TY - JOUR
T1 - Lymphocyte proliferation among major depressive and dysthymic patients with typical or atypical features
AU - Zaharia, Marilee D.
AU - Ravindran, Arun V.
AU - Griffiths, Jenna
AU - Merali, Zul
AU - Anisman, Hymie
N1 - Funding Information:
Supported in part by a grant from the Medical Research Council of Canada and the Pharmaceutical Manufacturers Associations of Canada (PMAC–MRC) in collaboration with Pfizer (Canada) Inc. H.A. is an Ontario Mental Health Foundation Senior Fellow. We are indebted to Lena DiPietro, Karen Gerbasi and Jerzy Kulczycki for their assistance.
PY - 2000/4
Y1 - 2000/4
N2 - Background: Depressive illness may be associated with immune and cytokine alterations. However, data are unavailable concerning functional immune changes associated with chronic, low-grade depression (dysthymia). Moreover, the contribution of the neurovegetative features of depression (e.g., altered sleep, eating) to the immune alterations remains to be determined. Methods: Mitogen-stimulated cell proliferation was assessed in major depressive and dysthymic patients exhibiting either typical or atypical features. In a subset of patients, lymphocyte proliferation was also assessed before and after pharmacotherapy to determine whether alleviation of symptoms would be accompanied by normalization of immune functioning. Results: Lymphocyte proliferation was reduced to a greater extent among dysthymic than among major depressive patients. Among dysthymic patients reduced cell proliferation was evident irrespective of symptom typicality; however, among major depressive patients the contribution of neurovegetative features varied with the specific mitogen used. Symptom alleviation following antidepressant treatment was not accompanied by normalization of cell proliferation. Limitations: Patients received 12 weeks of antidepressant treatment, and more sustained therapy may be required for normalization of immune activity. As well, conclusions concerning normalization of immune functioning in drug-treated major depressive patients requires that a greater number of patients be assessed. Conclusions: As the immune variations were more pronounced in dysthymia than in major depression, chronicity of illness may be a pertinent factor in promoting immune disturbances. This does not exclude the possibility that depression is associated with immune activation, which then provokes suppression of other aspects of immunity. As well, it is conceivable that immune alterations indirectly contribute to the symptoms accompanying depressive state, although it does not appear that variations of lymphocyte proliferation are associated with neurovegetative status. Copyright (C) 2000 Elsevier Science B.V.
AB - Background: Depressive illness may be associated with immune and cytokine alterations. However, data are unavailable concerning functional immune changes associated with chronic, low-grade depression (dysthymia). Moreover, the contribution of the neurovegetative features of depression (e.g., altered sleep, eating) to the immune alterations remains to be determined. Methods: Mitogen-stimulated cell proliferation was assessed in major depressive and dysthymic patients exhibiting either typical or atypical features. In a subset of patients, lymphocyte proliferation was also assessed before and after pharmacotherapy to determine whether alleviation of symptoms would be accompanied by normalization of immune functioning. Results: Lymphocyte proliferation was reduced to a greater extent among dysthymic than among major depressive patients. Among dysthymic patients reduced cell proliferation was evident irrespective of symptom typicality; however, among major depressive patients the contribution of neurovegetative features varied with the specific mitogen used. Symptom alleviation following antidepressant treatment was not accompanied by normalization of cell proliferation. Limitations: Patients received 12 weeks of antidepressant treatment, and more sustained therapy may be required for normalization of immune activity. As well, conclusions concerning normalization of immune functioning in drug-treated major depressive patients requires that a greater number of patients be assessed. Conclusions: As the immune variations were more pronounced in dysthymia than in major depression, chronicity of illness may be a pertinent factor in promoting immune disturbances. This does not exclude the possibility that depression is associated with immune activation, which then provokes suppression of other aspects of immunity. As well, it is conceivable that immune alterations indirectly contribute to the symptoms accompanying depressive state, although it does not appear that variations of lymphocyte proliferation are associated with neurovegetative status. Copyright (C) 2000 Elsevier Science B.V.
KW - Dysthymia
KW - Immune
KW - Lymphocyte proliferation
KW - Major depression
KW - Neurovegetative features
UR - http://www.scopus.com/inward/record.url?scp=0034175941&partnerID=8YFLogxK
U2 - 10.1016/S0165-0327(99)00100-7
DO - 10.1016/S0165-0327(99)00100-7
M3 - Article
C2 - 10760553
AN - SCOPUS:0034175941
SN - 0165-0327
VL - 58
SP - 1
EP - 10
JO - Journal of Affective Disorders
JF - Journal of Affective Disorders
IS - 1
ER -