Do antidepressants enhance immune...( Philadelphia PA May 8 2008 Infectio...),Health

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 bodys 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. '/>"/>