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.
KeywordsAcute Lung Injury Chromaffin Cell Adrenal Medulla Phagocytic Cell Endogenous Catecholamine
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).
- BaerwaldC. G.Laufenberg, M., Specht, T., von Wichert, P., Burmester, G. R., and Krause, A. (1997) Impaired sympathetic influence on the immune response in patients with rheumatoid arthritis due to lymphocyte subset-specific modulation of beta 2-adrenergic receptors. Br J Rheumatol 36, 1262–1269PubMedCrossRefGoogle Scholar
- Czermak,B. J.Sarma, V., Bless, N. M., Schmal, H., Friedl, H. P., and Ward, P. A. (1999b) In vitro and in vivo dependency of chemokine generation on C5a and TNF-alpha. J Immunol 162, 2321–2325Google Scholar
- Flierl, M. A.Rittirsch, D., Nadeau, B. A., Chen, A. J., Sarma, J. V., Zetoune, F. S., McGuire, S. R., List, R. P., Day, D. E., Hoesel, L. M., Gao, H., Van Rooijen, N., Huber-Lang, M. S., Neubig, R. R., and Ward, P. A. (2007) Phagocyte-derived catecholamines enhance acute inflammatory injury. Nature 449, 721–725PubMedCrossRefGoogle Scholar
- Loeper, andM.Crouzon,O.(1904) L’action de l’adrenaline sur le sang. Arch Med Exp Anat Pathol 16, 83–108Google Scholar
- Wang, H., Yu, M., Ochani, M., Amella, C. A., Tanovic, M., Susarla, S., Li, J. H., Wang, H., Yang, H., Ulloa, L., Al-Abed, Y., Czura, C.J., and Tracey, K. J. (2003) Nicotinic acetylcholine receptor alpha7 subunit is an essential regulator of inflammation. Nature 421, 384–388PubMedCrossRefGoogle Scholar