Infl ammatory processes and social behavior are deeply interwoven. Proinfl ammatory factors, in primis cytokines, can trigger a concert of behavioral modifi cations that help the organism to navigate its social environment in periods of sickness, by increasing the neural sensitivity of salience/alarm networks to negative social stimuli (so to promptly identify and avoid potential risks) and the reactivity of reward circuits to positive social stimuli (thus promoting approachlike behavior towards close and supportive others). In turn, social adversities, such as abuse, separation, rejection, social exclusion, negative evaluation, can increase peripheral infl ammation (thus preparing the organism to situations in which wounding and infections are more likely to occur). Individuals who are more socially disconnected, or lonely, display a chronic elevation of peripheral infl ammatory markers, and an exaggerated production of pro-infl ammatory factors in response to infections and negative social experiences. This may have relevant clinical implications and shed light on the relationships between chronic stress, infl ammation, and neuropsychiatric disorders characterized by social dysbehavior, such as anxiety and depression.
Keywords: Psychoneuroendocrinoimmunology, Stress, Allostasis, Allostatic load, Social brain, Depression.