Our Research
Bacteria play many roles in human health and disease, thus investigating host-microbiome communication is of great importance. To this end, our research demonstrates that serotonin, a neurotransmitter responsible for mood in the brain and motility in the guy, can act as a bacterial communication molecule for pathogenic bacteria, specifically Pseudomonas aeruginosa. Serotonin increases Pseudomonas virulence factor and biofilm production in vitro and enhances virulence in vivo, in a Pseudomonas infection mouse model we developed. These findings are beneficial in understanding the impact of the microbiome on human health and further study may open the door for novel treatments for human disease.
Inflammatory bowel disease (IBD) is a classification of autoimmune disorder that affects the gastrointestinal tract by inducing pain, vomiting, and diarrhea, among other symptoms. Currently over one million Americans suffer from IBD. As of yet, the cause of IBD is not fully understood but evidence suggests the human microbiome plays a significant role. As such it is important to understand the signaling processes between bacteria and environmental factors that may influence these processes. Bacteria signal one another with a group of molecules known as quorum sensing molecules (QSMs). These signaling pathways influence bacterial growth and gene expression. Previously, our lab has developed whole-cell based biosensors to detect the presence of particular QSMs, N-acyl homoserine lactone (AHL).
The level of the CD36 scavenger receptor at the cellular surface may influence a number of cellular signaling and transport events mediated by ligands that require CD36 for their action, such as fatty acids, oxLDL, parasites and bacteria. CD36 mediates recognition and phagocytosis of a variety of bacteria and interacts with bacterial lipids together with Toll-like Receptors 2 und 6, leading to the modulation of signal transduction important for native immunity and for inflammatory processes in response to bacterial pathogens. In cell culture, CD36 mediates uptake of Escherichia coli and Staphylococcus aureus, and the activation of the PI3K/Akt signaling pathways is important for the internalization of these bacteria by endothelial and epithelial cells.
Although great progress has been made in understanding of spinal cord injuries, SCI, there continue to be limits to improving quality of life. Many SCI patients experience continued GI issues including incontinence. Research in our group has shown increase in pro-inflammatory cytokines such as IL-6 and TNF-alpha in intestines of rats post-injury, as well as changes in bacteria communication and serotonin levels. Continued research into these changes will hopefully allow us to properly elucidate the mechanisms behind the gut inflammation and bowel problems experienced by patients with SCI.
Current treatment methods for Inflammatory Bowel Disease (IBD) have proven to be insufficient in improving the quality of life of patients. These treatments have focused on suppressing the inflammatory response but have ignored the damage already present in the gut. Mesenchymal stem cells (MSC) have been shown to, not only have anti-inflammatory properties, but also promote tissue repair. Previous studies using MSCs have been hindered by venous complications arising from the stem cell infusion.
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