PMID- 9455873
OWN - NLM
STAT- MEDLINE
DCOM- 19980331
LR  - 20210526
IS  - 1071-412X (Print)
IS  - 1098-6588 (Electronic)
IS  - 1071-412X (Linking)
VI  - 5
IP  - 1
DP  - 1998 Jan
TI  - Induction of interleukin-4 and interleukin-5 expression in mast cells is 
      inhibited by glucocorticoids.
PG  - 18-23
AB  - Inflammation in asthma and other allergic diseases is characterized by excessive 
      production of immunoglobulin E (IgE) and the influx of leukocytes, especially 
      eosinophils. Interleukin 4 (IL-4) and IL-5 are essential for IgE production and 
      eosinophilia, respectively, and are produced by mast cells in allergic 
      conditions, for which glucocorticoids are widely used therapeutically. We 
      assessed the effect of glucocorticoids on IL-4 and IL-5 mRNA production by the 
      RBL-2H3 cell line, an analog of mucosal mast cells. IL-4 and IL-5 mRNAs were 
      induced by an antigen that is used to cross-link receptor bound IgE, by calcium 
      ionophore, or by ionophore with phorbol ester and were markedly inhibited by 
      dexamethasone. In cells activated with ionophore and phorbol ester, 10(-6) M 
      dexamethasone reduced the IL-4 and IL-5 mRNA levels to only 12.8 and 5.7%, 
      respectively, of those in cells without dexamethasone, and 10(-9) M dexamethasone 
      caused reductions to 27 and 56%, respectively. Hydrocortisone at 10(-6) and 
      10(-7) M almost completely inhibited IL-4 and IL-5 mRNA production. Dexamethasone 
      was markedly inhibitory even if it was added after the cells were activated, 
      provided that it was present in the cultures for at least 1.5 h. These studies 
      indicate that the expression of IL-4 and IL-5 mRNAs by mast cells is highly 
      sensitive to glucocorticoids. The data suggest that these inhibitory effects may 
      contribute to the clinical efficacy of glucocorticoids in the therapy of allergic 
      diseases.
FAU - Sewell, W A
AU  - Sewell WA
AD  - Centre for Immunology, University of New South Wales, and St. Vincent's Hospital, 
      Sydney, Australia. w.sewell@cfi.unsw.edu.au
FAU - Scurr, L L
AU  - Scurr LL
FAU - Orphanides, H
AU  - Orphanides H
FAU - Kinder, S
AU  - Kinder S
FAU - Ludowyke, R I
AU  - Ludowyke RI
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Clin Diagn Lab Immunol
JT  - Clinical and diagnostic laboratory immunology
JID - 9421292
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Glucocorticoids)
RN  - 0 (Interleukin-5)
RN  - 0 (RNA, Messenger)
RN  - 207137-56-2 (Interleukin-4)
RN  - 7S5I7G3JQL (Dexamethasone)
RN  - WI4X0X7BPJ (Hydrocortisone)
SB  - IM
MH  - Animals
MH  - Anti-Inflammatory Agents/pharmacology
MH  - Dexamethasone/pharmacology
MH  - Gene Expression
MH  - Glucocorticoids/*pharmacology
MH  - Hydrocortisone/pharmacology
MH  - Interleukin-4/analysis/*genetics
MH  - Interleukin-5/analysis/*genetics
MH  - Mast Cells/chemistry/*drug effects
MH  - RNA, Messenger/analysis/metabolism
MH  - Rats
MH  - Time Factors
MH  - Tumor Cells, Cultured/chemistry/drug effects
PMC - PMC121384
EDAT- 1998/02/10 00:00
MHDA- 1998/02/10 00:01
PMCR- 1998/01/01
CRDT- 1998/02/10 00:00
PHST- 1998/02/10 00:00 [pubmed]
PHST- 1998/02/10 00:01 [medline]
PHST- 1998/02/10 00:00 [entrez]
PHST- 1998/01/01 00:00 [pmc-release]
AID - 0070 [pii]
AID - 10.1128/CDLI.5.1.18-23.1998 [doi]
PST - ppublish
SO  - Clin Diagn Lab Immunol. 1998 Jan;5(1):18-23. doi: 10.1128/CDLI.5.1.18-23.1998.