Research paperPhysical abuse during childhood predicts IL-2R levels in adult panic disorder patients
Introduction
Childhood maltreatment is a complex problem that affects society greatly and is of immense importance to public health. Maltreatment during childhood afects fundamental biological processes and produces long-lasting epigenetic marks, leading to adverse mental health outcomes in adulthood (Szyf et al., 2011). Exposure to adverse life events in childhood has been linked to an increased susceptibility for a spread of psychiatric disorders, possibly via long-term influences on the immune system (Danese et al., 2007).
Childhood trauma is associated with systemic inflammation as assessed by measurements of C-reactive protein (CRP) and inflammatory cytokines including tumor necrosis factor-alpha and interleukin (IL)-6 (Danese et al., 2007). Childhood maltreatment was found to be associated with increased plasma CRP levels and inflammatory markers in subjects identified as being on the psychosis spectrum, depression and bipolar disorder (Aas et al., 2017)
Panic Disorder (PD) is a common and disabling anxiety disorder that is associate with a pro-inflammatory cytokines profile (Quagliato and Nardi, 2018a). Furthermore, this disorder has a high incidence of traumatic events during childhood (Safren et al., 2002). Individuals who experience early life stress have been shown to develop PD more frequently in adulthood than subjects with no history of early life stress (Safren et al., 2002; Goodwin et al., 2005). However, to the present date none study evaluated the impact of childhood trauma on inflammatory markers in PD patientes. Furthermore, it is unknow if any immune abnormalities could be specific to at least one or more sorts of early life trauma.
Several putative biological mechanisms by which childhood maltreatment may increase the risk for PD might be hypothesized. These include, but are not limited to, alterations in the hypothalamic-pituitary-adrenal (HPA) axis, and genetic and epigenetic processes as well as structural and functional brain imaging changes (Nemeroff, 2016). These biological mechanisms may provide insight into modifiable targets and provide direction to improve both treatment of PD and prevention strategies for individual with high PD risk.
The central aim of this case-control study was to search for evidence of peripheral inflammatory biomarkers that may be correlated with distinct biological modifications associated with the existence or absence of a history of childhood maltreatment in PD. This goal was addressed by interrogating the influence of early life trauma on cytokines expression in patients with PD.
Section snippets
Participants
Eighty-four people with a diagnosis of PD and 78 age-matched controls were recruited for this study (see Table 1). Patient recruitment was via either clinician or self/family referral. All patients were living in the community and had been receiving antidepressant medication for at least 3 months prior to entry in the study. Diagnostic status was determined by Structured Clinical Interview for DSM-IV-TR administered by a trained psychiatrist or psychologist and independently confirmed by
Demographic factors
The patient and control groups were not significantly different in any demographic factor. There were no significant associations of cytokine levels with age, sex, years of education, BMI, physical activity, ethnicity, age of onset, fluoxetine or diazepam equivalent dose, PAS, HAM-A, HAM-D or CGI scores. The patient and control groups were significantly different between levels of interleukins (Table 2).
Relationship between child trauma subtypes and cytokines
The multiple regression model showed that physical abuse explained 13.8% of the variance in
Discussion
The present study finds evidence that individual types of trauma exposure impact differentially on the inflammatory markers in PD patients, presenting a significant association between physical abuse and the inflammatory marker IL-2R in PD patients. As such, this provides strong evidence that childhood traumatic events significantly impact on the inflammatory system, thus offering a possible molecular pathway by which early life stress might contribute to vulnerability to developing psychiatric
Funding
None.
CRediT authorship contribution statement
Laiana A. Quagliato: Conceptualization, Data curation, Formal analysis, Writing – original draft. Danielle A. Coelho: Data curation. Ursula M.A. de Matos: Data curation. Antonio E. Nardi: Supervision, Validation, Writing – review & editing.
Declaration of Competing Interest
None.
Acknowledgement
None.
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