Cytokines stress response

In the ebb phase, there is increased activity of the sympathetic nervous system and increased plasma levels of adrenaline and glucocorticoids but a decreased level of insulin. This results in mobilisation of glycogen in the liver and triacylglycerol in adipose tissue, so that the levels of two major fuels in the blood, glucose and long-chain fatty acids, are increased. This is, effectively, the stress response to trauma. These changes continue and are extended into the flow phase as the immune cells are activated and secrete the proinflammatory cytokines that further stimulate the mobilisation of fuel stores (Table 18.2). Thus the sequence is trauma increased endocrine hormone levels increased immune response increased levels of cytokines metabolic responses. 

The mechanistic basis of the neuroprotective activity of FAEE appears to rely not only on its general free-radical trapping or antioxidant activity per se, but also on its activity in mediating the induction of stress response proteins (HO-1 and F1SP72), cytoprotective (phase 2) proteins, and the parallel suppression of genes induced by pro-inflammatory cytokines, such as nitric oxide synthase (iNOS). 

The stress or growth pathways modulated by vanadium involve specialized effectors and often can be activated by excess ROS. Cytokines, small proteins that effect communication between cells or cell behavior, can be involved in the cellular stress response. Tumor necrosis factor a (TNFa) is a cytokine stress signal that binds to a membrane receptor (tumor necrosis factor receptor, or TNFR). This interaction stimulates kinase activity that leads to cell injury and inflammation and also to the activation of caspases, a family of cysteine-dependent aspartate-directed proteases that are involved in apoptosis. The mitogen-activated protein (MAP) kinase cascade regulates both mitosis and apoptosis signaling pathways. 

Exposure to pathobiological stressors causes the formation or release of mediators other than cytokines and ROS. These include stress-induced hormones and nitric oxide (NO). Stress responses stimulate the hypothalamic-pituitary axis causing the release of adrenocorticotropin, thereby elevating glucocorticoid levels. Glucocorti-... 

It has become clear that cytokines are potent activators of the central stress response, serving as the afferent limb of the response system during acute or chronic inflammatory shess. Several pro-inflammatory cytokines, including tumor necrosis factor-a (TNF-a), inteiieukin-lp (IL-lp), and inteiTeukin-6 (IL-6), can activate the HPA axis (Chrousos, 1995 Tsigos et al., 1997). 

Keywords Alpha-melanocyte stimulating hormone Adre-nocorticotrophic hormone Corticotropin releasing hormone Cytokines Depression Hypothalamic-pituitary-adrenal axis Proenkephalin Proopiomelanocortin Schizophrenia Stress response... 

On the other hand, pro-inflammatory cytokines such as lL-1 and lL-6 are known to stimulate the HPA-axis via hypothalamic neurons. For example, the release of the CRH and GHRH is stimulated by lL-1 (Besedovsky et al., 1986 Berkenbosch et al., 1987), the central lL-1 upregulation leads to stimulation of CRH, the HPA-axis, and the sympathetic nervous system (Sundar et al., 1990 Weiss et al., 1994). Therefore, a vicious circle may be induced, if the stress response is not limited, as it is discussed in MD (see Figure 36.2). 

Wang KX, Denhardt DT (2008) Osteopontin role in immune regulation and stress responses. Cytokine Growth Factor Rev 19(5-6) 333-345. doi 10.1016/j. cytogfr.2008.08.001... 

Other relationships between fatty acids and cytokines and stress have been found. Recently, Zimmer et al. (2000) found that a chronic n-3-PUF A-deficient diet induced a marked decrease in dopamine vesicle density in the rat frontal cortex. This is an interesting finding because dopamine modifies the cell-mediated immune-response and mediates stress responses in mice (Inglis and, Konstandi, et al., 2000 Moghaddam, 1999 Nizoguchi, et al., 2000 Wu, et al., 1999). 

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