Stress is commonly thought to increase susceptibility to disease, but a new study in Brain, Behavior, and Immunity finds short-term stress can actually boost the immune system and help reduce the number of skin cancer tumors in mice.

Squamous cell carcinoma Image: Wikimedia Commons

"It does not make sense that stress should always or necessarily be harmful since its most basic form is the fight-or-flight response," Firdaus Dhabhar, the lead author of the paper and a neuroimmunologist from Stanford University, wrote in an email. "In nature, the ability to mount stress responses is essential for survival."

Previous studies, including several from Dhabhar's lab, have shown that acute stress can help fight infection and enhance immune function. But this latest paper, which appeared online at the journal's website ahead of print publication, is the first to demonstrate its effects on cancer.

"These findings are very exciting," said Rainer Straub, a neuroimmunologist at the University of Regensburg in Germany, who was not involved with the study. "They clearly show that [Dhabhar's] work is going in a clinical direction. It is promising research."

The researchers exposed healthy mice to ultraviolet B light (UVB) three times a week to induce squamous cell carcinoma tumor growth. For three weeks, half of the mice were placed in well-ventilated plastic tubes for two and a half hours before their UVB exposure, the restricted movement causing short-term psychological stress. The team then monitored tumor growth in 30 mice from each group for 21 weeks.

Fewer acutely stressed mice developed tumors than the non-stressed group, and the small percentage of stressed mice that did had less of them. Acutely stressed mice also showed higher levels of several cytokines and chemokines, proteins that regulate immune responses and cell trafficking. Specifically, UV-exposed skin in stressed mice showed elevated levels of CTACK and RANTES, both of which recruit T cells; interleukin-12, which increases the number of leukocytes and slows tumor growth; and interferon-y, which has been shown to suppress tumors.

Dhabhar and his colleagues were "pleasantly surprised" by their results, he said. However, short-term stress stopped helping curb tumor development after 26 weeks, despite the fact that cytokine and chemokine levels stayed elevated for the study's entire 32 weeks. It may be because cells in stressed mice developed into tumors more slowly, they hypothesized, or that the number of tumors exceeded a certain threshold and could no longer be suppressed.

The researchers are currently trying to understand the mechanisms involved in the immune response, ensure there are no adverse effects of eliciting such stress in mice, and determine how best to trigger the protective aspects of short-term stress in humans.


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