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Bilik, S. M.

Publications and source records attributed to Bilik, S. M..

2 recordsLinked to original sources

Multi-omics identification of activated T cells and spatial PD-1/PD-L1 signaling as biomarkers of diabetic foot ulcer healing

Diabetic foot ulcers (DFUs) are a common and debilitating complication of diabetes, and amputations from non-healing ulcers carry high morbidity and mortality. A critical need exists for biomarkers that can identify healing potential early and guide targeted interventions. To address this, we applied an integrated multi-omics approach across four patient cohorts comprising 51 DFUs (29 Healing, 22 Non-healing). Bulk RNA-sequencing revealed marked activation of Th1 and Th2 pathways (activation z-score +4.8, p = 3.8x10-{superscript 1}), and immune cell deconvolution predicted higher proportions of T cell populations in Healers. Spatial proteomics in a second cohort identified elevated CD3 T cell density and selective enrichment of PD-1 and PD-L1 expression in vascular niches of the papillary dermis in Healers (p < 0.001). Flow cytometry in a third cohort further demonstrated higher proportions of CD3PD-1 and CD3PD-L1 T cells in Healers compared with Non-healers. Single-cell RNA-sequencing from a fourth cohort showed upregulation of PD-1 and PD-L1 within CD4 T cells from Healers. Complementary immunofluorescence and serological profiling confirmed that both PD-1 and PD-L1 are elevated in tissue and circulating serum of healing DFUs, supporting their potential use as systemic biomarkers. Taken together, vascular-enriched PD-1/PD-L1 signaling and T cell activation were observed in association with healing DFUs, supporting PD-1/PD-L1 as candidate biomarkers in both tissue and blood with potential translational relevance for predicting DFU outcomes and informing precision therapies.

immunology↗

A human ex vivo model of radiation-induced skin injury reveals p53-driven DNA damage signaling and recapitulates a TGFβ fibrotic response

Radiation-induced skin injury is a poorly understood complication affecting cancer patients who undergo radiotherapy, with no current therapies able to prevent or halt its progression to debilitating radiation-induced skin fibrosis (RISF). Addressing the need for clinically relevant human models, this study developed and characterized a human ex vivo skin model that recapitulates the temporal molecular processes of cutaneous radiation injury, as demonstrated through bulk RNA-sequencing and tissue validation studies. Human skin explants subjected to ionizing radiation demonstrated rapid induction of DNA double-strand breaks, followed by a robust, p53-driven transcriptional program involving genes related to cell cycle arrest, apoptosis, and senescence. Over time, the irradiated skin exhibited increasing activation of pro-fibrotic pathways, notably epithelial-mesenchymal transition and TGF{beta}1-mediated signaling. This resulted in upregulation of classic fibrosis markers such as COL1A1, FN1, and increased collagen thickness. Importantly, regulators of the p53 axis, MDM2 and miR-34a, was observed, implicating these factors as potential therapeutic targets to modulate the balance between repair of radiation injury and pathologic fibrosis. Transcriptome analysis of irradiated and non-irradiated breast skin from post-mastectomy patients showed notable concordance of p53 and pro-fibrotic gene signatures comparable to the ex vivo model, underscoring its translational relevance. This work provides a platform for identifying early biomarkers and testing therapeutic strategies to prevent or mitigate cutaneous radiation toxicities, including RISF, beginning with elucidating the dynamic interplay between the p53-mediated DNA damage response and the onset of fibrosis following radiation. Ultimately, this work aims to improve long-term skin health and quality of life for cancer patients. One Sentence SummaryHuman ex vivo skin recapitulates a clinically relevant p53-mediated DNA damage and pro-fibrotic response to radiation.

genomics↗