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Biology subjects

Helmy, E.

Publications and source records attributed to Helmy, E..

2 recordsLinked to original sources

Lipid Nanoparticles for Spleen-Targeted RNA delivery

Lipid nanoparticles (LNPs) formulated with neutral helper lipids efficiently deliver RNA to the liver in pre-clinical models and humans but achieving clinically relevant delivery to other tissues remains a major challenge. To reduce liver uptake, targeting strategies often range from active targeting relying on antibodies to quasi-active targeting by employing permanently charged helper lipids which influence biodistribution after administration. In this study, we present an alternative approach based on varying ionizable lipids and stabilizers, along with optimizing formulation parameters for targeted delivery of circular RNA via a passive targeting approach. We generated a library of 216 LNP formulations and evaluated their performance in vitro in Jurkat cells and human primary T cells. The lead LNPs showcasing activity in both Jurkat and T cells were explored for their efficacy in vivo via multiple routes of administrations. Our results show that both the identity of stabilizer and ionizable lipid had effects on decreasing hepatic vs. splenic delivery while enhancing splenic accumulation. In line with this improved tissue tropism, spleen-tropic LNPs induced distinct transcriptomic remodeling in vivo compared with conventional, FDA-approved SM-102 LNPs. These findings demonstrate that extrahepatic targeting of LNPs can be achieved without altering charge of the LNPs and further reveal that hepatic de-targeting efficiency could be influenced by the immune status of the recipient.

bioengineering↗

SARS-CoV-2 spike protein induces abnormal inflammatory blood clots neutralized by fibrin immunotherapy

Blood clots are a central feature of coronavirus disease-2019 (COVID-19) and can culminate in pulmonary embolism, stroke, and sudden death. However, it is not known how abnormal blood clots form in COVID-19 or why they occur even in asymptomatic and convalescent patients. Here we report that the Spike protein from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) binds to the blood coagulation factor fibrinogen and induces structurally abnormal blood clots with heightened proinflammatory activity. SARS-CoV-2 Spike virions enhanced fibrin-mediated microglia activation and induced fibrinogen-dependent lung pathology. COVID-19 patients had fibrin autoantibodies that persisted long after acute infection. Monoclonal antibody 5B8, targeting the cryptic inflammatory fibrin epitope, inhibited thromboinflammation. Our results reveal a procoagulant role for the SARS-CoV-2 Spike and propose fibrin-targeting interventions as a treatment for thromboinflammation in COVID-19. One-Sentence SummarySARS-CoV-2 spike induces structurally abnormal blood clots and thromboinflammation neutralized by a fibrin-targeting antibody.

immunology↗