| Abstract | In 2020, nearly 8 in 10 adults said that the coronavirus pandemic was a significant stressor in their life, with nearly half of American adults reporting that their behavior has been negatively affected by stress. Stressors, much like the coronavirus, have been linked to altering acute and long-term inflammatory responses. One component of the stress response is inflammation. Inflammation acts as an adaptive part of the innate immune system that is activated in response to harmful stimuli. Though acute inflammation is critical in the process of fighting off disease and infection, prolonged inflammation has been shown to be correlated with neurodegenerative diseases such as Alzheimer's Disease. Exposure to stress at early periods of development, known as early life stress (ELS) has been shown to negatively impact the hypothalamic-pituitary-adrenal (HPA) axis, leading to disruption of the negative feedback loop. The goal of this study is to investigate the downstream effects of a combination early life stress model on targets and markers of the inflammatory pathway, including glucocorticoid receptor (GR) and DNMT1. Utilizing a restricted bedding stress paradigm, mice were exposed to stress prenatally and postnatally, with the prenatal stress induced via maternal stress. Preliminary results from this study indicate that the combination-stress (CS) condition resulted in an immunosuppressive effect given the downregulation of pro-inflammatory cytokines. However, quantification of data on GR suggests that exposure to stress early in life does not have a significant effect on levels of GR in the hippocampi of mice. Our study does provide support for increases in epigenetic modification in these CS mice with DNMT1 being present in higher levels in the CS mice compared to the no-stress (NS) control. |
