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Sponsored by: |
National Institute of General Medical Sciences (NIGMS) |
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Information provided by: | National Institute of General Medical Sciences (NIGMS) |
ClinicalTrials.gov Identifier: | NCT00294697 |
Our overall hypothesis is that genetic variations in innate immunity genes predispose patients to varying responses after injury by altering the systemic and local inflammatory responses. In addition, we hypothesize that these genetic differences are associated with different clinical outcomes
Condition |
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Sepsis Pneumonia Trauma Burn Injury |
Study Type: | Observational |
Study Design: | Cohort, Prospective |
Official Title: | Genetics of Innate Immune Response After Burn Trauma |
Blood, Tissue, Fluids
Estimated Enrollment: | 1500 |
Study Start Date: | August 2003 |
Estimated Study Completion Date: | October 2009 |
The goal of this research proposal is to identify relationships that exist between specific genetic markers, immune responses to injury and infection (sepsis), and post injury clinical outcomes. Specifically, we will investigate the clinical impact of mutations involved in the innate immune response, which likely influence host response. To accomplish this goal we will collect and analyze data from patients with acute thermal injury, the most quantitative inflammatory stimulus experienced by humans. In addition, we propose to further characterize the immunologic response parameters to injury and infection, and their role in complicated sepsis. In this way, we will identify parameters associated with unfavorable clinical outcomes, and determine how these parameters differ among individuals with different genotypes. We propose to 1) evaluate associations between candidate SNPs within the NOD2/RIP2 signaling pathway and clinical outcome following burn injury, 2) evaluate the functional effects of alternate alleles at candidate SNPs; finally 3), we will use genetically engineered animal models to determine whether mutations in the NOD2 or RIP2 genes alter myocardial signal transduction mechanisms shown to play a role in myocardial inflammation/dysfunction after burn trauma. These approaches should allow us to evaluate more extensively clinically relevant interactions between specific genetic polymorphisms, the cellular expression of immune mediators, and burn-induced immune dysfunction. The proposed research should uncover genetic and/or acute immune-inflammatory parameters that identify patients who are at "high risk" and could as a result make possible the targeted design of pharmacologic intervention strategies that will inhibit the toxic effects of LPS and other bacterial pathogen components without paralyzing the host immunity of patients
Genders Eligible for Study: | Both |
Accepts Healthy Volunteers: | Yes |
Sampling Method: | Probability Sample |
Burn, Trauma, and Surgical Patients
Inclusion Criteria: All burn or trauma victims admitted to the burn or trauma center within 24 hours of injury will be considered for inclusion.
Exclusion Criteria:severe immunosuppression, DNR, severe trauma, terminal diseases.
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Contact: Fernando A Rivera, MD | 214-648-3534 | fernando.rivera@utsouthwestern.edu |
United States, Texas | |
UT Southwestern Medical Center at Dallas | Recruiting |
Dallas, Texas, United States, 75390-9160 | |
Principal Investigator: Fernando A Rivera, MD |
Principal Investigator: | Fernando A Rivera, MD | UT Southwestern Medical center |
Responsible Party: | UT Southwestern Medical Center ( Perry Adams ) |
Study ID Numbers: | 5K08GM071646-03 |
Study First Received: | February 21, 2006 |
Last Updated: | October 9, 2008 |
ClinicalTrials.gov Identifier: | NCT00294697 |
Health Authority: | United States: Institutional Review Board; United States: Federal Government |
polymorphisms innate immune response immunomonitoring immuno paralysis |
Burns Paralysis Sepsis Respiratory Tract Infections |
Respiratory Tract Diseases Lung Diseases Wounds and Injuries Pneumonia |