Chronic stress is a major risk factor in the pathophysiology of many neuropsychiatric disorders. Further, chronic stress conditions can promote neuroinflammation and inflammatory responses in both humans and animal models. Type I interferons (IFN-I) are critical mediators of the inflammatory response in the periphery and responsible for the altered mood and behavior. However, the underlying mechanisms are not well understood. In the present study, we investigated the role of IFN-I signaling in chronic stress-induced changes in neuroinflammation and behavior. Using the chronic restraint stress model, we found that chronic stress induces a significant increase in serum IFNβ levels in mice, and systemic blockade of IFN-I signaling attenuated chronic stress-induced infiltration of macrophages into prefrontal cortex and behavioral abnormalities. Furthermore, complement component 3 (C3) mediates systemic IFNβ-induced changes in neuroinflammation and behavior. Also, we found significant increases in the mRNA expression levels of IFN-I stimulated genes in the prefrontal cortex of depressed suicide subjects and significant correlation with C3 and inflammatory markers. Together, these findings from animal and human postmortem brain studies identify a crucial role of C3 in IFN-I-mediated changes in neuroinflammation and behavior under chronic stress conditions.

Type 1 interferon mediates chronic stress-induced neuroinflammation and behavioral deficits via complement component 3-dependent pathway.

https://doi.org/10.1016/j.ynstr.2022.100495

Microglia-specific transcriptional repression of interferon-regulated genes after prolonged stress in mice

Stress to Inflammation and Anhedonia: Mechanistic Insights from Preclinical and Clinical Models

Healthy individuals show a tendency towards positive cognitions that is reversed during depression. This tendency is revealed by the Scrambled Sentences Task (SST), an experimental procedure that was also shown to be associated with vulnerability to suffer from depressive episodes. Here, we used the SST to map the prevalence of negative cognitions across the personality domains of criterion B of the Alternative Model of Personality Disorder (AMPD) of the DSM-5 in healthy individuals. The AMPD was developed to characterize personality in a dimensional approach spanning both healthy and pathological individuals. We expected negative cognitions to be more frequent among individuals with high negative affectivity and detachment scores, as these dimensions are thought to be associated with disorders of affect. This association was stable and significant in three separate experiments and persisted for detachment after adjusting for current depression levels. In the Five-Factor Model of Personality (FFM), in contrast, only openness failed to show any association with negative cognitions. Negative affectivity and detachment differed in the preferential association with negative and positive cognitions, respectively. This finding suggests a possible role of motivational factors related to sensitivity to negative and positive incentives in linking personality dimensions and cognitive tendencies, with an anhedonic dimension of negative cognitions being present alongside current depressive symptoms. 

Negative Cognitions in the Personality Domains of the AMPD

Microglia-Specific Transcriptional Repression of Interferon-Stimulated Genes after Prolonged Stress in Mice

Interferon-beta-induced changes in neuroimaging phenotypes of appetitive motivation and reactivity to emotional salience.

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Interferon-beta-induced changes in neuroimaging phenotypes of appetitive motivation and reactivity to emotional salience.