Do Antidepressants Enhance Immune Function? Ex Vivo Results From HIV Positive Individuals With and Without Depression
New study published in Biological Psychiatry
Philadelphia, PA, May 8, 2008 – Infection with human immunodeficiency virus (HIV), which leads to acquired immunodeficiency syndrome (AIDS), is an epidemic of global concern. According to the most recent estimates, released in November 2007, by the Joint United Nations Programme on HIV/AIDS (UNAIDS) and the World Health Organization (WHO), an estimated 33.2 million worldwide are living with HIV infection currently. Although the rates of infection appear to be decreasing, there are obviously immense implications for achieving improvements in HIV/AIDS treatment.
The functioning of natural killer (NK) cells, which are a major element of the innate immunity system and are involved in the body’s first line of defense against infections such as HIV, is decreased in both HIV and depression. A group of researchers who have previously found that stress and depression impair NK cell function and accelerate the course of HIV/AIDS are now publishing a new report in the May 1st issue of Biological Psychiatry.
In this study, they recruited both depressed and non-depressed HIV-infected women and studied the ex vivo effects of three drugs, a selective serotonin reuptake inhibitor (SSRI), a substance P antagonist, and a glucocorticoid antagonist, on their NK cell activity. These drugs were selected because, as the authors state, each “affect[s] underlying regulatory systems that have been extensively investigated in both stress and depression research as well as immune and viral research.” The scientists found that the SSRI citalopram, and the substance P antagonist CP 96,345, but not the glucocorticoid receptor antagonist RU486, increased NK cell activity. According to Dr. Dwight Evans, corresponding author of the article: “The present findings provide evidence that natural killer cell function in HIV infection may be enhanced by selective serotonin reuptake inhibition and also by substance P antagonism in both depressed and non-depressed individuals.”
John H. Krystal, M.D., Editor of Biological Psychiatry and affiliated with both Yale University School of Medicine and the VA Connecticut Healthcare System, comments: “There has been growing evidence that the compromise of immune function associated with depression influences the outcomes of infectious diseases and cancer. Antidepressant treatments are beginning to be studied for their potential positive effects on immune function.” He adds that “the paper by Evans et al. suggests that antidepressant treatment may have positive effects on natural killer cell activity in cells isolated from individuals infected with HIV with and without depression. This type of bridge between the brain and the rest of the body deserves further attention.” Dr. Evans agrees, noting that “these findings begin to pave the way towards initiating clinical studies addressing the potential role of serotonergic agents and substance P antagonists in improving natural killer cell innate immunity, possibly delaying HIV disease progression and extending survival with HIV infection.”
# # #Notes to Editors:
The article is “Selective Serotonin Reuptake Inhibitor and Substance P Antagonist Enhancement of Natural Killer Cell Innate Immunity in Human Immunodeficiency Virus/Acquired Immunodeficiency Syndrome” by Dwight L. Evans, Kevin G. Lynch, Tami Benton, Benoit Dubé, David R. Gettes, Nancy B. Tustin, Jian Ping Lai, David Metzger and Steven D. Douglas. Drs. Evans, Lynch, Benton, Dubé, and Metzger and Mr. Gettes are affiliated with the Department of Psychiatry, with Dr. Evans also with the Departments of Medicine and Neuroscience, and Dr. Douglas is with the Department of Pediatrics, all at the University of Pennsylvania School of Medicine in Philadelphia, Pennsylvania. Ms. Tustin and Drs. Lai and Douglas are with the Division of Allergy and Immunology, Joseph J. Stokes Research Institute of The Children’s Hospital of Philadelphia, in Philadelphia, Pennsylvania. The article appears in Biological Psychiatry, Volume 63, Issue 9 (May 1, 2008), published by Elsevier.
Full text of the article mentioned above is available upon request. Contact Jayne M. Dawkins at (215) 239-3674 or firstname.lastname@example.org to obtain a copy or to schedule an interview.
About Biological Psychiatry
This international rapid-publication journal is the official journal of the Society of Biological Psychiatry. It covers a broad range of topics in psychiatric neuroscience and therapeutics. Both basic and clinical contributions are encouraged from all disciplines and research areas relevant to the pathophysiology and treatment of major neuropsychiatric disorders. Full-length and Brief Reports of novel results, Commentaries, Case Studies of unusual significance, and Correspondence and Comments judged to be of high impact to the field are published, particularly those addressing genetic and environmental risk factors, neural circuitry and neurochemistry, and important new therapeutic approaches. Concise Reviews and Editorials that focus on topics of current research and interest are also published rapidly.
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