Dr. Chung's research interest involves the differential effects of SOCS proteins on immune cell/organ function in mouse models of shock and/or sepsis.
She also examines the mechanisms of how these proteins regulate cytokine/chemokine expression through JAK-STAT and other signaling pathways during the pathological process of shock and/or septic insults.
Biography
Dr. Chun-Shiang Chung is an Assistant Professor of Surgery (Research) at Rhode Island Hospital and The Warren Alpert School of Medicine.
Dr. Chung obtained her B.S and M.S degrees in botany at the Chinese Culture University and the National Chun-Hsing University in Taiwan. In 1992, Dr. Chung obtained a second M.S. degree in Microbiology and received her Ph.D. from the University of Rhode Island in 1997. Dr. Chung completed her postdoctoral training in Dr. Alfred Ayala's lab in the Department of Surgery's Division of Surgical Research at Rhode Island Hospital, and in 2002 received a faculty appointment to Instructor in Surgery (Research).
With a broad background in immunology and biochemistry and more than 15 years' expertise in the application of the murine model of sepis-cecal ligation and puncture, Dr. Chung has served as co-investigator on several of Dr. Ayala's NIH-funded grants over the past decade. In 2004, she was promoted to the rank of Assistant Professor of Surgery (Research) and continues to produce many peer-reviewed publications related to sepis-induced changes in apoptosis, immune and organ function. Dr. Chung has also served as an Ad Hoc reviewer for several journals in her field and as a mentor for many undergraduates, graduate and medical students and residents.
Research Overview
Trauma is the fifth leading cause of death in the United States. Of those trauma victims who survive the initial traumatic insult, sepsis and multiple organ failure are still reported to account for upwards of 40% of the mortality encountered in the surgical intensive unit. Despite the provision of the best surgical/medical/ pharmacological care. Many studies indicate that trauma/sepsis induces a marked suppression in both lymphocyte and macrophage function. In order to design better management of this devastating condition, it is critical to identify the precise mechanisms behind this immunosuppression of trauma/sepsis.
Research Statement
Inflammatory cells secret a wide variety of immunoregulatory mediators, such as pro- and anti-inflammatory cytokines, chemokines, prostanoids etc., at different stages during the course of the development of trauma/sepsis. Both pro- and anti-inflammatory cytokines are critical for the host to eliminate invasive agents after injury. However, many of these cytokines have also been implicated in having detrimental effects on organ function and eventual mortality seen in patients with severe traumatic injuries and/or sepsis. Following trauma and shock there appears to be loss of the normal regulatory function controlling the pro-inflammatory response. Over the years, the traditional studies on cytokines have focused on the mechanisms of how they set forth their actions. Recent investigations concerning regulation of the negative feedback of cytokine signaling have advanced considerably. Dysregulation of the negative feedback loops of JAK/STAT pathway has been implicated in autoimmune and inflammatory diseases, hematopoietic disorders, and cancers. Thus, it is important to understand the mechanisms by which signaling through the JAK/STAT pathway is negatively (downregulated) controlled. Several negative regulators of JAK/STAT pathway have been identified such as SH2-containing protein-tyrosine phosphatase (SHP-1), SH2-containing inositol phosphatase (SHIP), PTEN, CD45, and a new family of proteins, the suppressor of cytokines signaling (SOCS) family proteins. Using a mouse model of traumatic injury/shock, current studies are focused on the role of SOCS-1 and SOCS-3 in the immune response after injury. By understanding the molecular mechanism of negative regulatory pathways of the immune system should improve our knowledge of cytokine signaling associated with diseases and their contribution to pathology that could lead to the design of potentially novel therapeutic strategies for the treatment of trauma/shock.
Funded Research
- The US Shock Society/Novo Nordisk Grant
P.I.: Chun-Shiang Chung
Project: "Immune Hypo-Responsiveness in Shock: Role of SOCS-1 & SOCS-3 Proteins."
- NIH Research Grant R01-GM46354-11
P.I.: Alfred Ayala
Project: "Differential Effects of Sepsis on Macrophage Function."
Award: $1,562,905. 2008-2012
- NIH Research Grant R01-HL63898-01
P.I.: Alfred Ayala
Project: "Regulatory Mechanisms of Acute Lung Injury: Phagocyte Apoptosis."
Award: $1,413,967. 2008-2012
- NIH Research Grant R01-GM53209-10
P.I.: Alfred Ayala
Project: "Programmed Cell Death: Role In Septic Immune Suppression."
Award: $1,106,943. 2004-2009
- Brown University Health Developmental Grant
P.I.: Chun-Shiang Chung
Project: "Mechanisms of Immune Hypo-responsiveness in Shock."
Award: $28,490. 2004-2005
- Rhode Island Foundation Grant
P.I.: Chun-Shiang Chung
Project: "Mechanisms of Immune Hypo-responsiveness in Shock."
Award: $10,000. 2005-2005