title: Are adhesion molecules involved in stress-induced changes in lymphocyte distribution?
abstract: Acute psychological stress is associated with important changes in circulating cell populations and reductions in cell-mediated immune responses. However, the mechanisms underlying these phenomena are poorly understood. In this study, we investigated (i) acute and chronic restraint stress effects in Sprague-Dawley rats on peripheral lymphocyte subsets and (ii) adhesion molecule (beta2 integrins) expression and (iii) also determined whether glucocorticoids could underlie stress-related changes in cellular redistribution. We observed time-dependent changes in lymphocyte distribution including decreased (-21%) percentages of peripheral T helper cells and increased (88%) NK cell numbers following acute brief restraint. Acute stress was also found to overall upregulate beta2-integrin (CD11a and CD11b) expression on T cells and to raise (1049%) plasma corticosterone levels. However, this stress response was found habituated (-75% vs. acute) in the animals previously exposed to chronic restraint stress. Stress effects on circulating lymphocytes were not observed in animals previously exposed to chronic intermittent restraint stress or chronically stressed animals re-exposed to the same stressor. Our results indicate that 1) stress alters lymphocyte distribution, 2) that adhesion molecules may be involved in stress-induced alterations of T-cell distribution and 3) that these changes may be related to circulating glucocorticoids and subjected to adaptation with repeated stress exposure.
authors.affiliation: Division of Medicine, Dorothy Crowfoot Hodgkin Laboratories, University of Bristol, UK. mebauer@pucrs.br
authors.forename: M E
authors.initials: ME
authors.lastname: Bauer
authors.forename: P
authors.initials: P
authors.lastname: Perks
authors.forename: S L
authors.initials: SL
authors.lastname: Lightman
authors.forename: N
authors.initials: N
authors.lastname: Shanks
mesh_terms: D000208:Acute Disease; D000311:Adrenal Glands / Q000166:cytology / Q000502:physiology; D000818:Animals; D018821:CD18 Antigens / Q000378:metabolism*; D002452:Cell Count; D002908:Chronic Disease; D003345:Corticosterone / Q000097:blood; D016130:Immunophenotyping; D007694:Killer Cells, Natural / Q000166:cytology; D016169:Lymphocyte Function-Associated Antigen-1 / Q000096:biosynthesis; D016131:Lymphocyte Subsets / Q000166:cytology / Q000378:metabolism*; D016177:Macrophage-1 Antigen / Q000096:biosynthesis; D008297:Male; D009929:Organ Size; D051381:Rats; D017207:Rats, Sprague-Dawley; D012149:Restraint, Physical / Q000523:psychology; D013315:Stress, Psychological / Q000378:metabolism*; D006377:T-Lymphocytes, Helper-Inducer / Q000166:cytology / Q000378:metabolism; D013950:Thymus Gland / Q000166:cytology / Q000502:physiology; D013997:Time Factors; D015854:Up-Regulation
chemical_list: D018821:CD18 Antigens; D016169:Lymphocyte Function-Associated Antigen-1; D016177:Macrophage-1 Antigen; D003345:Corticosterone