Effects of stress on susceptibility and severity of inflammation in adjuvant-induced arthritis

被引:14
作者
Chover-Gonzalez, AJ
Harbuz, MS
Tejedor-Real, P
Gibert-Rahola, J
Larsen, PJ
Jessop, DS
机构
[1] Univ Bristol, Div Med, Dept Clin Med, Bristol BS2 8HW, Avon, England
[2] Univ Cadiz, Dept Neurosci, Cadiz, Spain
[3] Univ Copenhagen, Panum Inst, Dept Med Anat B, DK-2200 Copenhagen, Denmark
来源
NEUROENDOCRINE IMMUNE BASIS OF THE RHEUMATIC DISEASES | 1999年 / 876卷
基金
英国惠康基金;
关键词
D O I
10.1111/j.1749-6632.1999.tb07650.x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
We have utilized the open field and learned helplessness (LH) models of psychological stress to determine whether a differential response to stress can affect the severity of adjuvant-induced arthritis (AA) within a single rat strain,In response to open field stress, the corticosterone response of the low emotivity rats was significantly lower than that of the high emotivity rats, In spite of the differential corticosterone response to stress, no significant difference was found in paw volumes between the AA high and low emotivity groups, In another study, rats were subjected to a learned LH paradigm and separated into two groups based on failed (LH+) or successful (LH-) avoidance. Plasma corticosterone levels in response to avoidable foot shock in the LH- rats were significantly greater than in the LH+ group. Following injection with adjuvant, paw inflammation occurred earlier and was more severe in the LH- rats compared to the LH+ group, These data show that rats with a greater tendency to avoid foot shock have more severe inflammation, despite having a greater corticosterone response to stress, We conclude that an increased corticosterone I response to stress does not affect susceptibility: to or severity! of inflammation in;AA, Indeed, in the LH model a more robust response to stress is associated with increased inflammation and earlier onset of the disease.
引用
收藏
页码:276 / 286
页数:11
相关论文
共 37 条
[31]   CORTICOTROPIN RELEASING HORMONE RELATED BEHAVIORAL AND NEUROENDOCRINE RESPONSES TO STRESS IN LEWIS AND FISCHER RATS [J].
STERNBERG, EM ;
GLOWA, JR ;
SMITH, MA ;
CALOGERO, AE ;
LISTWAK, SJ ;
AKSENTIJEVICH, S ;
CHROUSOS, GP ;
WILDER, RL ;
GOLD, PW .
BRAIN RESEARCH, 1992, 570 (1-2) :54-60
[32]  
VANDELANGERIJT AGM, 1993, CLIN EXP IMMUNOL, V94, P150
[33]   CORTICOSTEROID METABOLISM AND RHEUMATOID ARTHRITIS [J].
WEST, HF .
ANNALS OF THE RHEUMATIC DISEASES, 1957, 16 (02) :173-182
[34]  
WICK G, 1993, ENDOCR REV, V14, P539, DOI 10.1210/er.14.5.539
[35]   THYMUS-DEPENDENT AND THYMUS-INDEPENDENT REGULATION OF IA-ANTIGEN EXPRESSION INSITU BY CELLS IN THE SYNOVIUM OF RATS WITH STREPTOCOCCAL CELL WALL-INDUCED ARTHRITIS - DIFFERENCES IN SITE AND INTENSITY OF EXPRESSION IN EUTHYMIC, ATHYMIC, AND CYCLOSPORINE-A-TREATED LEW AND F344 RATS [J].
WILDER, RL ;
ALLEN, JB ;
HANSEN, C .
JOURNAL OF CLINICAL INVESTIGATION, 1987, 79 (04) :1160-1171
[36]   THE VALIDITY OF ANIMAL-MODELS OF DEPRESSION [J].
WILLNER, P .
PSYCHOPHARMACOLOGY, 1984, 83 (01) :1-16
[37]   Examination of changes in interpersonal stress as a factor in disease exacerbations among women with rheumatoid arthritis [J].
Zautra, AJ ;
Hoffman, J ;
Potter, P ;
Matt, KS ;
Yocum, D ;
Castro, L .
ANNALS OF BEHAVIORAL MEDICINE, 1997, 19 (03) :279-286