Publications by authors named "David A Padgett"

Immunological memory (MEM) development is affected by stress-induced neuroendocrine mediators. Current knowledge about how a behavioral interaction, such as social defeat, alters the development of adaptive immunity, and MEM is incomplete. In this study, the experience of social disruption stress (SDR) prior to a primary influenza viral infection enhanced the frequency and function of the T cell memory pool.

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Psychological stress is associated with an increased expression of markers of peripheral inflammation, and there is a growing literature describing a link between periodontal pathogens and systemic inflammation. The hypothesis of the present work is that exposing mice to the social stressor, called social disruption (SDR), would enhance the inflammatory response to lipopolysaccharide (LPS) derived from the oral pathogen, Porphyromonas gingivalis. Mice were exposed to SDR for 2h per day on 6 consecutive days.

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This article summarizes the endocrine and immune changes induced by an experimental model for social stress characterized by repeated defeat. Data indicate that mice facing a social stressor may use different behavioral coping responses based on the environmental conditions and previous experiences. Although chronic stressors generally suppress immune function and increase a host's susceptibility to disease, this may not be always true in all cases.

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Social stress has long been known to affect physical and psychological health in humans and a variety of animal species. In mice, disruption of the social hierarchy (social disruption, SDR) resulted in significant changes in the phenotype and function of immune cells taken from the spleen. Interestingly, there were considerable individual differences in the development of this splenic response to SDR.

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Over the past decade it has become clear that stress can significantly slow wound healing: stressors ranging in magnitude and duration impair healing in humans and animals. For example, in humans, the chronic stress of caregiving as well as the relatively brief stress of academic examinations impedes healing. Similarly, restraint stress slows healing in mice.

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Phagocytes of the innate immune system, such as monocytes/macrophages, represent a first line of defense against invading microorganisms. Psychological stress is often thought to suppress the functioning of these cells, in part due to the immunosuppressive activity of stress-induced glucocorticoid hormones. However, exposure to the stressor social disruption (SDR) has been shown to increase cytokine production by monocytes/macrophages and to reduce their sensitivity to corticosterone.

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We have previously shown that moderate exercise significantly increased survival after influenza virus (A/PR/8/34) infection in mice. We hypothesized that this brief duration of exercise would either increase innate immune defences and/or shift the immune response from a Th1 inflammatory to a Th2 anti-inflammatory response resulting in decreased lung pathology. Adult male BALB/cByJ mice (5-6 months old) were infected with 50 microL of A/PR/8/34 virus (40HAU) intranasally and randomized to either an exercise (EX) or sedentary (SED) group.

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The experimental model, social disruption (SDR), is a model of social stress in which mice are repeatedly attacked and defeated in their home cage by an aggressive conspecific. In terms of the impact of this stressor on the immune response, SDR has been reported to cause hyperinflammation and glucocorticoid insensitivity. To this point however, the behavioral consequences of SDR have not been thoroughly characterized.

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For 20 years, Brain, Behavior, and Immunity has provided an important venue for the publication of studies in psychoneuroimmunology. During this time period, psychoneuroimmunology has matured into an important multidisciplinary science that has contributed significantly to our knowledge of mind, brain, and body interactions. This review will not only focus on the primary research papers dealing with psychoneuroimmunology, viral infections, and anti-viral vaccine responses in humans and animal models that have appeared on the pages of Brain, Behavior, and Immunity during the past 20 years, but will also outline a variety of strategies that could be used for expanding our understanding of the neuroimmune-viral pathogen relationship.

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This review summarizes the endocrine and immune changes induced by an experimental model for social stress that is termed SDR. Further, the differences between this stressor and other chronic stress models in mice are compared and contrasted. Individual differences in the response to SDR are described and discussed in the context of the unique characteristics of this stressor and the importance of a variety of behavioral and environmental factors in modulating the response to social stress.

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Restraint stress (RST) delays wound closure and suppresses pro-inflammatory gene expression by a glucocorticoid-dependent mechanism. Because androstenediol (AED) ameliorates many of the anti-inflammatory influences of glucocorticoids (GC) in vitro, it was hypothesized that treatment of stressed animals with AED would ameliorate the suppressive influence of restraint and restore healing to control levels. To test this hypothesis, male CD1 mice were subjected to nightly cycles of RST beginning 3 days prior to placement of two 3.

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Epstein-Barr virus (EBV) encodes for several enzymes that are involved in viral DNA replication. There is evidence that some viral proteins, by themselves, can induce immune dysregulation that may contribute to the pathophysiology of the virus infection. In this study, we focused on the EBV-encoded deoxyuridine triphosphate nucleotidohydrolase (dUTPase) and present the first evidence that the dUTPase is able to induce immune dysregulation in vitro as demonstrated by the inhibition of the replication of stimulated peripheral blood mononuclear cells (PBMCs) and the upregulation of several proinflammatory cytokines including TNF-alpha, IL-1beta, IL-8, IL-6, and IL-10 produced by unstimulated PBMCs treated with purified EBV-encoded dUTPase.

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We wanted to determine if different doses of exercise, performed in the initial days after infection when the host is mounting an immune response, altered mortality, and morbidity to influenza virus infection in mice. Forty hemagglutinating units of influenza virus (A/Puerto Rico/8/34) were administered intranasally to lightly anesthetized mice. Male Balb/cByJ mice were randomized to one of three groups: sedentary control (CON); moderate (MOD) exercise (20-30 min at 8-12 m/min); or prolonged (PRO) exercise (2.

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In the present study the global effect of restraint stress on gene expression in the murine lung during an experimental influenza A/PR8 viral infection was examined. Gene expression profiling using high density oligonucleotide microarrays revealed that the expression of 95 genes was altered on day 3 post infection (p.i.

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Activation of the hypothalamic-pituitary-adrenal axis (HPA) and sympathetic nervous system by stress has been shown to modulate both innate and adaptive immunity during an experimental influenza A/PR8 viral infection. HPA activation alters levels of glucocorticoids (GC) and opioids which are associated with suppression of lymphoid cellularity and NK activity. These experiments were designed to investigate the role that stress-induced GC and opioids have in modulating NK activity during an influenza viral infection.

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Antibodies to several Epstein-Barr virus (EBV)-encoded enzymes are observed in patients with different EBV-associated diseases. The reason for these antibody patterns and the role these proteins might play in the pathophysiology of disease, separate from their role in virus replication, is unknown. In this series of studies, we found that purified EBV deoxyuridine triphosphate nucleotidohydrolase (dUTPase) can inhibit the replication of human peripheral blood mononuclear cells in vitro and upregulate the production of TNF-alpha, IL-1beta, IL-6, IL-8, and IL-10.

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Epstein-Barr virus (EBV) is the causative agent of infectious mononucleosis (IM). In addition, latent infections with EBV are associated with nasopharyngeal carcinoma (NPC) and Burkitt's Lymphoma (BL). Antibodies to several EBV-encoded early antigens (EA) are often observed in patients with NPC and BL, however, the role of EBV-encoded proteins in the etiology of these and other EBV-associated diseases is not completely understood.

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These experiments were designed to examine the influences of restraint stress (RST) on natural killer (NK) activity and to determine its consequences on influenza A/PR8 (A/PR8) viral replication in mice. The data showed that RST delayed the recruitment of NK1.1+ cells into the lung parenchyma during infection.

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Social disruption (SDR) in male mice reduces the sensitivity of their splenocytes to the actions of glucocorticoids. To determine whether physical defeat is necessary for the development of this reduced sensitivity, a modification of the SDR paradigm was employed in which mice were exposed to fighting conspecifics in the presence or absence of physical contact. This was accomplished by dividing a cage of 5 resident male C57BL/6 mice in half with a wire mesh partition so that 2 of the mice in the cage (SDR Physical Contact mice) fought and were defeated by an aggressive male C57BL/6 intruder that was placed into the cage for 2h for up to 6 days, while the remaining 3 resident mice (SDR Sensory Contact mice) were on the opposite side of the partition and thus prevented from physically interacting with the intruder.

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Experimental animal models have been used to examine stress-induced interactions among the nervous, endocrine, and immune systems. Generally, the response to stress results in a body-wide set of physiologic adaptations, mediated through the activation of neuroendocrine pathways that intersect and modulate inflammatory and immune responses. These interacting responses modulate diverse physiological processes including the initiation of tissue repair and wound healing.

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Stimulation of splenocytes from socially stressed mice [social disruption (SDR)] with Gram-negative bacterial lipopolysaccharide (LPS) revealed a state of functional glucocorticoid (GC) resistance. LPS-stimulated splenocytes were less sensitive to the inhibitory effects of corticosterone. This study demonstrated that activation signals were required for the expression of splenic GC resistance.

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Stress has a negative impact on wound healing. This murine study evaluated the effect of restraint stress (RST) on interleukin-1 (IL-1) and keratinocyte growth factor-1 (KGF-1) gene expression in cutaneous wounds by in situ hybridization. At day 1, RST mice had reduced frequency of IL-1beta mRNA-expressing fibroblasts compared to control mice.

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