Adrenergic Regulation of Complement-Induced Acute Lung Injury

It is well established that catecholamines regulate immune trod inflammatory responses. Until recently, they have been thought to derive from the adrenal medulla and from presynaptic neurons, when studies revealed that T cells, macrophages and neutrophils can also de novo synthesize and release endogenous catecholamines, which can then regulate immune cell functions in an autocrine/paracrine manner via engagement of adrenergic receptors. Accordingly, it appears that phagocytic cells and lymphocytes may represent a major, newly recognized source of catecholamines that regulate inflammatory responses.