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Biology subjects

Ricordi, C.

Publications and source records attributed to Ricordi, C..

2 recordsLinked to original sources

Optimizing 3D-printed Scaffold Geometry Decreases Foreign Body Response and Enhances Allogeneic Islet Transplant Outcomes

Cellular therapy, such as beta cell transplantation for Type 1 diabetes, is a promising approach to durably alleviate disease states. Implanting cells within porous scaffolds is beneficial as they distribute the cells and mechanically support implantation; however, scaffolds can exacerbate foreign body responses (FBR). While the geometric features of a scaffold are known to impact FBR, there is limited consensus on what makes an ideal implant. Some have explored the role of pore size and interconnectivity; however, the impact of rung thickness between pores on FBR is broadly understudied. To investigate this parameter, we created a scaffold with reproducible geometric features and high biostability by combining 3D-printing with the polymer polydimethylsiloxane (PDMS). We tested 3D-printed scaffold prototypes with identical pore sizes but distinct PDMS rung thicknesses ranging from 150 to 300 {micro}m. Upon transplantation, biocompatibility screening in a mouse model revealed that scaffolds with thicker PDMS rungs led to increased intra-device fibrosis. Additional spatio-proteomic analysis revealed distinct differences in host responses to rung changes, with alterations in macrophage and adaptive immune cell markers, as well as fibrotic proteins, within scaffolds containing thicker rungs. Selecting the optimized rung size, we evaluated its efficacy in rat syngeneic and allogeneic islet transplant models. In the allogeneic model, 3D-printed scaffold islet implants demonstrated robust efficacy and stability, yielding improved outcomes compared to PDMS scaffolds without optimized geometric features. Results from this study reveal how specific geometric scaffold features critically influence FBR to biomaterial implants, accelerating or mitigating fibrotic responses, and ultimately determining transplant success.

bioengineering↗

Senescent cells in Giant Cell Arteritis have inflammatory phenotype participating in tissue injury via IL-6 dependent pathways

ObjectivesAge is the strongest risk factor of Giant Cell Arteritis (GCA), implying a possible pathogenetic role of cellular senescence. To address this question, we applied an established senescence specific multi-marker algorithm in tissue artery biopsies (TABs) of GCA patients. MethodsSeventy five positive TABs from GCA patients and 22 negative from patients with Polymyalgia Rheumatica (PMR) were retrospectively retrieved and analyzed. Senescent cells and their histologic origin were identified with specific cellular markers; IL-6 and MMP-9 were investigated as components of the senescent associated secretory phenotype (SASP) by triple co-staining. GCA or PMR artery culture supernatants were applied to primary skin fibroblasts with or without IL-6 blocking agent to explore the induction of IL-6 associated cellular senescence. ResultsSenescent cells were mainly present in GCA arteries at higher proportion compared to PMR (9.50% vs 2.66% respectively, p<0.0001) and were mainly originated from fibroblasts, macrophages and endothelial cells. IL-6 was expressed by senescent fibroblasts and macrophages while MMP-9 by fibroblasts only. IL-6 positive senescent cells were associated with the extension of vascular inflammation (adventitial limited disease vs transmural inflammation: 10.02% vs 4.37% respectively, p<0.0001). GCA but not PMR artery culture supernatant could induce IL-6-associated senescence that was partially inhibited by IL-6 blockade. ConclusionsSenescent cells with inflammatory phenotype are present in GCA arteries and are associated with the tissue inflammatory bulk. These findings might suggest a potential implication in disease pathogenesis by perpetuating inflammation and affecting vascular remodeling via IL-6 dependent mechanisms.

cell biology↗