"Feeling good" stimulates immune system
Feeling good may help our bodies fight germs better, according to results from experiments with mice. When activated, nerve cells that signal emotional reward also boost mouse immune systems.
Scientists in the Department of Immunology, Rappaport Faculty of Medicine, at Technion Israel Institute of Technology in Haifa, Israel, have observed positive feelings are linked with a supercharged immune system.
Their research may partially explain the placebo effect — a phenomenon in which a fake treatment can sometimes improve a patient's condition — simply because that person expects it will help.
results were reported on July 4th in Nature Medicine.
Scientists artificially increased the activity of nerve cells in the mice brains' ventral tegmental area (VTA) — a part of the brain thought to help produce feelings of reward. Tamar L. Ben-Shaanan PhD and his colleagues, found that VTA activation had a big effect on mice immune systems.
After confirmation that nerve cells in the VTA were activated, mice were then infected with E. coli bacteria. E. coli normally live in the intestines of people and animals. Most varieties are harmless. But a few nasty strains cause severe abdominal cramps, bloody diarrhea and vomiting.
Follow-up tests revealed fewer E. coli survived in mice with artificially stimulated VTA nerve cells, than in mice without stimulation of VTA nerve cells.
Immune cells also ramped up, as well. The number of monocytes increased. Monocytes are the largest of white blood cells which replenish macrophage blood cells in response to inflammation. Macrophages, too, increased thus becomming more effective at killing E. coli.
If a similar effect is found in humans, a biological explanation that positive thinking influences health will have been confirmed.
Positive expectations contribute to the clinical benefits of the placebo effect1, 2. Such positive expectations are mediated by the brain's reward system3, 4; however, it remains unknown whether and how reward system activation affects the body's physiology and, specifically, immunity. Here we show that activation of the ventral tegmental area (VTA), a key component of the reward system, strengthens immunological host defense. We used 'designer receptors exclusively activated by designer drugs' (DREADDs) to directly activate dopaminergic neurons in the mouse VTA and characterized the subsequent immune response after exposure to bacteria (Escherichia coli), using time-of-flight mass cytometry (CyTOF) and functional assays. We found an increase in innate and adaptive immune responses that were manifested by enhanced antibacterial activity of monocytes and macrophages, reduced in vivo bacterial load and a heightened T cell response in the mouse model of delayed-type hypersensitivity. By chemically ablating the sympathetic nervous system (SNS), we showed that the reward system's effects on immunity are, at least partly, mediated by the SNS. Thus, our findings establish a causal relationship between the activity of the VTA and the immune response to bacterial infection.
Return to top of page
Jul 6, 2016 Fetal Timeline Maternal Timeline News News Archive
(LEFT) immune cells from control mice infected with E. coli.
(RIGHT) activated VAT reward system has killed more E. coli.
Image Credit: Tamar Ben-Shaanan, Technion-Israel Institute of Technology, Haifa