow the accurate reconstruction of in vivo cellular networks and uncover cooperativity amongst intracellular pathways.

immunology↗

Plasma microbiome in COVID-19 subjects: an indicator of gut barrier defects and dysbiosis

The gut is a well-established route of infection and target for viral damage by SARS-CoV-2. This is supported by the clinical observation that about half of COVID-19 patients exhibit gastrointestinal (GI) symptoms. We asked whether the analysis of plasma could provide insight into gut barrier dysfunction in patients with COVID-19 infection. Plasma samples of COVID-19 patients (n=30) and healthy control (n=16) were collected during hospitalization. Plasma microbiome was analyzed using 16S rRNA sequencing, metatranscriptomic analysis, and gut permeability markers including FABP-2, PGN and LPS in both patient cohorts. Almost 65% (9 out 14) COVID-19 patients showed abnormal presence of gut microbes in their bloodstream. Plasma samples contained predominately Proteobacteria, Firmicutes, and Actinobacteria. The abundance of gram-negative bacteria (Acinetobacter, Nitrospirillum, Cupriavidus, Pseudomonas, Aquabacterium, Burkholderia, Caballeronia, Parabhurkholderia, Bravibacterium, and Sphingomonas) was higher than the gram-positive bacteria (Staphylococcus and Lactobacillus) in COVID-19 subjects. The levels of plasma gut permeability markers FABP2 (1282{+/-}199.6 vs 838.1{+/-}91.33; p=0.0757), PGN (34.64{+/-}3.178 vs 17.53{+/-}2.12; p<0.0001), and LPS (405.5{+/-}48.37 vs 249.6{+/-}17.06; p=0.0049) were higher in COVID-19 patients compared to healthy subjects. These findings support that the intestine may represent a source for bacteremia and may contribute to worsening COVID-19 outcomes. Therapies targeting the gut and prevention of gut barrier defects may represent a strategy to improve outcomes in COVID-19 patients.

microbiology↗

Selective LXR agonist, DMHCA, corrects the retina-bone marrow axis in type 2 diabetes

In diabetic dyslipidemia, cholesterol accumulates in the plasma membrane, decreasing fluidity and thereby suppressing the ability of cells to transduce ligand-activated signaling pathways. Liver X receptors (LXRs) are the main cellular mechanism by which intracellular cholesterol is regulated and play important roles in inflammation and disease pathogenesis. N,N-dimethyl-3{beta}-hydroxy-cholenamide (DMHCA), a selective LXR agonist, specifically activates the cholesterol efflux arm of the LXR pathway without stimulating triglyceride synthesis. Thus, DMHCA possesses superior clinical potential as a cholesterol lowering agent than current LXR pan-agonist. In this study, we use a multi-systems approach to understand the effects and molecular mechanisms of DMHCA treatment in type 2 diabetic db/db mice and human -derived circulating angiogenic cells (CACs), which are vascular reparative cells. We find that DMHCA is sufficient to correct the retina-bone marrow (BM) axis in diabetes, thereby restoring retinal structure, function, and cholesterol homeostasis, rejuvenating membrane fluidity in circulating vascular reparative cells, hampering systemic inflammation, and correcting BM dysfunction. Using single-cell RNA-seq on lineage-sca1+cKit+ (LSK) hematopoietic stem cells (HSCs) from untreated and DMHCA-treated diabetic mice, we provide novel insights into hematopoiesis and reveal DMHCAs mechanism of action in correcting diabetic HSCs by reducing myeloidosis and increasing CACs and erythrocyte progenitors. Taken together, these findings demonstrate the broad and pleiotropic effects of DMHCA treatment, which has exciting potential to correct the retina-BM axis in diabetic subjects.

cell biology↗