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 Indian J Med Microbiol  
 

Figure 2: Central nervous system regulation of innate immune response gene programs. (a) The HPA axis distributes glucocorticoid hormones through the blood to regulate gene expression in virtually every cell of the body. Hormone activation of the glucocorticoid receptor in leukocytes results in profound suppression of both pro-inflammatory gene networks (for example, NF-κB-mediated transcription of proinflammatory cytokine genes, such as IL1β, IL6 and TNF) and antiviral gene programs (for example, IRF-mediated transcription of type I interferon (IFN) genes, such as IFNA and IFNB). Activation of cytokine receptors in the hypothalamus triggers the production of glucocorticoids by the HPA axis. This constitutes the body's primary systemic mechanism for negative feedback control of pro-inflammatory gene expression triggered by microbial pattern recognition receptors (PRRs). (b) During fight-or-flight responses and acute injury, nerve fibers from the sympathetic nervous system (SNS) release the neurotransmitter noradrenaline into primary and secondary lymphoid organs, all other major organ systems (including the vasculature and perivascular tissues) and many peripheral tissues in which pro-inflammatory reactions occur. SNS nerve fibers can also stimulate the adrenal glands to release stored adrenaline into the systemic circulation. Both of these neuromediators regulate vascular function and stimulate leukocyte adrenergic receptors (for example, ADRB2) to activate transcription factors such as CREB and GATA family factors. SNS-induced transcriptional alterations can modulate hematopoiesis, redeploy leukocytes between tissue and blood, and repress IRF-mediated antiviral immune response gene programs while enhancing many NF-κB-mediated proinflammatory programs. ACTH: Adrenocorticotropic hormone; ADRB2: β2-adrenergic receptor, CRH: Corticotropin-releasing hormone, HPA: Hypothalamic–pituitary–adrenal, IL: Interleukin, IRF: Interferon regulatory factor, NF-κB: Nuclear factor-κB, TNF: Tumor necrosis factor[28]

Figure 2: Central nervous system regulation of innate immune response gene programs. (a) The HPA axis distributes glucocorticoid hormones through the blood to regulate gene expression in virtually every cell of the body. Hormone activation of the glucocorticoid receptor in leukocytes results in profound suppression of both pro-inflammatory gene networks (for example, NF-κB-mediated transcription of proinflammatory cytokine genes, such as <i>IL1β, IL6</i> and <i>TNF</i>) and antiviral gene programs (for example, IRF-mediated transcription of type I interferon (IFN) genes, such as <i>IFNA</i> and <i>IFNB</i>). Activation of cytokine receptors in the hypothalamus triggers the production of glucocorticoids by the HPA axis. This constitutes the body's primary systemic mechanism for negative feedback control of pro-inflammatory gene expression triggered by microbial pattern recognition receptors (PRRs). (b) During fight-or-flight responses and acute injury, nerve fibers from the sympathetic nervous system (SNS) release the neurotransmitter noradrenaline into primary and secondary lymphoid organs, all other major organ systems (including the vasculature and perivascular tissues) and many peripheral tissues in which pro-inflammatory reactions occur. SNS nerve fibers can also stimulate the adrenal glands to release stored adrenaline into the systemic circulation. Both of these neuromediators regulate vascular function and stimulate leukocyte adrenergic receptors (for example, ADRB2) to activate transcription factors such as CREB and GATA family factors. SNS-induced transcriptional alterations can modulate hematopoiesis, redeploy leukocytes between tissue and blood, and repress IRF-mediated antiviral immune response gene programs while enhancing many NF-κB-mediated proinflammatory programs. ACTH: Adrenocorticotropic hormone; ADRB2: β2-adrenergic receptor, CRH: Corticotropin-releasing hormone, HPA: Hypothalamic–pituitary–adrenal, IL: Interleukin, IRF: Interferon regulatory factor, NF-κB: Nuclear factor-κB, TNF: Tumor necrosis factor<sup>[28]</sup>