Literature DB >> 22999161

Catecholamine production is differently regulated in splenic T- and B-cells following stress exposure.

Marcela Laukova1, Peter Vargovic, Miroslav Vlcek, Katarina Lejavova, Sona Hudecova, Olga Krizanova, Richard Kvetnansky.   

Abstract

OBJECTIVES: Stress is accompanied also by a rise in splenic catecholamines (CAs). However, indications about endogenous CA production in the spleen exist but there are no data about the cellular source of this production and possible modification by stress. Therefore, our aim was to investigate whether splenic T- and B-cells are one of main sources in the spleen expressing tyrosine hydroxylase (TH), enzyme crucial for CA biosynthesis, and phenylethanolamine N-methyltransferase (PNMT) which is necessary for epinephrine production. We also investigated whether stress is able to modify expression of both enzymes and CA levels within these cell fractions as well as tried to explain functional consequences of changes observed.
RESULTS: T-cells contain higher levels of TH mRNA than B-cells although protein levels appeared similar. On contrary, the PNMT mRNA and protein were higher in B-cells, which appeared to be the main source of PNMT in the spleen. T-cells increased TH and PNMT expression after acute stress while similar rise was observed in B-cells after repeated stress, most probably as a consequence of higher CA turnover in both cell populations. The rise in TH and PNMT was accompanied by an elevation of Bax/Bcl-2 mRNA ratio, number of apoptotic cells and also by a decline of IFN-γ mRNA in both cell types. Reduction of IL-2 and IL-4 mRNA was also observed in B-cells.
CONCLUSION: Stress-induced stimulation of endogenous CA biosynthesis in lymphocytes is dependent on the type of lymphocyte population and duration of stressor and leads to attenuated IFN-γ expression and induction of apoptosis. These changes might contribute to dysregulation of specific immune functions involving T- and B-cells and may decrease the ability to cope with intracellular agents following stress situations.
Copyright © 2012 Elsevier GmbH. All rights reserved.

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Year:  2012        PMID: 22999161     DOI: 10.1016/j.imbio.2012.08.279

Source DB:  PubMed          Journal:  Immunobiology        ISSN: 0171-2985            Impact factor:   3.144


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