Document Detail


Non-genomic rapid inhibition of Na+/H+-exchange 1 and apoptotic immunosuppression in human T cells by glucocorticoids.
MedLine Citation:
PMID:  20143335     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Glucocorticoids (GCs) have been employed as immunosuppressive agents for many years. However, it is still unclear how GCs instantly uncouple T cells from acute stressful inflammatory. In terms of time scale, the genomic activity of the classic GC receptor cannot fulfill this role under crisis; but a rapid non-genomic response can. In a previous study, intracellular acidification was found to be due to a rapid non-genomic inhibition of Na(+)/H(+)-exchange 1 (NHE1) and this event led to the immunosuppression of T cell proliferation by progesterone. The aim of this study was to examine whether there is a rapid acidification response caused by an inhibition of NHE1 activity and to explore the differential non-genomic effect on immunosuppression of hydrocortisone and dexamethasone. The IC(50) values for NHE1-dependent pH(i) recovery by hydrocortisone and dexamethasone are 250 and 1 nM, respectively. Co-stimulation of GCs with phytohemagglutinin (PHA) is able to inhibit PHA-induced IL-2 secretion, IL-4 secretion, and T-cell proliferation. Furthermore, apoptosis in PHA-activated T cells is not induced by hydrocortisone but by dexamethasone. The mechanism of immunosuppression on proliferation by dexamethasone was found to be different of hydrocortisone and seems to involve cytotoxicity against T cells. Moreover, apoptosis induced by dexamethasone and impermeable dexamethasone-bovine serum albumin suggests that the apoptotic immunosuppression occurs through both the plasma membrane and cytoplasmic sites. The rapid inhibitory responses triggered by GCs would seem to release T cells instantly when an acute stress-related response is needed. Nonetheless, the apoptotic immunosuppression by dexamethasone is attributable to its severe cytotoxicity.
Authors:
Ching-Pang Chang; Shyi-Wu Wang; Zih-Ling Huang; Olivia Ya-Hsuan Wang; Michael I-Ta Huang; Li-Ming Lu; Der-Cherng Tarng; Chau-Heng Chien; Eileen Jea Chien
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of cellular physiology     Volume:  223     ISSN:  1097-4652     ISO Abbreviation:  J. Cell. Physiol.     Publication Date:  2010 Jun 
Date Detail:
Created Date:  2010-04-07     Completed Date:  2010-04-21     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0050222     Medline TA:  J Cell Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  679-86     Citation Subset:  IM    
Copyright Information:
(c) 2010 Wiley-Liss, Inc.
Affiliation:
Institute of Physiology, School of Medicine, National Yang-Ming University, Taipei, Taiwan, Republic of China.
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MeSH Terms
Descriptor/Qualifier:
Adult
Amiloride / analogs & derivatives,  pharmacology
Apoptosis / drug effects*
Cation Transport Proteins / antagonists & inhibitors*
Cell Survival / drug effects
Dexamethasone / pharmacology*
Dose-Response Relationship, Drug
Genome, Human / genetics
Glucocorticoids / pharmacology*
Humans
Hydrocortisone / pharmacology*
Hydrogen-Ion Concentration / drug effects
Immunosuppression*
Interleukin-2 / secretion
Interleukin-4 / secretion
Lymphocyte Activation / drug effects
Male
Sodium-Hydrogen Antiporter / antagonists & inhibitors*
T-Lymphocytes / immunology*,  secretion
Tetradecanoylphorbol Acetate / pharmacology
Thymidine / metabolism
Tritium
Young Adult
Chemical
Reg. No./Substance:
0/Cation Transport Proteins; 0/Glucocorticoids; 0/Interleukin-2; 0/SLC9A1 protein, human; 0/Sodium-Hydrogen Antiporter; 10028-17-8/Tritium; 1214-79-5/5-dimethylamiloride; 16561-29-8/Tetradecanoylphorbol Acetate; 207137-56-2/Interleukin-4; 2609-46-3/Amiloride; 50-02-2/Dexamethasone; 50-23-7/Hydrocortisone; 50-89-5/Thymidine

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