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Objective: The present study aimed to test the role of the autonomic nervous system (ANS) in modulating the impact of family stress induced by harsh parenting on youths' inflammation. First, we examined the direct effect of severity of adverse parenting behaviors on two serum biomarkers of systemic inflammation (C-reactive protein and interleukin-6) among youth. Second, we tested the moderating role of ANS reactivity in response to laboratory-induced stress in the association between harsh parenting and inflammation among these youth., Method: The sample included 101 low-income children (75.2% African American) between 9 and 12 years of age ( M age = 1.2) who participated in a conflict task with their primary caregiver in a laboratory setting. Heart rate variability reactivity (HRV-R), skin conductance level reactivity (SCL-R), and preejection period reactivity (PEPr-R) were used to index parasympathetic and sympathetic nervous system reactivity. Markers of low-grade inflammation (C-reactive protein and interleukin-6) were obtained from serum.SD age = 1.2) who participated in a conflict task with their primary caregiver in a laboratory setting. Heart rate variability reactivity (HRV-R), skin conductance level reactivity (SCL-R), and preejection period reactivity (PEPr-R) were used to index parasympathetic and sympathetic nervous system reactivity. Markers of low-grade inflammation (C-reactive protein and interleukin-6) were obtained from serum., Results: After adjusting for confounding variables, ANS activity moderated the associations between family stress and systemic inflammation. Specifically, elevated HRV-R buffered the effect of family stress on youths' inflammation, whereas elevated PEPr-R and SCL-R exacerbated the effect., Conclusion: These findings show that self-regulatory capacity and threat sensitivity, as indicated by ANS function, may have an impact on the associations between family stress and systemic inflammation. (PsycInfo Database Record (c) 2020 APA, all rights reserved).

Accumulating evidence suggests that the experience of early life adversity is a risk factor for a range of poor outcomes across development, including poor physical health in adulthood. The biological embedding model of early adversity (Miller, Chen, & Parker, 2011) suggests that early adversity might become embedded within immune cells known as monocytes/macrophages, programming them to be overly aggressive to environmental stimuli and insensitive to inhibitory signals, creating a "proinflammatory phenotype" that increases vulnerability to chronic diseases across the life span. We tested this hypothesis in the present study. Adolescent girls (n = 147) had blood drawn every 6 months across a 2.5-year period. To assess inflammatory responses to challenge, their monocytes were stimulated in vitro with a bacterial product, and production of the cytokine interleukin-6 was quantified. Hydrocortisone was added to cultures to assess the cells' sensitivity to glucocorticoids' anti-inflammatory signal. Using cluster analyses, we found that early life adversity was associated with greater odds of displaying a proinflammatory phenotype characterized by relatively larger interleukin-6 responses and relatively less sensitivity to glucocorticoids. In contrast, ongoing social stress was not associated with increasing odds of being categorized in the proinflammatory cluster. These findings suggest that early life adversity increases the probability of developing a proinflammatory phenotype, which, if sustained, could forecast risk for health problems later in life.

Asthma is a chronic respiratory disorder that affects over 7 million children in the United States. Evidence indicates that family stressors are associated with worsening of asthma symptoms, and some research suggests that these stressful experiences engender changes in children's immune systems in ways that exacerbate airway inflammation and contribute to both acute and chronic asthma symptoms. We examined the association between observed experiences of parent-child conflict and the expression of signaling molecules involved in the transduction of anti-inflammatory signals that regulate airway inflammation and obstruction. Fifty-seven children and their parents participated in a conflict task, and coders rated interactions for evidence of harsh and supportive behaviors. Children reported on their perceptions of parental support and reported on their daily asthma symptoms for 2 weeks. We collected peripheral blood in children to measure leukocyte expression of messenger RNA for the glucocorticoid receptor and the β2-adrenergic receptor. Analyses revealed that harsh conflict behaviors were associated with decreased expression of both messenger RNAs and more severe asthma symptoms. Neither supportive behaviors nor perceived parental support was associated with gene expression or asthma symptoms. These findings suggest that harsh interactions with parents are associated with downregulation of key anti-inflammatory signaling molecules and difficulties breathing in children with asthma. Children with asthma who are also victims of maltreatment may be particularly susceptible to transcriptional changes in immune cells that could worsen asthma over time.

Individuals' social experiences are associated with their mental health, physical health, and even mortality. Over the last 30 years, researchers have examined the ways in which these social experiences might be associated with chronic inflammation - a component underlying many of the chronic diseases of aging. Little research, however, has examined the role of adults' attachment style as a specific social component that might be associated with inflammation. In the present study, we utilized data from a sample of 59 African-American adults from the Maryland Adolescent Development in Context Study (MADICS) to examine the links between attachment avoidance and attachment anxiety and C-reactive protein (CRP) and interleukin (IL)-6. After controlling for demographic characteristics, body mass index, and depressive symptoms, attachment avoidance and anxiety were associated with IL-6 but not CRP. This study adds to the growing body of research identifying the wide range of social experiences associated with inflammation and further suggests that attachment relationship experiences may have implications for biological processes relevant to many chronic diseases of aging.

Within the field of relationship science there is increasing interest in the connections between close relationships and physical health. In the present study, we examined whether adolescents' (~12 years old) and young adults' (~20 years old) perceptions of their parents as a secure base prospectively predict C-reactive protein (CRP), a commonly used marker of inflammatory activity, at age 32 in a well-characterized sample of African Americans. We utilized existing data collected as part of the Maryland Adolescent Development in Context Study (MADICS) to construct measures of perceptions of parental secure base support (SBS), general parental support, and peer support in early adolescence and early adulthood. In the present study, SBS was operationalized as the perceived ability to depend on parents in times of need. Fifty-nine African American MADICS participants who reported on perceived support in early adolescence and early adulthood participated in a follow-up home visit at age 32 during which serum CRP was measured via a blood draw. After controlling for inflammation-related confounds (e.g., tobacco use, body mass index), adolescents' perceptions of parental SBS, but not peer support or general parental support, predicted lower CRP values at age 32 (b = -.92, SE = .34, p < .05). None of the support variables in early adulthood predicted CRP at 32 years. This study adds to a growing literature on relationships and health-related outcomes and provides the first evidence for a link between parental SBS in adolescence and a marker of inflammatory activity in adulthood.

Links between child maltreatment and low‐grade inflammation in adulthood are well documented, but these studies often rely on adults to report retrospectively on experiences of childhood abuse. Furthermore, these findings raise questions about whether exposure to childhood maltreatment needs time to "incubate," only giving rise to nonresolving inflammation in adulthood, or whether heightened inflammation may be observable in childhood, closer in time to the maltreatment exposure. The present study examined this question in a sample of 155 low‐income children (ages 8–12), half of whom had been exposed to maltreatment. Trained coders evaluated case reports to classify maltreatment based on timing and exposure type. Blood samples from children assessed C‐reactive protein and cytokines, which were used to form a composite of low‐grade inflammation. Analyses revealed a marginally significant Maltreatment Exposure × Sex interaction, which suggested that maltreatment exposure was associated with higher inflammation for girls but not boys. Additionally, analyses focused on the accumulation of maltreatment experiences (through multiple forms of maltreatment or across multiple time points) revealed that girls with greater diversity in their maltreatment experiences and those who experienced maltreatment at multiple time points were at greatest risk. Finally, examination of timing of first onset of maltreatment suggested that girls whose exposures occurred before the age of 5 had the highest low‐grade inflammation. These findings add new evidence linking maltreatment to inflammation in childhood, which could increase the risk for mental and physical health problems across the lifespan. [ABSTRACT FROM AUTHOR]

Researchers have identified cross-sectional links between interpersonal stress and inflammation. Little is known, however, about how these dynamics unfold over time, what underlying immune pathways might exist, or whether moderators such as race could alter the strength of the connection between interpersonal stress and inflammatory processes. We examined whether adolescent girls whose relationship trajectories were characterized by chronic stress would exhibit a proinflammatory phenotype marked by systemic inflammation, heightened cytokine responses to bacterial challenges, and resistance to the anti-inflammatory properties of cortisol. Significant Stress × Race interactions revealed that family stress trajectories predicted glucocorticoid sensitivity and peer stress trajectories predicted cytokine production for White but not Asian girls. Relationship stress trajectories were not associated with systemic inflammation, however. These findings suggest that particular subgroups of adolescent girls who face chronic and elevated stress in their close relationships may be at risk for disruptions to the immune system. [ABSTRACT FROM PUBLISHER]

Objective We examined prospective connections among parental depressive symptoms, family dysfunction, and eosinophil activity in children with asthma. Methods 81 children with asthma and their parents completed two laboratory visits across a 1-year period. At baseline and 1 year later, parents reported about their depressive symptoms and family dysfunction. We collected peripheral blood in children to measure eosinophil counts and eosinophil cationic protein. Following visits, children recorded their asthma symptoms for 2 weeks. Results After controlling for demographic and biomedical covariates, a significant T1×T2 Family Dysfunction interaction emerged, suggesting that the links between family dysfunction at T1 and eosinophil counts and activity at T2 depended on family functioning at T2. Parental depressive symptoms were unrelated to eosinophil activity and asthma symptoms. Conclusions These findings suggest that improvements in family functioning are associated with decreases in eosinophil activity, which may contribute to inflammatory processes that affect airway function. [ABSTRACT FROM AUTHOR]