The ties that bind: Ingroup ties are linked with diminished inflammatory immune responses and fewer mental health symptoms through less rumination

<div><p>The present research explored whether components of social identity, namely ingroup ties, affect, and centrality, were differentially linked to mental health and inflammatory immune responses, and whether rumination mediated those relations. Study 1 (<i>N</i> = 138) indicated that stronger ingroup ties were associated with fewer mental health (depressive and post-traumatic stress) symptoms; those relations were mediated by the tendency for individuals with strong ties to rely less on ruminative coping to deal with a stressful life event. Study 2 (<i>N</i> = 54) demonstrated that ingroup ties were negatively associated with depressive symptoms, dispositional rumination, as well as stress-linked inflammatory elements at the physiological level. Consistent associations for centrality and ingroup affect were absent, suggesting that ingroup ties may have unique health benefits.</p></div

Effects of chronic, subchronic-intermittent and acute stressors on anxiety-related behaviors in male mice.

<p>Mean (± SEM) stretch attend responses (A), latency to enter the open arms (B), Time in the open Arms (C), Number of entries into the open arms (D), Time in the closed arms (E) and number of entries into the closed arms 2 he and again 2 weeks following treatment. Male mice had either not been stressed (control), exposed to an acute stressor (resident intruder paradigms for the two sexes), a subchronic-intermittent stressor followed by the resident-intruder paradigm, or a chronic stressor followed by the resident-intruder stressor. *p<.05 relative to nonstressed mice. ^o p<.05 relative to performance measured 2 hr following the treatment.</p

5-HT variations in the prefrontal cortex following chronic, subchronic-intermittent and acute stressors.

<p>Mean (± SEM) concentration of 5-HIAA and 5-HT in the prefrontal cortex of male (Panels A and B) and female mice (Panel C and D) that had not been stressed (control),exposed to an acute stressor (resident intruder paradigms for the two sexes), a subchronic-intermittent stressor (7 stress sessions over 21 days) followed by the resident-intruder paradigm on Day 22, or a chronic stressor (variable stressor exposure on each off 21 days) followed by the resident-intruder stressor. *p<.05 relative to nonstressed mice.</p

NE variations in the central amygdala following chronic, subchronic-intermittent and acute stressors.

<p>Mean (± SEM) concentration of MHPG and NE in the central amygdala of male (Panels A and B) and female mice (Panel C and D) that had not been stressed (control), exposed to an acute stressor (resident intruder paradigms for the two sexes), a subchronic-intermittent stressor followed by the resident-intruder paradigm, or a chronic stressor followed by the resident-intruder stressor. *p<.05 relative to nonstressed mice of the same sex. # p<.05 relative to acutely stressed mice.</p

Corticosterone levels following an acute stressor.

<p>Mean (± SEM) plasma corticosterone concentrations (µg/dl) among male (upper) and female (lower) mice that had experienced either no stress, restraint for 15 min, or a resident-intruder stressor. *p<.05 relative to nonstressed mice of the same sex. # p<.05 relative to acutely stressed mice.</p

NE variations in the hippocampus following chronic, subchronic-intermittent and acute stressors.

<p>Mean (± SEM) concentration of MHPG and NE in the hippocampus of male (Panels A and B) and female mice (Panel C and D) that had not been stressed (control), exposed to an acute stressor (resident intruder paradigms for the two sexes), a subchronic-intermittent stressor followed by the resident-intruder paradigm, or a chronic stressor followed by the resident-intruder stressor. *p<.05 relative to nonstressed mice.</p

NE and 5-HT variations in the amygdala following an acute stressor.

<p>Mean (± SEM) concentration of MHPG and NE (Panels A and B) and 5-HIAA and 5-HT (Panels C and D) of the central amygdala among male and female mice that had experienced either no stress, restraint for 15 min, or a resident-intruder stressor. *p<.05 relative to nonstressed mice of the same sex.</p

Effects of chronic, subchronic-intermittent and acute stressors on anxiety-related behaviors in female mice.

<p>Mean (± SEM) stretch attend responses (A), latency to enter the open arms (B), Time in the open Arms (C), Number of entries into the open arms (D), Time in the closed arms (E) and number of entries into the closed arms 2 he and again 2 weeks following treatment. Female mice had either not been stressed (control), exposed to an acute stressor (resident intruder paradigms for the two sexes), a sub subchronic-intermittent chronic stressor followed by the resident-intruder paradigm, or a chronic stressor followed by the resident-intruder stressor. *p<.05 relative to nonstressed mice. ^o p<.05 relative to performance measured 2 hr following the treatment.</p

NE and 5-HT variations in the hippocampus following an acute stressor.

<p>Mean (± SEM) concentration of hippocampal MHPG and NE (Panels A and B) and 5-HIAA and 5-HT (Panels C and D) among male and female mice that had experienced either no stress, restraint for 15 min, or a resident-intruder stressor. *p<.05 relative to nonstressed mice of the same sex.</p

Summary of changes in MHPG, NE, 5-HIAA and 5-HT following acute, subchronic-intermittent and chronic stressors (Experiment 2).

↑<p>relative to control group;</p>↑↑<p>relative to control, acute stressor and subchronic-intermittent stressor groups.</p