The linear model included allowance for probe-specific dye-effects, increasing the precision of the statistical tests. The p-values were adjusted for multiple testing, across all genes and all comparisons, using the method of Benjamini and Hochberg to control the expected false discovery rate at less than 5%. For each gene and each comparison, the comparison was considered to be statistically significant if the Dabrafenib 1195765-45-7 q-value was less than 5% and the fold change was greater than 50%. The linear model included allowance for probespecific dye-effects, increasing the precision of the statistical tests. During an immune response, the central nervous system and the immune system communicate with each other. The major pathway systems involved in this cross-talk are the hypothalamicpituitary-adrenal axis and the autonomic nervous system. Activation of the vagus-dominated parasympathetic, cholinergic nervous system is known to greatly attenuate and dampen the inflammatory response via nicotinergic cholinergic receptors expressed on macrophages and other immune cells. According to its afferent and efferent arms, this effect has been termed “inflammatory reflex” or “cholinergic anti-inflammatory pathway”. In contrast, the role of the sympathetic nervous system during inflammation seems to be more complex and less well understood. On the one hand, SNS activation seems to target immune cells that express adrenoreceptors, exacerbating the local inflammatory response , and increase the general immune and proinflammatory mediator response. On the other hand, several studies indicate an inhibitory effect of the SNS on the inflammatory response, suppressing the immune response by decreasing the activity of natural killer cells and T cell immunity. In addition, catecholamines released from presynaptic sympathetic nerve terminals lead to localized vasoconstriction, preventing invading pathogens from becoming systemic. Over two decades ago, lymphocytes were described as sources of catecholamines. These lymphocyte-derived catecholamines seem to act in an autocrine/paracrine fashion that affects lymphocyte trafficking , vascular perfusion, cell proliferation , cytokine production and the functional activity of lymphocytes. Recently, phagocytes have also been identified as a newly recognized source of catecholamines that exert a similar autocrine/paracrine regulation of phagocytes following release of norepinephrine or epinephrine. Additional experiments demonstrated that blockade of these phagocyte-derived catecholamines greatly attenuated lung inflammatory injury, while the opposite was the case when the catecholamine-inactivating enzymes catechol-O-methyltransferase and monoamine oxidase were inhibited. Therefore, activation of the adrenergic system during an inflammatory response may greatly enhance the local inflammatory response, resulting in neutrophil accumulation and enhanced cytokine production.