الفهرس 
Biological characteristics Of CytokinesOnly 14 pages are availabe for public view
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Abstract
Cytokines play a key role in modulation of immune response, Cytokine networks regulate lymphocyte turnover, differentiation, and activation. Many different cell types, in addition to immune cells, produce cytokines and express receptors for cytokines. Cell-to-cell communication (cellular “crosstalk”) is maintained via cytokine networks. In disease, these networks undergo imbalance. By measuring amplification or downregulation of cytokine signaling cascades in response to pathological insults or therapeutic interventions, it might be possible to evaluate disease progression or regression. Multiplex formats for cytokine profiling are now available and appear to be especially useful in monitoring cytokine profile alterations in a variety of human diseases (Theresa L Whiteside, 2007).
Cytokines play a pivotal role in the coordination and regulation of immune responses. Surgical trauma and anesthesia are associated with a complex dysregulation of the immune system with the activation of both proinflammatory and anti-inflammatory responses. Interleukin-1, tumor necrosis factor-α and interleukin-6 have local and systemic effects that may limit injury and the spread of infection and provide a suitable environment for tissue healing and repair (Whiteside, 2002).
Cytokines may show the following features; Pleiotropy, Ambiguity, Redundancy, Synergy, and Antagonism.
Sepsis is defined as an infection or suspected infection that triggers a particular inflammatory response. This is called the systemic inflammatory response syndrome and is characterised by the presence of more than one of the following: body temperature outside 36-38°C; heart rate >90 beats/min; hyperventilation, seen as a respiratory rate of >20 breaths/min or a PCO2<32 mm Hg; white blood cell count outside 4000-12 000 cells/l.
Although not universally accepted terminology, severe SIRS and SIRS shock are terms that some authors have proposed. These terms suggest organ dysfunction or refractory hypotension related to an ischemic or inflammatory process rather than to an infectious etiology.
Multiple organ dysfunction syndrome is the presence of altered organ function in acutely ill patients such that homeostasis cannot be maintained without intervention. Primary MODS is the direct result of a well defined insult in which organ dysfunction occurs early and can be directly attributable to the insult itself. Secondry MODS develops as a consequence of a host response and is identified witin the context of SIRS.
Systemic inflammatory response syndrome (SIRS) is non specific and may follow a variety of clinical insults, including infection, pancreatitis, ischemia, multiple trauma, tissue injury, hemorrhagic shock, or immune-mediated organ injury.
Trauma, inflammation, or infection leads to the activation of the inflammatory cascade. When SIRS is mediated by an infectious insult, the inflammatory cascade is often initiated by endotoxin. Tissue macrophage, monocytes, mast cells, platelets, and endothelial cells are able to produce a multitude of cytokines. The cytokines tissue necrosis factor-α (TNF-α) and interleukin-1 (IL-1) are released first and initiates several cascades. The release of IL-1 and TNF-α (or the presence of endotoxin or exotoxin) leads to cleavage of the nuclear factor β(NF-β) inhibitor. Once the inhibitor is removed. NF-β is able to initiate the production of mRNA, which induces the production other pro-inflammatory cytokines.
IL-6, IL-8, and interferon gamma are the primary pro-inflammatory mediators induced by NF-β. Invitro research suggests that glucocorticoids may function by inhibiting NF-β. TNF-α and IL-1have been shown to be released in large quantities within 1 hour of an insult and have both local and systemic effects. In vitro studies have shown that these 2 cytokines given individually produce no significant hemodynamic response but cause severe lung injury and hypotension when given together. TNF-α and IL-1 are responsible for fever and the release of stress hormones (norepinephrine, vasopressin, activation of the renin-angiotensin-aldosterone system).
The severity and rising incidence of sepsis, combined with a need to rationalise its treatment, has resulted in the recent release of joint international guidelines from US and European critical care societies. Using the latest evidence, they provide a logical approach to sepsis, The latest guidelines on sepsis will affect how we practise medicine.
The initial medical care should include prompt initiation of pertinent laboratory testing and imaging studies after obtaining a history and performing a physical examination. Treatment should then be focused based on possible inciting causes of systemic inflammatory response syndrome (e.g. appropriate treatment of acute myocardial infarction differs from the treatment of community-acquired pneumonia or pancreatitis). Treatment also includes embirical antibiotics, steroids, TNF and IL-1 receptor antagonists, antibradykinin, platelet activating factor receptor antagonists, and anticoagulants (antithrombin ΙΙΙ) and supplemental oxygen.