Dr. Tammy Ozment and Dr. Kun Yang Present Posters at Annual Shock Society Conference
Associate Professor Tammy Ozment and Assistant Professor Kun Yang, both of the Department of Surgery at Quillen College of Medicine, presented posters at the 46th annual Shock Society conference in Portland, Oregon.
Dr. Ozment presented a poster titled, “Neutrophil Dectin-3 Expression Correlates with Uptake ofE. Coli.” Invasive candidiasis (IC) is an increasingly common cause of hospital acquired infections.The mortality rate for IC can exceed 40%.Patients who develop IC are frequently critically ill with some degree of immunosuppression, most notably neutropenia or neutrophil dysfunction.Neutrophils are the first cellular line of defense against systemic fungal infections and are the best equipped to eliminate Candida.In the critically ill, neutrophils have been shown to have defects in their ability to internalize and kill pathogens. However, very little is known about the function of Dectin-3 in neutrophils in general and in human neutrophils in particular. Dr. Ozment said, “From the data we conclude that Dectin-1 stimulation, but not TLR2, TLR4, or Dectin-3 stimulation, increases neutrophil Dectin-3 expression.Additionally, Dectin-3 expression positively correlates with neutrophil uptake of E. coli, though it is not known to interact with E. coli ligands.This suggests that Dectin-3 could play a role in the neutrophil response to non-fungal infections.”
Dr. Yang’s poster was titled, “Lactate Inhibits Bacterial Phagocytosis and Clearance by Suppressing Hippo/YAP and NLRP3 in Macrophages.” Sepsis is a life-threatening disease that is characterized by organ dysfunction and dysregulated host innate and inflammatory responses to the infection. The defective eradiation of invading bacterial or other pathogens is a major cause of multiple organ dysfunction and death in sepsis. Elevated blood lactate levels are associated with severity and mortality of sepsis.
Dr. Yang said, “We recently observed that elevated serum lactate levels impair bacterial clearance in septic mice, as evidenced by increased bacterial burden, and increased mortality rate of septic mice. Mechanistically, we found that lactate suppresses NLRP3 inflammasome activation and induces YAP phosphorylation. Our results indicate a novel role of lactate in inhibiting macrophage phagocytosis and bacterial clearance during polymicrobial sepsis. Therefore, lactate/lactate-associated signaling may be promising target for sepsis treatment.”