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Bio
The major basic science research focus of my research is clinical inflammation biology and the mechanisms and management of infection after injury and surgery. My lab is especially interested in the role of cellular “Danger” molecules, or “damage-associated molecular patterns” (aka “DAMPs” or “alarmins”) in inflammation. Our laboratory is a world leader in investigating the role of intracellular DAMPs derived from mitochondria. Our original work on this subject was published in Nature (March 4, 2010). It has been widely cited as a groundbreaking conceptual advance in sepsis and inflammation research, and has been cited more than 1,000 times. The known mitochondrial DAMPs include mitochondrial DNA, formyl peptides, and some of the mitochondrial lipids. Our recent work has shown that mitochondrial formyl peptides act as potent DAMPs. They circulate in plasma after injury where they activate innate immune cells while simultaneously causing heterologous suppression of cell-surface G-protein coupled receptors for critically important chemoattractants like chemokines and leukotrienes. Mitochondrial DNA is also a potent agonist that targets toll-like receptor 9 (TLR-9) and we have found that it is also a potent activator of neutrophil (PMN) extracellular traps (“NETs”). Signaling downstream from this receptor, however, may result in tolerance and so plays a critical role in suppression of immune function after injury.
Research Interests
Papers共 291 篇Author StatisticsCo-AuthorSimilar Experts
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Elsevier eBookspp.227-237.e1, (2024)
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Woon Yong Kwon,Yoon Sun Jung,Gil Joon Suh,Sung Hee Kim, Arum Lee,Jeong Yeon Kim,Ha Young Kim,Heesu Park,Jieun Shin,Taegyun Kim, Kyoung Su Kim,Kiyoshi Itagaki,
CRITICAL CARE MEDICINE (2024)
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Annals of surgery (2023)
The journal of trauma and acute care surgeryno. 2 (2022): 187-196
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