Fibroblast activation in response to TGFβ1 is modulated by co-culture with endothelial cells in a vascular organ-on-chip platform.

Tissue fibrosis is a major healthcare burden that affects various organs in the body for which no effective treatments exist. An underlying, emerging theme across organs and tissue types at early stages of fibrosis is the activation of pericytes and/or fibroblasts in the perivascular space. In hepatic tissue, it is well known that liver sinusoidal endothelial cells (EC) help maintain the quiescence of stellate cells, but whether this phenomenon holds true for other endothelial and perivascular cell types is not well studied.

A high-throughput microfluidic bilayer co-culture platform to study endothelial-pericyte interactions.

Microphysiological organ-on-chip models offer the potential to improve the prediction of drug safety and efficacy through recapitulation of human physiological responses. The importance of including multiple cell types within tissue models has been well documented. However, the study of cell interactions in vitro can be limited by complexity of the tissue model and throughput of current culture systems.

Histone-like nucleoid-structuring protein represses transcription of the ehx operon carried by locus of enterocyte effacement-negative Shiga toxin-expressing Escherichia coli.

Shiga toxin-producing Escherichia coli (STEC) are a significant cause of zoonotic foodborne diarrheal disease in industrialized nations. In addition to Shiga toxin most STEC produce the enterohemolysin (EhxA) toxin. The EhxA toxin is encoded by the ehxCABD operon located on the large plasmid carried by STEC, yet its role in pathogenesis is unknown.