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Texas A&M University · Pharmacology and Toxicology
Active 2013–2024
M. Karen Newell-Rogers, PhD, is a professor at Texas A&M University Naresh K. Vashisht College of Medicine with a background in microbiology and immunology. Her research broadly involves studying how an individual's immune response genes contribute to infectious and post-infectious chronic inflammatory syndromes, including Post-Traumatic Brain Injury Syndromes, Lyme Disease, Multiple Sclerosis, preeclampsia, and virally-induced autoimmune syndromes. She has also collaborated on work revealing a link between immune response and the progression of heart failure. Her research further explores how a cell's energy demands and strategies impact immune recognition, particularly targeting metabolic disruption in tumor cells to induce susceptibility to cell death or immune detection. A significant aspect of her work involves using peptide replacement strategies to reverse effects of chronic inflammatory diseases such as HIV/AIDS, MS, Lyme, and Crohn's disease. Her contributions have been recognized through awards, including the 2011 Hope Award from the Time for Lyme Foundation and her nomination as a TAMEST innovator protégé. Many of her technological innovations have been licensed to biotech companies and are in various stages of commercialization, including a Phase I clinical trial based at the University of Texas Health Sciences Center.
International Journal of Molecular Sciences · 2022-08-30 · 11 citations
TBI induces splenic B and T cell expansion that contributes to neuroinflammation and neurodegeneration. The vagus nerve, the longest of the cranial nerves, is the predominant parasympathetic pathway allowing the central nervous system (CNS) control over peripheral organs, including regulation of inflammatory responses. One way this is accomplished is by vagus innervation of the celiac ganglion, from which the splenic nerve innervates the spleen. This splenic innervation enables modulation of the splenic immune response, including splenocyte selection, activation, and downstream signaling. Considering that the left and right vagus nerves have distinct courses, it is possible that they differentially influence the splenic immune response following a CNS injury. To test this possibility, immune cell subsets were profiled and quantified following either a left or a right unilateral vagotomy. Both unilateral vagotomies caused similar effects with respect to the percentage of B cells and in the decreased percentage of macrophages and T cells following vagotomy. We next tested the hypothesis that a left unilateral vagotomy would modulate the splenic immune response to a traumatic brain injury (TBI). Mice received a left cervical vagotomy or a sham vagotomy 3 days prior to a fluid percussion injury (FPI), a well-characterized mouse model of TBI that consistently elicits an immune and neuroimmune response. Flow cytometric analysis showed that vagotomy prior to FPI resulted in fewer CLIP+ B cells, and CD4+, CD25+, and CD8+ T cells. Vagotomy followed by FPI also resulted in an altered distribution of CD11bhigh and CD11blow macrophages. Thus, transduction of immune signals from the CNS to the periphery via the vagus nerve can be targeted to modulate the immune response following TBI.
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