Posted by SLS on January 3, 2013, at 7:37:50
In reply to T. gondii infection linked to bipolar risk, posted by firemonkey on January 3, 2013, at 2:04:18
Interesting.
Depressive disorders (MDD and BD) actually *suppress* the immune response to infection. It is not unexpected that someone with these illnesses should be less resistant to T. gondii. The "good" immune processes are reduced while the "bad" immune processes (inflammation) are increased. The whole immune system suffers from dysregulation in depressive disorders.
- Scott
---------------------------------------------
http://www.ncbi.nlm.nih.gov/pubmed/20955778Immune suppression and immune activation in depression.
Blume J, Douglas SD, Evans DL.
SourceDepartment of Psychiatry, University of Pennsylvania School of Medicine, 423 Guardian Drive, 305 Blockley Hall, Philadelphia, PA 19104, USA.
AbstractDepression has been characterized as a disorder of both immune suppression and immune activation. Markers of impaired cellular immunity (decreased natural killer cell cytotoxicity) and inflammation (elevated IL-6, TNFα, and CRP) have been associated with depression. These immunological markers have been associated with other medical illnesses, suggesting that immune dysregulation may be a central feature common to both depression and to its frequent medical comorbidities. Yet the significant associations of findings of both immune suppression and immune activation with depression raise questions concerning the relationship between these two classes of immunological observations. Depressed populations are heterogeneous groups, and there may be differences in the immune profiles of populations that are more narrowly defined in terms of symptom profile and/or demographic features. There have been few reports concurrently investigating markers of immune suppression and immune activation in the same depressed individuals. An emerging pre-clinical literature suggests that chronic inflammation may directly contribute to the pathophysiology of immune suppression in the context of illnesses such as cancer and rheumatoid arthritis. This literature provides us with specific immunoregulatory mechanisms mediating these relationships that could also explain differences in immune disturbances between subsets of depressed individuals We propose a research agenda emphasizing the assessment of these immunoregulatory mechanisms in large samples of depressed subjects as a means to define the relationships among immune findings (suppression and/or activation) within the same depressed individuals and to characterize subsets of depressed subjects based on shared immune profiles. Such a program of research, building on and integrating our knowledge of the psychoneuroimmunology of depression, could lead to innovation in the assessment and treatment of depression and its medical comorbidities.
Copyright © 2010 Elsevier Inc. All rights reserved.
--------------------------------------
Some see things as they are and ask why.
I dream of things that never were and ask why not.- George Bernard Shaw
poster:SLS
thread:1034536
URL: http://www.dr-bob.org/babble/20121231/msgs/1034546.html