New Publications highlight SynVivo's Inflammation model in Sepsis and Inflammation Research

New Publications highlight the utility of SynVivo's Inflammation model to study Neutrophil-Endothelial Interactions during Sepsis and Inflammation

Dear Colleagues,

SynVivo's Inflammation Model is highlighted in two new publications that report on neutrophil-endothelial interactions and endothelial barrier function during Sepsis and Inflammation. See Download links below.

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“Experimental Approaches to Evaluate Leukocyte-Endothelial Cell Interactions in Sepsis and Inflammation”.

Laurie E. Kilpatrick , Mohammad F. Kiani (2020) SHOCK

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In sepsis, patients often die of organ failure and therapies directed against endothelial cell dysfunction and tissue damage are important targets for treatment of this disease. Novel approaches are required to understand the underlying pathophysiology of neutrophil dysregulation and neutrophil–endothelial cell interactions that play a critical role in the early course of organ damage and disruption of endothelial protective barrier. This review article presents methodologies to study neutrophil–endothelial interaction and endothelial barrier function in our in vivo and in vitro models of sepsis. We will focus on rodent models of sepsis and in vitro tools that use human cell culture models under static conditions and the more physiologically relevant biomimetic microfluidic assays.

" Neutrophil‐endothelial interactions of murine cells is not a good predictor of their interactions in human cells "

Fariborz Soroush , Yuan Tang , Omar Mustafa , Shuang Sun , Qingliang Yang , Laurie E. Kilpatrick , Mohammad F. Kiani (2020) FASEB

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All drugs recently developed in rodent models to treat inflammatory disease have failed in clinical trials. We therefore used our novel biomimetic microfluidic assay (bMFA) to determine whether the response of murine cells to inflammatory activation or anti‐inflammatory treatment is predictive of the response in human cells. Under physiologically relevant flow conditions, permeability and transendothelial electrical resistance (TEER) of human or mouse lung microvascular endothelial cells (HLMVEC or MLMVEC), and neutrophil‐endothelial cell interaction was measured. The differential impact of a protein kinase C‐delta TAT peptide inhibitor (PKCδ‐i) was also quantified. Results show that responses to activation and anti‐inflammatory treatment in mice may not always be predictive of their response in humans.