PMID- 8777955
OWN - NLM
STAT- MEDLINE
DCOM- 19960917
LR  - 20190821
IS  - 0903-1936 (Print)
IS  - 0903-1936 (Linking)
VI  - 9
IP  - 2
DP  - 1996 Feb
TI  - Role of cyclic AMP in the modulation of IgE production by the beta 2-adrenoceptor 
      agonist, fenoterol.
PG  - 220-5
AB  - We have previously demonstrated that the beta 2-adrenoceptor agonist, salbutamol, 
      potentiates the effect of interleukin-4 (IL-4) on immunoglobulin E (IgE) 
      production by human peripheral blood mononuclear cells (PBMC). This study was 
      undertaken to further define the activities of these drugs and the role of 
      cyclic-adenosine monophosphate (cAMP) in the modulation of IgE production. Our 
      results indicate that fenoterol (1 microM) potentiated IL-4-induced IgE 
      production and IgE messenger ribonucleic acid (mRNA) expression. Moreover, this 
      effect was associated with an increase in intracellular cAMP levels. The 
      activities of this drug on IgE production were mimicked by cell permeable cAMP 
      analogues, such as dibutyryl-cAMP (db-cAMP) (100 microM) or Sp-AMP (10 microM). 
      The potentiating effect of fenoterol on IgE production was markedly inhibited in 
      the presence of protein kinase A (PKA) inhibitors: H8 (10 microM) and Rp-AMP (10 
      microM), suggesting that its effects are likely to depend on the activation of 
      the cAMP pathway. Additionally, the potentiating effect of fenoterol was also 
      blocked in the presence of indomethacin. Fenoterol potentiated IL-4-induced IgE 
      production from purified B-cells activated through their CD40 antigen. This 
      effect was associated with an increase in cellular viability. Therefore, the 
      activities of this drug on PBMC are likely to be mediated by the activation of 
      another cellular type. Taken together, these results show that fenoterol 
      potentiates the IL-4-induced IgE production via the cAMP pathway, but that this 
      enhancement could not be explained by a direct effect on B-lymphocytes.
FAU - Coqueret, O
AU  - Coqueret O
AD  - Departement d'Immunologie, Institut Henri Beaufour, Les Ulis, France.
FAU - Demarquay, D
AU  - Demarquay D
FAU - Lagente, V
AU  - Lagente V
LA  - eng
PT  - Journal Article
PL  - England
TA  - Eur Respir J
JT  - The European respiratory journal
JID - 8803460
RN  - 0 (Adrenergic beta-Agonists)
RN  - 0 (Cyclooxygenase Inhibitors)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (RNA, Messenger)
RN  - 207137-56-2 (Interleukin-4)
RN  - 22M9P70OQ9 (Fenoterol)
RN  - 37341-29-0 (Immunoglobulin E)
RN  - E0399OZS9N (Cyclic AMP)
RN  - EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases)
RN  - XXE1CET956 (Indomethacin)
SB  - IM
MH  - Adrenergic beta-Agonists/*pharmacology
MH  - B-Lymphocytes/drug effects/metabolism
MH  - Blotting, Northern
MH  - Cyclic AMP/metabolism/*physiology
MH  - Cyclic AMP-Dependent Protein Kinases/antagonists & inhibitors
MH  - Cyclooxygenase Inhibitors/pharmacology
MH  - Drug Synergism
MH  - Enzyme Inhibitors/pharmacology
MH  - Fenoterol/antagonists & inhibitors/*pharmacology
MH  - Humans
MH  - Immunoglobulin E/*biosynthesis/genetics
MH  - Indomethacin/pharmacology
MH  - Interleukin-4/pharmacology
MH  - Leukocytes, Mononuclear/drug effects/metabolism
MH  - RNA, Messenger/biosynthesis
EDAT- 1996/02/01 00:00
MHDA- 1996/02/01 00:01
CRDT- 1996/02/01 00:00
PHST- 1996/02/01 00:00 [pubmed]
PHST- 1996/02/01 00:01 [medline]
PHST- 1996/02/01 00:00 [entrez]
AID - 10.1183/09031936.96.09020220 [doi]
PST - ppublish
SO  - Eur Respir J. 1996 Feb;9(2):220-5. doi: 10.1183/09031936.96.09020220.