Subordinate social status modulates the vulnerability to the immunological effects of social stress

被引:19
作者
Avitsur, Ronit [1 ]
Kinsey, Steven G. [2 ]
Bidor, Kineret [1 ]
Bailey, Michael T. [3 ]
Padgett, David A. [3 ,4 ]
Sheridan, John F. [3 ,4 ]
机构
[1] Acad Coll Tel Aviv Yaffo, Sch Behav Sci, Yaffo, Israel
[2] Ohio State Univ, Dept Psychol, Columbus, OH 43210 USA
[3] Ohio State Univ, Sect Oral Biol, Coll Dent, Columbus, OH 43210 USA
[4] Ohio State Univ, Inst Behav Med Res, Columbus, OH 43210 USA
关键词
social hierarchy; social status; social disruption; glucocorticoid resistance; spleen; mice;
D O I
10.1016/j.psyneuen.2007.09.005
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Social stress has long been known to affect physical and psychological health in humans and a variety of animal species. In mice, disruption of the social hierarchy (social disruption, SDR) resulted in significant changes in the phenotype and function of immune cells taken from the spleen. Interestingly, there were considerable individual differences in the development of this splenic response to SDR. Studies have suggested that these individual differences were mediated by behavioral factors such as social hierarchy. To test this hypothesis, social status within cages of mate mice was identified before and after SDR. Results showed that in the majority of the cages social order was stable over time. In addition, examination of the association between social status and splenic function showed that the splenic response to SDR in subordinate mice was significantly augmented compared to dominants. This relationship between subordinate social status and the splenic response to social stress was more notable in cages with stable social hierarchies. To sum up, the current study showed a role for socio-behavioral factors in determining the response to stress. This study further demonstrated the complexity of factors playing a role in mediating the physiological response to social stress resulting in considerable individual differences in the response to stress. (C) 2007 Elsevier Ltd. All rights reserved.
引用
收藏
页码:1097 / 1105
页数:9
相关论文
共 20 条
  • [1] [Anonymous], BIOL LAB MOUSE
  • [2] Social stress and the regulation of tumor necrosis factor-α secretion
    Avitsur, R
    Kavelaars, A
    Heijnen, C
    Sheridan, JF
    [J]. BRAIN BEHAVIOR AND IMMUNITY, 2005, 19 (04) : 311 - 317
  • [3] Expression of glucocorticoid resistance following social stress requires a second signal
    Avitsur, R
    Padgett, DA
    Dhabhar, FS
    Stark, JL
    Kramer, KA
    Engler, H
    Sheridan, JF
    [J]. JOURNAL OF LEUKOCYTE BIOLOGY, 2003, 74 (04) : 507 - 513
  • [4] Social experience alters the response to social stress in mice
    Avitsur, R
    Stark, JL
    Dhabhar, FS
    Kramer, KA
    Sheridan, JF
    [J]. BRAIN BEHAVIOR AND IMMUNITY, 2003, 17 (06) : 426 - 437
  • [5] Social disruption-induced glucocorticoid resistance: kinetics and site specificity
    Avitsur, R
    Stark, JL
    Dhabhar, FS
    Padgett, DA
    Sheridan, JF
    [J]. JOURNAL OF NEUROIMMUNOLOGY, 2002, 124 (1-2) : 54 - 61
  • [6] Social stress alters splenocyte phenotype and function
    Avitsur, R
    Stark, JL
    Dhabhar, FS
    Sheridan, JF
    [J]. JOURNAL OF NEUROIMMUNOLOGY, 2002, 132 (1-2) : 66 - 71
  • [7] Social stress induces glucocorticoid resistance in subordinate animals
    Avitsur, R
    Stark, JL
    Sheridan, JF
    [J]. HORMONES AND BEHAVIOR, 2001, 39 (04) : 247 - 257
  • [8] Social interactions, stress, and immunity
    Avitsur, Ronit
    Padgett, David A.
    Sheridan, John F.
    [J]. NEUROLOGIC CLINICS, 2006, 24 (03) : 483 - +
  • [9] Physical defeat reduces the sensitivity of murine splenocytes to the suppressive effects of corticosterone
    Bailey, MT
    Avitsur, R
    Engler, H
    Padgett, DA
    Sheridan, JF
    [J]. BRAIN BEHAVIOR AND IMMUNITY, 2004, 18 (05) : 416 - 424
  • [10] Chronic psychosocial stress-induced down-regulation of immunity depends upon individual factors
    Bartolomucci, A
    Sacerdote, P
    Panerai, AE
    Peterzani, T
    Palanza, P
    Parmigiani, S
    [J]. JOURNAL OF NEUROIMMUNOLOGY, 2003, 141 (1-2) : 58 - 64