Emerging evidence has revealed that noradrenaline (NA), the main neurotransmitter of the sympathetic nervous system (SNS), regulates a variety of immune functions via binding to adrenergic receptors (ARs) present on immune cells. Recently, we found that treatment of neutrophils with NA significantly impaired neutrophil chemotaxis, and induced an anti-inflammatory phenotype with reduced expression of the genes critical for cytoskeleton remodelling and inflammation. Furthermore, superfusion of NA over the cremaster muscle almost completely inhibited fMLP-induced neutrophil adhesion/arrest and transmigration. Although the findings from our study indicate that neutrophil chemotaxis, activation and phagocytosis can all be negatively regulated in an NA-dependent manner, it is unclear how NA mediate impairment of neutrophil chemotaxis. In this project, we will examine the effect of adrenergic receptor deficiency on immune responses in a number of models of inflammation.
inflammation, neurotransmitter, neutrophils
School of Clinical Sciences at Monash Health / Hudson Institute of Medical Research » Medicine - Monash Medical Centre
Top-up scholarship funding available
Monash Health Translation Precinct (Monash Medical Centre)