Sungkyunkwan University · Medicine
Professor Doo Ryeon Chung's research lab focuses on the immunological mechanisms underlying bacterial infections and post-surgical complications, particularly in the context of antimicrobial resistance and host immune responses. The lab investigates how T cells, especially CD4+ alphabeta T cells, contribute to the pathogenesis of conditions such as intra-abdominal abscesses, peritoneal adhesions, and hospital-acquired pneumonia. Using translational animal models, the lab explores the role of bacterial antigens—such as zwitterionic capsular polysaccharides—in driving aberrant immune activation and tissue remodeling. Their work aims to identify novel therapeutic targets and improve clinical outcomes in severe infections and surgical complications.
Figures are computed from collected data and may differ slightly.
Acinetobacter spp., P. aeruginosa, S. aureus, and K. pneumoniae are the most frequent isolates from adults with HAP or VAP in Asian countries. These isolates are highly resistant to major antimicrobial agents, which could limit the therapeutic options in the clinical practice. Discordant initial empirical antimicrobial therapy significantly increases the likelihood of pneumonia-related mortality.
Abscess formation associated with intra-abdominal sepsis causes severe morbidity and can be fatal. Previous studies have implicated T cells in the pathogenesis of abscess formation, and we have recently shown that CD4(+) T cells activated in vitro by zwitterionic capsular polysaccharides from abscess-inducing bacteria such as Staphylococcus aureus and Bacteroides fragilis initiate this host response when transferred to naive rats. In this study, we show that mice deficient in alphabetaTCR-bearin
In patients with GNBSI, DTR was associated with higher mortality than those in other resistance categories. Our findings suggest that DTR could be useful for surveillance and prognostication.
The development of adhesions in the peritoneal and pelvic cavities, which commonly form after surgery or infection, cause significant morbidity and mortality. However, the pathogenesis of adhesion formation is still poorly understood. Because T cells are important in orchestrating fibrinogenic tissue disorders, we hypothesized that they play a critical role in the pathogenesis of peritoneal adhesion formation. Using a cecal abrasion surgical model in rodents, T cell depletion and adoptive transf
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