Inflammation levels increased with depression

Researchers explore link between depression and immune system

Approximately one-third of patients with depressive symptoms have high levels of inflammation. However, inflammation is often measured using only very broad and nonspecific markers. To better understand the link between depression and the immune system, researchers at the Max Planck Institute for Psychiatry measured many different biological factors and identified patterns in the data.

In the newly published study, scientists from Project Group Medical Genomics, led by first author Jonas Hagenberg and Janine Knauer-Arloth, measured more than 40 immune markers in the blood of 237 participants. This was a transdiagnostic study; That is, the researchers included not only participants affected by depression but also participants with other disorders such as anxiety or substance use. In addition to immune markers, the scientists also measured the activity of more than 12,000 different genes in immune cells and depressive symptom burden. They also included body mass index (BMI) and participants’ age because both of these factors affect inflammation. The researchers then tried to recognize patterns in the data using machine learning methods.

The team identified four different clusters of participants. Besides CRP, the standard marker used to measure inflammation, immune markers IL-1RA, TNF-alpha, and various chemokines were helpful in identifying these clusters. Chemokines are a specific class of immune markers. 121 participants were included in the largest cluster; these patients had fewer depressive symptoms, lower levels of inflammation, and tended to be younger. The next two clusters consisted of a total of 77 participants, characterized by high depressive symptom burden, high inflammation levels, and increased BMI. The final group consisted of 39 participants who exhibited high depressive symptom burden but low levels of inflammation.

Gene activity levels differed mainly between the cluster containing patients with fewer symptoms and the remaining three clusters where patients had more symptoms. Interestingly, the analysis showed that some of the genes associated with depression are linked to specific immune cells; This suggested that certain types of immune cells may be more relevant to depression than others.

“Our results tell us that although CRP is a good marker, there are other markers, such as IL-1RA and chemokines, that may be useful and require further investigation,” Hagenberg explains. “Furthermore, the link between depressive symptom burden, inflammatory markers and BMI suggests that depression should be treated holistically – this is not a new finding, but underlines the importance of body weight.”

Including data beyond CRP allows researchers to gain a deeper understanding of the connection between the immune system and depression. This information may help develop more personalized and precise treatments for subgroups of depressed patients in the future.