Peter Chen's research while affiliated with University of Toronto and other places

Publications (10)

Article
Although sepsis in burn patients is a major contributor to mortality, treatments are not always effective and underlying mechanisms have yet to be completely elucidated. NLRP3 inflammasome orchestrates burn‐induced, inflammatory‐driven pathophysiologic processes. Here, we determined the mechanism of NLRP3 inflammasome activation on bacterial cleara...
Article
Background: During the past decades' sepsis has become the major cause of death in severely burned patients. Despite the importance of burn sepsis, its diagnosis, let alone its prediction, is difficult if not impossible. Recently, we have demonstrated burn patients have increased NLRP3 inflammasome activation in white adipose tissue. We aimed to d...
Article
The hypermetabolic stress response after burn contributes to multi-organ failure, sepsis, morbidity, and mortality. The cytokine interleukin 6 (IL-6) has been hypothesized to mediate not only white adipose tissue (WAT) browning in burns, but also other hypermetabolic conditions. In addition to its inflammatory effects, IL-6 also acts as a metabolic...
Article
Objective: Comparing the inflammatory and immunological trajectories in burned adults versus burned elderly patients to gain novel insights and better understanding why elderly have poor outcomes. Summary background data: Despite receiving the same treatment and clinical consideration as all other burn patients, elderly patients continue to have...
Article
Full-text available
Burn is accompanied by long-lasting immuno-metabolic alterations referred to as hypermetabolism that are characterized by a considerable increase in resting energy expenditure and substantial whole-body catabolism. In burned patients, the length and magnitude of the hypermetabolic state is the highest of all patients and associated with profoundly...
Article
Full-text available
Over the last decades advancements have improved survival and outcomes of severely burned patients except one population, elderly. The Lethal Dose 50 (LD50) burn size in elderly has remained the same over the past three decades, and so has morbidity and mortality, despite the increased demand for elderly burn care. The objective of this study is to...
Article
Sepsis can be defined as a systemic inflammatory response syndrome occurring in the presence of an infectious source. Over the past 25 years, numerous guidelines have been established to clarify definitions and improve the overall management of clinical sepsis. In light of these multiple paradigm shifts, this review attempts to summarize the innate...
Article
Severe thermal injury is associated with extreme and prolonged inflammatory and hypermetabolic responses, resulting in significant catabolism that delays recovery or even leads to multiple organ failure and death. Burned patients exhibit many symptoms of stress-induced diabetes, including hyperglycemia, hyperinsulinemia, and hyperlipidemia. Recentl...

Citations

... Sepsis is a common complication post burn injury and the leading cause of mortality in burn patients [1,2]. Indeed, burn patients are more prone to developing sepsis than other traumatic diseases, which is ascribed to a severe loss of skin barrier causing uncontrolled burn wound infection and inducing a persistent hyperinflammatory status [3]. Macrophages are a ubiquitous group of innate immune cells in host tissues and compartments where they serve as gatekeepers to recognize and respond to infection and tissue injury [4]. ...
... The ebb phase is present for a limited duration and is a period that dictates whether a patient will survive or succumb to burn injury-associated complications. Chen et al. previously showed that patients demonstrating abnormally high levels of proinflammatory IL-1b and decreased macrophages at the site of injury are highly susceptible to the development of sepsis (35). Furthermore, septic patients also had increased anti-inflammatory plasma cytokines such as interleukin-10 (IL-10) and interleukin-1RA (IL-1RA) (35). ...
... IL-6 levels are notably heightened after a burn injury, and the magnitude of elevation correlates to the severity of the injury, organ dysfunction, and poorer outcomes [122,123]. Data from animal studies suggest that IL-6 plays a role in the browning of the WAT, a major adverse event of burn hypermetabolism [124]. WAT browning caused hepatic steatosis and dysfunction and was associated with increased morbidity and mortality in burned mice [62]. ...
... New variants emerge rapidly, and vaccination, particularly when not recently boosted, has not consistently prevented infection by variants such as omicron (36), indicating more effective treatments are needed. In severe burns, cytokine storms are a threat to patient survival (37). These storms have been less severe in patients treated with nanosilver dressings, based on clinical observations. ...
... However, this process may not always be beneficial. Recent studies have discovered beiging of WAT in the development of hypermetabolic diseases such as burns and cancer, and it was thought to be a driver for fat wasting [43][44][45]. Recently, there have been limited studies reporting the beiging of WAT in HF. ...
... Burns affect seemingly every age group 2 . However, the mortality rate is signi cantly higher in elderly burn patients 35 . Regardless of age, severe burns cause damage to multiple organs distant from the original burn wound, leading to severe clinical problems such as multiple organ dysfunction syndrome (MODS) 3 . ...
... LPS-induced sepsis is considered an intoxication model, in which LPS is delivered as a single, large bolus of toxin, in contrast to the complex and repeated interactions between the microbial PAMPs and host PRRs that occur during polymicrobial IAI-mediated sepsis in mice and humans (Remick and Ward, 2005;Lewis et al., 2016). LPS administration in mice rapidly induces high circulating inflammatory cytokine levels, which peak much earlier than infection-induced sepsis (Rittirsch et al., 2007;Chen et al., 2014). Additionally, physiological effects are dose-dependent and large doses of LPS are required to induce responses similar to septic shock in mice (van der Poll, 2012;Chen et al., 2014). ...
... The nucleotide-binding domain and the leucine-rich, repeat-containing family, pyrin-containing 3 (NLRP3) inflammasome, mediate obesity-induced inflammation and insulin resistance (see Figure 3) [108]. Moreover, NLRP3 inflammasome was activated in the WAT of burn patients, indicating a possible function in conciliating burn-induced insulin resistance [109]. ...