Browsing by Subject "Stress"
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Item Autism: Association Between Autism and Parenting Stress(2009-12-01) Banini, Simon D.; Bae, SejongAutism is a developmental disorder, whose etiology is still an active research. Objectives of this study are to identify: risk factors of parenting stress; statistical tools for analysis and interpretations of data to ascertain and reinforce risk factors; and recommendations to mitigate parenting stress of autistic children. Data: National Survey of Children with Special Care Needs (NS-CSHCN), 2005-06. Analysis was performed on NS-CSHCN (n=40,723). Among parents with autistic children (n=2,123), the highest adjusted odds of stress were reported associated with primary language (OR= 9.44), insurance (OR=0.34), and Respite care (OR=3.71). Parents with non-autistic children (n=38,133) was the reference population with 467 missing values. Recommendations: Re-evaluation to improve provider language services especially for CSHCN; Family centered public health delivery rather than patient-provider interactive approach.Item Diverse Immune Responses Mediated by Beta-Adrenergic and Corticotropin-Releasing Hormone Receptors in a Model of Pneumococcal sepsis(2010-08-01) Kim, Byung-Jin; Harlan JonesNeuroendocrine stimulation can impact disease states by regulating immune function. The purpose of our studies was to define the functional role of stress-induced neuroendocrine factors, catecholamines and corticotropin-releasing hormone (CRH) on immune responses involved in the pathogenesis of Streptococcus pneumoniae (S. pneumoniae) infection implementing both in vitro and in vivo methodology. Dendritic cells play a pivotal role in antigen presentation and cytokine production, influencing both innate and adaptive immunity. Initial studies examined the potential immunomodulatory effect of epinephrine and CRH on DC cytokine production in response to the bacterial pathogenic ligand, lipopolysaccharide (LPS). In addition, the ability of DC to dictate CD4+ T cell activation as a consequence of CRH or epinephrine pre-treatment was examined using an in vitro co-culture system. Epinephrine and CRH pre-treatment resulted in a preferential increase in IL-23 and IL-10 cytokine production. In contrast, IL-12p70 was significantly attenuated in response to epinephrine and CRH pre-treatment. Preferences in IL-23 and IL-10 cytokine production by DC pre-treated with epinephrine and CRH corresponded with an increase in IL-4 and IL-17A, but not IFN-y cytokine production by CD4+ T cells. These results suggest that exposure to stress-derived epinephrine/CRH dictates dendritic cells to generate a dominant Th2/Th17 phenotype in the context of subsequent exposure to a pathogen. Our second study examined the functional properties of IL-23 during pulmonary S. pneumoniae infection. IL-23 plays a crucial role in establishing host defenses against extracellular pathogens. Further investigation is still required to define the impact of IL-23 on acute pulmonary S. pneumoniae infection. Utilizing IL-23p19 genetic deficient mice, we determined bacterial load, cytokine production and the contribution of neutrophils against S. pneumoniae infection using monoclonal antibody-mediated systemic neutrophil depletion. The absence of IL-23 induced a higher bacterial load in lung and blood as compared to IL-23 competent counterparts. In the absence of IL-23, production of proinflammatory cytokines such as IL-6, IL-12p70 as well as IL-17A and IFN- were dampened as compared to wild type mice. In addition, neutrophil distribution was also altered in IL-23-deficient mice, suggesting impaired neutrophil recruitment into lung. Interestingly, neutrophil depletion did not impact bacterial load in lung and blood in both IL-23 competent and deficient mice. These findings, suggest a novel role of IL-23 in pulmonary S. pneumoniae infection, potentially independent of neutrophil function. We next examined the possible impact of CRH and catecholamines as regulators of immune function against acute bacterial infection in response to stress. Utilizing a murine model of acute pulmonary S. pneumoniae infection and restraint stress, we selectively blocked CRH receptors (CRHR1 and CRHR2) as well as the 2 adrenergic receptor prior to restraint stress followed by intranasal pulmonary S. pneumoniae infection. Antagonist administration did not impact restraint stress-induced physiological responses as compared to restraint stressed mice, which did not receive receptor antagonists. However, following S. pneumoniae infection, physiological changes including weight and temperature were altered in response to administration of selective CRH receptor and β2 adrenergic receptor antagonists. Survival rate, bacterial load and cytokine production corresponded with physiological differences observed in response to selective CRH receptor and 2 adrenergic receptor antagonists. Importantly, preferential differences in bacterial colonization and survival corresponded with distinct differences in inflammatory cytokine production and immune cell distribution along pulmonary airways. In particular, opposing effects in IL-17A and neutrophil accumulation was found among mice administered the CRHR1 versus the CRHR2 antagonists. Together, these findings indicate that activation of each receptor can influence immune responses against S. pneumoniae infection. Thus, our findings provide further understanding of how stress-derived neuroendocrine factors directly impact immune responses related to immunopathology and immunoprotection.Item Investigating the Role of Stress in a Murine Model of Asthma(2008-07-01) Deshmukh, Aniket; Harlan Jones; P. Mathew; Jerry SimeckaThe mechanisms by which stress can exacerbate asthma are still unknown. The purpose of this study was to examine the immunological links between stress controllability and asthma pathogenesis. Our studies reveal specificity of stress control and immune activation resulting in hyper-inflammatory reactions in response to allergic airway challenge. We anticipate that these studies can serve as a translational piece to facilitate clinical studies of stress and asthma prevalence. The purpose of this project was to establish a murine model of stress controllability and demonstrate the impact of stress on the development of immune allergic airway hypersensitivity as a major feature of asthma. I hypothesized that given the ability to control the degree of stress would translate into less severe allergic airway hypersensitivity. We also hypothesized that distinct changes in immune responses generated in response to uncontrolled stress would reflect the extent of airway hypersensitivity. Mice were exposed to daily regimen of uncontrollable stress, controllable stress or no stress concurrently with allergen exposure. Behavioral disposition to stress was monitored in conjunction with evaluation of severity of asthma and immune status. Our results demonstrate that exerting control over stress conditions leads to distinct changes in immunological status corresponding with positive behavioral responses and less disease severity. We anticipate that our studies will facilitate application of stress management in control of immune status as a biomarker for asthma progression.Item Stress and Social Support as Risk Factors for the Occurrence of Neural Tube Defect-Affected Pregnancies in Women Living Along the Texas-Mexico Border(1999-06-01) Herron, Kathryn M.; Antonio Rene; John Licciardone; Gilbert RamirezHerron, Kathryn M., Stress and Social Support as Risk Factors for the Occurrence of Neural Tube Defect-Affected Pregnancies in Women Living Along the Texas-Mexico Border. Master of Public Health, June, 1999, 59 pp., 8 tables, 1 figure, references, 78 titles. Data were derived from the case-control study of the Texas Department of Health’s Neural Tube Defect Project, involving women living along the Texas-Mexico border, June 1995 to October 1998. Social support and stress information was obtained from a questionnaire, and a residual stress scale was created to determine an aggregate measure for each subject. Interviews were conducted with 261 women, with 1.2 controls to each case. Having high residual stress was found to be a significant risk factor for NTDs. Other significant risk factors included periconceptional injury, residential mobility, having no relatives to talk about private matters, and discontent with relationships.Item The Association Between Depressive Symptoms and Accumulation of Stress Among Black Men in the Health and Retirement Study(Oxford University Press, 2020-09-29) Thorpe, Roland J., Jr.; Cobb, Ryon; King, Keyonna; Bruce, Marino A.; Archibald, Paul; Jones, Harlan P.; Norris, Keith C.; Whitfield, Keith E.; Hudson, DarrellBACKGROUND AND OBJECTIVES: Among the multiple factors posited to drive the health inequities that black men experience, the fundamental role of stress in the production of poor health is a key component. Allostatic load (AL) is considered to be a byproduct of stressors related to cumulative disadvantage. Exposure to chronic stress is associated with poorer mental health including depressive symptoms. Few studies have investigated how AL contributes to depressive symptoms among black men. The purpose of the cross-sectional study was to examine the association between AL and depressive symptoms among middle- to old age black men. RESEARCH DESIGN AND METHODS: This project used the 2010 and 2012 wave of the Health and Retirement Study enhanced face-to-face interview that included a biomarker assessment and psychosocial questionnaire. Depressive symptoms, assessed by the endorsement of 3 or more symptoms on the Center for Epidemiological Studies-Depression 8-item scale, was the outcome variable. The main independent variable, AL, score was calculated by summing the number values that were in the high range for that particular biomarker value scores ranging from 0 to 7. black men whose AL score was 3 or greater were considered to be in the high AL group. Modified Poisson regression was used to estimate prevalence ratios (PRs) and corresponding 95% confidence intervals (CIs). RESULTS: There was a larger proportion of black men in the high AL group who reported depressive symptoms (30.0% vs. 20.0%) compared with black men in the low AL group. After adjusting for age, education, income, drinking, and smoking status, the prevalence of reporting 3 or more depressive symptoms was statistically significant among black men in the high AL group (PR = 1.61 [95% CI: 1.20-2.17]) than black men in the low AL group. DISCUSSION AND IMPLICATIONS: Exposure to chronic stress is related to reporting 3 or more depressive symptoms among black men after controlling for potential confounders. Improving the social and economic conditions for which black men work, play, and pray is key to reducing stress, thereby potentially leading to the reporting of fewer depressive symptoms.