title: Dobutamine inhibits monocyte chemoattractant protein-1 production and chemotaxis in human monocytes.
abstract: It has been reported that, in patients with acute myocardial infarction or congestive heart failure, monocyte chemoattractant protein-1 (MCP-1) plays an important role in the development of inflammatory responses and that the level of MCP-1 is correlated with the severity of the disease. We conducted this study to investigate the effects of dobutamine and dopamine on lipopolysaccharide (LPS)-induced MCP-1 production in human monocytic THP-1 cells. Monocytes were incubated in vitro with LPS for 16 h at 37 degrees C in the presence or absence of dobutamine or dopamine. Enzyme-linked immunosorbent assay was used to examine the effect of dobutamine on MCP-1 synthesis, with the MCP-1 messenger RNA expression examined by reverse transcriptase-polymerase chain reaction. Dobutamine inhibited LPS-induced production of MCP-1, as well as messenger RNA expression, in a dose-dependent manner, whereas dopamine had no significant effect. Furthermore, we demonstrated that dobutamine suppressed MCP-1-induced chemotaxis and peak [Ca(2+)](i) in monocytic THP-1 cells. These findings suggest that dobutamine may modulate monocyte activation, such as chemotaxis and [Ca(2+)](i), as well as MCP-1 production, during therapy for congestive heart failure.
  
  
  CONCLUSIONS
  Monocyte chemoattractant protein-1 (MCP-1) plays important roles in the inflammatory processes associated with pathogenesis of cardiovascular diseases. In this study, dobutamine was found to inhibit lipopolysaccharide-induced MCP-1 production and messenger RNA expression, as well as MCP-1-induced chemotaxis and peak [Ca(2+)](i), in human monocytes.
authors.affiliation: Department of Anesthesiology, Tri-Service General Hospital, Taipei, Taiwan, Republic of China. cyli@ndmctsgh.edu.tw
authors.forename: Chi-Yuan
authors.initials: CY
authors.lastname: Li
authors.forename: Chien-Sung
authors.initials: CS
authors.lastname: Tsai
authors.forename: Sheau-Huei
authors.initials: SH
authors.lastname: Chueh
authors.forename: Ping-Ching
authors.initials: PC
authors.lastname: Hsu
authors.forename: Jia-Yi
authors.initials: JY
authors.lastname: Wang
authors.forename: Chih-Shung
authors.initials: CS
authors.lastname: Wong
authors.forename: Shung-Tai
authors.initials: ST
authors.lastname: Ho
mesh_terms: D000318:Adrenergic beta-Agonists / Q000494:pharmacology*; D000420:Albuterol / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism; D002465:Cell Movement / Q000187:drug effects; D018932:Chemokine CCL2 / Q000037:antagonists & inhibitors* / Q000096:biosynthesis*; D002633:Chemotaxis / Q000187:drug effects*; D003864:Depression, Chemical; D004280:Dobutamine / Q000494:pharmacology*; D004298:Dopamine / Q000494:pharmacology; D004591:Electrophoresis, Polyacrylamide Gel; D006801:Humans; D066298:In Vitro Techniques; D008070:Lipopolysaccharides / Q000494:pharmacology; D009000:Monocytes / Q000187:drug effects* / Q000378:metabolism*; D012333:RNA, Messenger / Q000096:biosynthesis; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D000318:Adrenergic beta-Agonists; D018932:Chemokine CCL2; D008070:Lipopolysaccharides; D012333:RNA, Messenger; D004280:Dobutamine; D000420:Albuterol; D002118:Calcium; D004298:Dopamine