Presentation Title

Hyperglycemic attenuation of the innate immune response of the pulmonary system in diabetic patients with acute respiratory distress syndrome

Abstract

Acute respiratory distress syndrome (ARDS) is associated with 74500 deaths and 3.6 million hospital days in the United States ¹. It has been found that patients who suffer from Types I and II diabetes mellitus (DM) have consequently better recovery and survival from acute lung injury, yet the mechanism of the disease that is responsible for this outcome is unknown. It was hypothesized that that the factor that these types of the disease have in common, the presence of hyperglycemia, is responsible for the mediation of the immune response to lung inflammation. Murine models of Type I DM were injected daily intraperitoneally with STZ for five days until they exhibited a diabetic state. Subcutaneous osmotic insulin pumps were placed to restore insulin levels in experimental mice, while control mice received subcutaneous osmotic saline pumps. Fourteen days post pump placement, ARDS was induced through lipid polysaccharide nebulization and 24 hours post injury, the mice were euthanized for sample collection. Inflammation was measured through polymorphonuclear neutrophilic (PMN) counts relative to glucose, fructosamine, and insulin. Glucose levels served as real-time measurements of the metabolic state of the model, where fructosamine represented a long- term state of the model. Mediation of inflammation was demonstrated by a significant negative relationship between glucose and its corresponding PMN, a negative relationship between fructosamine and PMN, and a positive relationship between insulin and PMN. The hypothesis of the attenuated response of chronic hyperglycemia was supported due to the decreased inflammatory responses in an increasingly diabetic model, both acutely and chronically.

Primary Faculty Mentor Name

Benjamin Suratt

Secondary Mentor NetID

glenda.euceda (@uvmhealth.org)

Secondary Mentor Name

Glenda Euceda

Status

Undergraduate

Student College

College of Arts and Sciences

Program/Major

Neuroscience

Primary Research Category

Biological Sciences

This document is currently not available here.

Share

COinS
 

Hyperglycemic attenuation of the innate immune response of the pulmonary system in diabetic patients with acute respiratory distress syndrome

Acute respiratory distress syndrome (ARDS) is associated with 74500 deaths and 3.6 million hospital days in the United States ¹. It has been found that patients who suffer from Types I and II diabetes mellitus (DM) have consequently better recovery and survival from acute lung injury, yet the mechanism of the disease that is responsible for this outcome is unknown. It was hypothesized that that the factor that these types of the disease have in common, the presence of hyperglycemia, is responsible for the mediation of the immune response to lung inflammation. Murine models of Type I DM were injected daily intraperitoneally with STZ for five days until they exhibited a diabetic state. Subcutaneous osmotic insulin pumps were placed to restore insulin levels in experimental mice, while control mice received subcutaneous osmotic saline pumps. Fourteen days post pump placement, ARDS was induced through lipid polysaccharide nebulization and 24 hours post injury, the mice were euthanized for sample collection. Inflammation was measured through polymorphonuclear neutrophilic (PMN) counts relative to glucose, fructosamine, and insulin. Glucose levels served as real-time measurements of the metabolic state of the model, where fructosamine represented a long- term state of the model. Mediation of inflammation was demonstrated by a significant negative relationship between glucose and its corresponding PMN, a negative relationship between fructosamine and PMN, and a positive relationship between insulin and PMN. The hypothesis of the attenuated response of chronic hyperglycemia was supported due to the decreased inflammatory responses in an increasingly diabetic model, both acutely and chronically.