title: Adrenergic regulation of complement-induced acute lung injury.
abstract: 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.
authors.affiliation: Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
authors.forename: Michael A
authors.initials: MA
authors.lastname: Flierl
authors.forename: Daniel
authors.initials: D
authors.lastname: Rittirsch
authors.forename: J Vidya
authors.initials: JV
authors.lastname: Sarma
authors.forename: Markus
authors.initials: M
authors.lastname: Huber-Lang
authors.forename: Peter A
authors.initials: PA
authors.lastname: Ward
mesh_terms: 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
chemical_list: D002395:Catecholamines; D011942:Receptors, Adrenergic, alpha; D011943:Receptors, Adrenergic, beta; D003165:Complement System Proteins; D009638:Norepinephrine