Depressive disorders and Immune cell changes 

Depressive disorders and Immune cell changes

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Depressive disorders

Low-grade inflammation and increased glucocorticoid production are common pathophysiological characteristics of depressive illnesses.

For the first time, a link between depressive illnesses and mechanical alterations in blood cells is established in a new study published in the prominent journal Translational Psychiatry. To accomplish so, the researchers used image-based morpho-rheological characterization of unmanipulated blood samples to facilitate real-time deformability cytometry in a cross-sectional case-control study (RT-DC).

The Composite International Diagnostic Assessment, a widely established clinical interview for psychiatric illnesses, was used to assess 69 pre-screened patients at high risk for depressive disorders and 70 matched healthy controls.

The main blood cell types were categorized and morpho-rheological properties such as cell size and cell deformability of each cell were quantified using the AI method of deep learning applied to over 16 million blood cell photos.

As a result, the researchers discovered that patients with depressive illnesses had more deformable peripheral blood cells than control people, while cell size was unaffected.

Monocytes and neutrophils were more deformable in people who had suffered from persistent depressive disorder in the past, while erythrocytes were more deformable in people who were now suffering from a persistent depressive disorder.

In addition, lymphocytes were more deformable in people who were currently depressed.

Following that, the study indicates for the first time that depressive disorders, particularly persistent depression disorders that last longer than two years, are linked to increased blood cell deformability.

Lymphocytes, monocytes, and neutrophils are the most affected, while all major blood cells show greater deformability. This shows that in depressive illnesses, mechanical alterations in immune cells occur, which could be the cause of a persistent immunological response.

The discovery of this pathomechanism could lead to novel therapeutic options in the future, such as enhancing cell mechanical processes to restore defective cell function.