Too much stress makes you sick – this is the widely held opinion. But exactly how chronic psychological stress affects our body is not yet fully understood. This is the question Dr. Annette Sommershof and her team from the University of Konstanz are trying to answer. The scientists are exploring stress-related changes in the immune system and have found evidence for the observation that long-term stress weakens the immune system, resulting in increased susceptibility to infections.
Excessive workloads, family problems, traumatic experiences – stress in daily life can have positive and negative connotations. Studies have shown that short-term stress boosts our performance, but that chronic stress over a prolonged period of time can have negative effects on our health. It has been known for several years that the central nervous system, the psyche and the immune system mutually influence one another. “Numerous studies confirm that mental stress has a direct effect on the immune system, and therefore probably a decisive influence on the development of disease,” says Dr. Annette Sommershof, biologist in the Department of Immunology (director: Prof. Dr. Markus Groettrup) at the University of Konstanz. Sommershof's work specifically focuses on stress-induced changes in the immune system.
In stress situations, the effectiveness of the immune system is partially suppressed by stress hormones such as cortisol. This enables cellular energy to be used more effectively for a flight or fight response. “T lymphocytes, which specialise in recognising and killing diseased cells or foreign organisms in the body, seem to be particularly sensitive to these signals,” says Annette Sommershof.
Suppression of the immune response leads to increased susceptibility to infections by viruses, bacteria and other pathogens. The exact mechanisms that lead to the suppression of an immune response are not yet known in detail and this is what Dr. Sommershof and her colleagues are investigating. “To name just one example, we are interested in finding out whether chronically stressed individuals who have a viral infection completely lack virus-specific T cells or whether such T cells are present but limited in their specific effector functions,” says Sommershof.
Dr. Sommershof’s investigations involve blood samples of patients suffering from posttraumatic stress disorder (PTSD). PTSD is caused by traumatic events such as an accident, war or other life-threatening events. “Trauma patients are characterised by extremely high stress levels, which correlate with changes in certain immune parameters,” says the researcher. Sommershof has been able to show that the peripheral blood of PTSD patients contains fewer naïve, i.e. not yet specialised, T cells, whose job is to fight off unknown pathogens. These patients also have only half the number of regulatory T cells of healthy individuals. Regulatory T cells are essential for maintaining tolerance to self-antigens; however, little is yet known about their role in chronic stress situations.
“We believe that the large difference in the number of peripheral T cells is a major reason why PTSD patients have reduced immunity, increased susceptibility to infection and are more likely to develop autoimmune diseases,” Sommershof explains. One of Sommershof’s research projects deals with the consequences of exam stress on students and seeks to find out whether the PTSD findings can be transferred to chronic stress situations in daily life. “We’ve already seen similar effects, especially as far as the composition of the peripheral T-cell populations are concerned,” says Sommershof.
While data from human studies provide important insights into the immune system changes that lead to reduced immunity and increased susceptibility to infection, no conclusions can be drawn as to why stress leads to the changes observed. Annette Sommershof therefore also works with mouse models to obtain mechanistic insights into the connection between chronic stress and immunosuppression.
Placing a dominant, aggressive mouse into the cage of an existing group of mice disturbs the animals’ ranking and social status, triggering social stress. The animals’ response to infection is then assessed. “We are thus trying to elucidate the causal chain through which stress influences the cellular immune system and compromises the body’s response to infection,” says Sommershof, who has found out that the socially stressed mice had malfunctioning T lymphocytes.
While viral infections induce extensive T-cell proliferation in healthy mice, this was not the case in socially stressed mice. “This is an important prerequisite for the occurrence of cellular immune responses and hence the ability to combat infections. Without T-cell activation and proliferation, the immune system would not be able to cope with the virus,” says Dr. Sommershof. Whether the altered activation and proliferation of the T lymphocytes also has a direct effect on the altered composition of the peripheral T-cell populations in PTSD patients, is something that will have to be studied in greater detail in the future.
In addition to improving our understanding of the relationships between stress and the immune system, Dr. Sommershof’s research might also lead to the discovery of new biomarkers that will enable a simple and reliable assessment of immune defence disorders. “These biomarkers could potentially also help doctors decide on the best time for vaccinations or stressful immunotherapies from an immunological point of view,” says Sommershof.
Further information:Dr. Annette Sommershof Department of ImmunologyUniversity of KonstanzE-mail: annette.sommershof(at)uni-konstanz.de