title: Acute stress differently modulates β1, β2 and β3 adrenoceptors in T cells, but not in B cells, from the rat spleen.
abstract: OBJECTIVE
  Stress-induced rise in circulating catecholamines (CAs), followed by modulation of β-adrenergic receptors (adrenoceptors, ARs), is one of the pathways involved in the stress-mediated effects of immune functions. The spleen is an organ with a high number of lymphocytes and provides a unique microenvironment in which they reside. Thus, lymphocytes may respond differently to CAs in the spleen than in the circulation. No reports exist concerning the involvement of β-ARs in stress-mediated effects on T and B cells isolated from the spleen. Therefore, our aim was to investigate the effect of single stress exposure on gene expression and cellular localization of β-adrenoceptor subtypes in splenic T and B cells. We tried to correlate changes in adrenoceptors with the expression of apoptotic proteins.
  
  
  METHODS
  Immobilization (IMMO) was used as a stress model. T and B cells were isolated from rat spleen using magnetically labeled antibodies. The gene expression of individual adrenoceptors and apoptotic proteins was evaluated by real-time PCR. Immunofluorescence was used to evaluate localization and adrenoceptor expression.
  
  
  RESULTS
  We have found T cells to be more vulnerable to stress compared to B cells, because of increased β₁-, β₂- and β₃-ARs after a single IMMO. Moreover, β₂-ARs translocated from the nucleus to the plasma membrane in T cells after IMMO. The rise in β-ARs most probably led to the rise of Bax mRNA and Bax to Bcl-2 mRNA ratio. This might suggest the induction of an apoptotic process in T cells.
  
  
  CONCLUSIONS
  Higher susceptibility of T cells to stress via modulation of β-ARs and apoptotic proteins might shift the immune responsiveness in the spleen.
authors.affiliation: Institute of Experimental Endocrinology, Center of Excellence CENDO and Center of Excellence for Cardiovascular Research, Slovak Academy of Sciences, Bratislava, Slovakia. marcelalau@email.cz
authors.forename: Marcela
authors.initials: M
authors.lastname: Laukova
authors.forename: Peter
authors.initials: P
authors.lastname: Vargovic
authors.forename: Lucia
authors.initials: L
authors.lastname: Csaderova
authors.forename: Lucia
authors.initials: L
authors.lastname: Chovanova
authors.forename: Miroslav
authors.initials: M
authors.lastname: Vlcek
authors.forename: Richard
authors.initials: R
authors.lastname: Imrich
authors.forename: Olga
authors.initials: O
authors.lastname: Krizanova
authors.forename: Richard
authors.initials: R
authors.lastname: Kvetnansky
mesh_terms: D000208:Acute Disease; D000818:Animals; D001402:B-Lymphocytes / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D002462:Cell Membrane / Q000276:immunology / Q000378:metabolism; D002467:Cell Nucleus / Q000276:immunology / Q000378:metabolism; D008297:Male; D021381:Protein Transport / Q000276:immunology; D051381:Rats; D017207:Rats, Sprague-Dawley; D018342:Receptors, Adrenergic, beta-1 / Q000378:metabolism*; D018343:Receptors, Adrenergic, beta-2 / Q000378:metabolism*; D022702:Receptors, Adrenergic, beta-3 / Q000378:metabolism*; D013154:Spleen / Q000166:cytology / Q000276:immunology / Q000378:metabolism; D013315:Stress, Psychological / Q000276:immunology / Q000378:metabolism*; D013601:T-Lymphocytes / Q000276:immunology* / Q000378:metabolism / Q000473:pathology
chemical_list: D018342:Receptors, Adrenergic, beta-1; D018343:Receptors, Adrenergic, beta-2; D022702:Receptors, Adrenergic, beta-3