On the trail of space immunodeficiency: Researchers have gained insight into the causes of astronauts’ reduced resistance to pathogens. Stays in weightlessness change the activity of many genes in immune cells, which apparently affects the work of the body police. The study also provides indications of the time frame in which the immune system recovers after returning home. The results could thus benefit the medical care of astronauts, say the scientists.
Normally, gravity always pulls on the body – our physiology is well adapted to these conditions on the earth’s surface. It therefore seems almost surprising that humans can cope with weightlessness when staying in space. However, the unnatural floating state is not without problems, as experience and studies in the context of manned space flight have shown: It can cause various health problems, such as cardiac arrhythmias, drop in blood pressure, dehydration and bone loss. Impairment of the immune system is also known. Astronauts show reduced resistance to pathogens during and after their stay in space: they are more susceptible to infections and viruses that are dormant in the body can be dangerously reactivated, which cause shingles, for example.
The body police in sight
Scientists from the Canadian University of Ottawa have now devoted themselves to further research into the background of this space immunodeficiency. They chose a genetic approach: They investigated the extent to which the genetic activities of astronauts’ immune cells are influenced by weightlessness. Using RNA sequencing, the team examined gene expression in the white blood cells (leukocytes) of eleven male and three female astronauts. They had been aboard the ISS for between 4.5 and 6.5 months over the past decade. The immune cells were isolated from blood that was taken at ten different times: once before the journey into space, four times during the stay and five times after returning to earth.
As the researchers report, there were clear effects on gene expression in the leukocytes. Among the affected genes, they identified two clusters of 247 and 29 genes, respectively, with specific trends in activity: genes in the first group shut down upon reaching space and up again upon returning to Earth, while genes in the second cluster were reversed pattern applied. As far as the functions of these hereditary traits are concerned, it became apparent that the predominant importance of the genes in the first cluster is linked to immune functions, while the genetic traits in the second cluster are more likely to play a role in cellular metabolism. “We have now been able to document that the expression of many genes in immune cells changes when astronauts reach space,” summarizes senior author Odette Laneuville from the University of Ottawa.
Normalization after landing
Regarding recovery after return, the data indicate that while it remains unclear whether and when complete recovery occurs, most genes in both clusters had returned to their pre-flight return expression levels within a year. A clear effect was also usually apparent after a few weeks. The results thus suggest that returning astronauts are still at significantly increased risk of infection for at least a month after landing on Earth.
The question remains as to what caused the change in gene expression in the leukocytes. So far, scientists have only been able to distort assumptions. It could therefore be that the effect has to do with the fluid displacement in weightlessness. As is well known, blood plasma is redistributed from the lower to the upper part of the body and the lymphatic system is also affected by relocations. This may be related to altered gene expression.
The researchers hope that their findings can now help to develop methods that counteract suppression of the immune system during space travel – especially on long-term flights. For the time being, the study once again underlines the importance of screening astronauts, Laneuville concludes: “It would be beneficial for the health of space travelers on long missions if both immune dysfunction and subclinical inflammation were detected. Such information offers the opportunity to intervene to prevent the progression of severe symptoms.
Source: Frontiers, professional article: Frontiers in Immunology, doi: 10.3389/fimmu.2023.1171103