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.
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Acknowledgments
This work was supported by NIH grants GM 29507, GM 61656 and HL-31963 (to P.A.W.) and Deutsche Forschungsgemeinschaft grants DFG HU 823/2-2 and HU 823/2-3 (to M.H.-L).
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Flierl, M., Rittirsch, D., Vidya Sarma, J., Huber-Lang, M., Ward, P. (2008). Adrenergic Regulation of Complement-Induced Acute Lung Injury. In: Lambris, J. (eds) Current Topics in Complement II. Advances in Experimental Medicine and Biology, vol 632. Springer, New York, NY. https://doi.org/10.1007/978-0-387-78952-1_8
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