Researchers at Vanderbilt University Medical Center and the Nashville Veterans Affairs Medical Center have 'cracked' the genomic code for sepsis in the lungs and kidneys.
Sepsis-Causing Microbial Agents Sensed by Toll-Like Receptors and Other Extracellular and Intracellular Detectors Activate Multiple Transcription Factors in Immune and Non-Immune Cells . Credit:Researchers at Vanderbilt University Medical Center and the Nashville Veterans Affairs Medical Center have"cracked" the genomic code for sepsis in the lungs and kidneys.
"The problem of sepsis has been close to my heart and mind for the past two-and-a-half decades, since my mother succumbed to sepsis as a complication of stroke," he noted. Sepsis is rising at an alarming rate around the world, exceeding 49 million cases a year, as bacteria, viruses and other infectious organisms become resistant to the multiple drugs available to control them.
In 2014 Hawiger and his colleagues reported that the next-generation, cell-penetrating Nuclear Transport Checkpoint Inhibitor they developed blocked signaling pathways leading to lethal shock in animals exposed to the endotoxin lipopolysaccharide . This peptide selectively suppressed transport into the nucleus of transcription factors that turn on the genes responsible for the out-of-control inflammatory response. It also dramatically increased survival in mice exposed to high doses of LPS.
In the current study, which was supported in part by the U.S. Department of Veterans Affairs, the researchers used next-generation sequencing and quantitative reverse transcription techniques to determine the differential expression of thousands of genes in the lungs and kidneys of mice exposed to multiple, sepsis-causing microbes.
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