One of the major clinical sequelae of critically injured burn patients is the subsequent development of septic complications. Loss of dermal barrier and significant immune dysregulation following burn injury set them at particular risk for septic complications. Initiation and orchestration of innate immune signals through neutrophils, monocyte/macrophages and dendritic cells are considered early responses to injury and infection. Another primitive and early response system in host-defense is the sympathetic activation resulting in massive release of adrenergic hormones (catecholamines) commonly referred to as "fight or flight" phenomenon. Currently, adrenergic agonists and antagonists are extensively used as a therapeutic modality in several patient populations including critically injured burn and septic patients. Therefore it is essential to know the impact of catecholamines on macrophages that are considered central to robust host-defense. Since tissue macrophages are constantly replenished from the bone marrow compartment- a highly innervated organ, it becomes an important target for neuro-immune modulation. The focus of Dr. Muthu’s laboratory is to study the impact of adrenergic mechanisms regulating hematopoietic development and function of macrophages. More specifically, they are 1) elucidating adrenergic receptor expression in bone marrow progenitors, 2) studying the phenotypic and phagocytic responses of bone marrow progenitor derived macrophages to adrenergic stimuli during differentiation, and 3) investigating the mechanistic links between adrenergic stimulation and the transcriptional regulation of monocytopoiesis (monocyte commitment) following burn injury and sepsis. Understanding adrenergic regulation of innate immune cell production and function can provide new insights into the immunological impact adrenergic drugs can have especially in the critically injured patients.