Adrenergic regulation of complement-induced acute lung injury.
It is well established that catecholamines regulate immune and 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.
Flierl
Michael A
MA
Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
Rittirsch
Daniel
D
Sarma
J Vidya
JV
Huber-Lang
Markus
M
Ward
Peter A
PA
D055371:Acute Lung Injury / Q000378:metabolism*; D000313:Adrenal Medulla / Q000378:metabolism; D000818:Animals; D002395:Catecholamines / Q000378:metabolism; D003165:Complement System Proteins / Q000494:pharmacology*; D006801:Humans; D008954:Models, Biological; D009504:Neutrophils / Q000187:drug effects / Q000378:metabolism; D009638:Norepinephrine / Q000378:metabolism; D010586:Phagocytes / Q000187:drug effects / Q000378:metabolism; D011942:Receptors, Adrenergic, alpha / Q000502:physiology*; D011943:Receptors, Adrenergic, beta / Q000502:physiology*; D012128:Respiratory Distress Syndrome / Q000378:metabolism*; D013601:T-Lymphocytes / Q000187:drug effects / Q000378:metabolism
D002395:Catecholamines; D011942:Receptors, Adrenergic, alpha; D011943:Receptors, Adrenergic, beta; D003165:Complement System Proteins; D009638:Norepinephrine