Social stress enhances sympathetic innervation of primate lymph nodes: Mechanisms and implications for viral pathogenesis
ABSTRACT Behavioral processes regulate immune system function in part via direct sympathetic innervation of lymphoid organs, but little is known about the factors that regulate the architecture of neural fibers in lymphoid tissues. In the present study, we find that experimentally imposed social stress can enhance the density of catecholaminergic neural fibers within axillary lymph nodes from adult rhesus macaques. This effect is linked to increased transcription of the key sympathetic neurotrophin nerve growth factor and occurs predominately in extrafollicular regions of the paracortex that contain T-lymphocytes and macrophages. Functional consequences of stress-induced increases in innervation density include reduced type I interferon response to viral infection and increased replication of the simian immunodeficiency virus. These data reveal a surprising degree of behaviorally induced plasticity in the structure of lymphoid innervation and define a novel pathway by which social factors can modulate immune response and viral pathogenesis.
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ABSTRACT: Although we generally experience our bodies as being biologically stable across time and situations, an emerging field of research is demonstrating that external social conditions, especially our subjective perceptions of those conditions, can influence our most basic internal biological processes-namely, the expression of our genes. This research on human social genomics has begun to identify the types of genes that are subject to social-environmental regulation, the neural and molecular mechanisms that mediate the effects of social processes on gene expression, and the genetic polymorphisms that moderate individual differences in genomic sensitivity to social context. The molecular models resulting from this research provide new opportunities for understanding how social and genetic factors interact to shape complex behavioral phenotypes and susceptibility to disease. This research also sheds new light on the evolution of the human genome and challenges the fundamental belief that our molecular makeup is relatively stable and impermeable to social-environmental influence.07/2013; 1(3):331-348. DOI:10.1177/2167702613478594
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ABSTRACT: Chronic Psychological stress (CPS) has several adverse effects both on HIV people and on HIV+patient. HIV-people with CPS are more susceptible to HIV infection than the HIV- people without CPS. T-cells have CXCR4 receptor and Macrophages have CCR5 receptor which can bind with both glucocorticoid and catecholamine hormone. HIV has GP120 residue which is able to bind with both CD4 and CXCR4/CCR5 receptor for its entry into the host cells. CPS increases glucocorticoid and catecholamine concentration in blood and thereby activates cAMP signaling pathway through binding the CXCR4/CCR5 receptors expressed on T cells and macrophages. This signal transduction pathway leads to the synthesis of more CXCR4 and CCR5 receptors by those cells, and in turn the cells become more susceptible to HIV infection. On HIV+patient stress hormones arrest the infected cell in G2 phase which is favorable for HIV replication. At the same time T-cells and macrophage are more susceptible to HIV, so HIV can infects a lot of immune cells and thereby makes the immune system weak. Stress also inhibits Th2 when the cell produces INF-γ as a response to viral attack. So that other cells remain vulnerable to viral infection. When T-cell count is decreased in the blood, the body cannot protect itself from other opportunistic infectious pathogens. As a result progression of AIDS increases rapidly.
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ABSTRACT: Genomics-based analyses have provided deep insight into the basic biology of cancer and are now clarifying the molecular pathways by which psychological and social factors can regulate tumor cell gene expression and genome evolution. This review summarizes basic and clinical research on neural and endocrine regulation of the cancer genome and its interactions with the surrounding tumor microenvironment, including the specific types of genes subject to neural and endocrine regulation, the signal transduction pathways that mediate such effects, and therapeutic approaches that might be deployed to mitigate their impact. Beta-adrenergic signaling from the sympathetic nervous system has been found to up-regulated a diverse array of genes that contribute to tumor progression and metastasis, whereas glucocorticoid-regulated genes can inhibit DNA repair and promote cancer cell survival and resistance to chemotherapy. Relationships between socio-environmental risk factors, neural and endocrine signaling to the tumor microenvironment, and transcriptional responses by cancer cells and surrounding stromal cells are providing new mechanistic insights into the social epidemiology of cancer, new therapeutic approaches for protecting the health of cancer patients, and new molecular biomarkers for assessing the impact of behavioral and pharmacologic interventions.Brain Behavior and Immunity 11/2012; 30. DOI:10.1016/j.bbi.2012.11.008 · 6.13 Impact Factor