Daniel G. Remick, M.D.
Chairman of Pathology and Laboratory Medicine
The laboratory focuses on investigating the inflammatory response with particular emphasis on cytokines. We are attempting to determine how the inflammatory response results in tissue/organ injury and death. To achieve this goal the laboratory uses a variety of methods ranging from whole animal models to isolated cells with reporter gene constructs. The ultimate focus of the lab is to understand the reaction to inflammation so that it may be modulated to improve health outcomes. It should be specifically noted that the modulation may include either blocking excessive inflammation or augmenting immunosuppression. The primary theme which ties together all of the projects is the careful measurement of cytokines. Cytokines are peptide mediators of the inflammatory response which represent critical components. They have been successfully modulated to improve health in patients with severe diseases.
There are several discrete projects within the laboratory.
Sepsis. Sepsis represents the host response to severe infections and results in substantial morbidity and mortality. The mortality for a septic patient exceeds 30% even in the best care situations. Our laboratory attempts to decipher the mechanisms for sepsis induced organ injury and mortality using a combination of a cell based approaches, whole animal experiments, and exploration of biomarker profiles in patients.
Asthma. Asthma represents another significant inflammatory condition with tremendous annual health-care costs. Our laboratory has developed a novel model of asthma like a pulmonary inflammation. Among children in inner cities, the major allergen which induces asthma comes from cockroaches rather than dog or cat allergens, or pollen. We collected dust from the homes were children had asthma and used this to induce asthma in the mouse. The mediators of inflammation are being explored and regulated.
Regulation of progression of acute inflammation Several aspects of the inflammatory response work together to induce a synthesis of specific inflammatory mediators. We are attempting to define the molecular events which allow the progression of acute inflammation, which may be different from those that start the response.
1. Osuchowski MF, Welch K, Yang H, Siddiqui J, Remick DG: Chronic sepsis mortality characterized by an individualized inflammatory response. J Immunol 179:623-630, 2007
2. Xing L, Remick DG: Promoter elements responsible for antioxidant regulation of MCP-1 gene expression. Antioxid Redox Signal 9:1979-1989, 2007
3. Natarajan S, Kim J, Remick DG: Acute pulmonary lipopolysaccharide tolerance decreases TNF-alpha without reducing neutrophil recruitment. J Immunol 181:8402-8408, 2008