Acute phase response, initiation

The Acute-Phase Response, an important pathophysiologic phenomenon, replaces the normal homeostatic mechanisms with new set points that are presumably contributing to defensive or adaptive capabilities. The functions of these changes are highly variable and diverse some participate in initiating or sustaining the inflammatory process, others modulate it, and still others have adaptive roles... 

Acute Phase Response. Plasma AAG levels show a threefold to fourfold increase in most conditions associated with inflammation or tissue necrosis, with peak concentrations around 3 to 5 days after the initial insult. AAG may be one of the most reflable indicators of clinical activity of ulcerative colitis. 

Acute Phase Response, Hp synthesis is increased in the presence of acute inflammatory processes, tissue necrosis, or malignancy. Increased plasma levels are seen approximately 4 to 6 days after the initiation of these processes and take... 

The concentrations of C-reactive protein increase up to 1000 -fold in inflammatory conditions and in tissue necrosis. In addition, it can initiate reactions of agglutination, precipitation, and opsonization for phagocytosis and can activate the complement system. Other biological activities with platelets and lymphocytes have also been described, but the full biological functions of CRP have not yet been completely elucidated. Review of CRP and the acute phase response H. Gewurz el aL. Advan. Int. Med. 27, 345 -372 (1982). Review of structure and function M. B. Pepys. Bur. J. Rheumatol Inflammation S, 386-397 (1982). Book Arm. N. Y. Acad. Set 389, entitled "C-Reactive Protein and the Plasma Protein Response to Tissue Injury , I. Rushner et al, Eds. (1982) 482 pp. 

KOJ A. Initiation of acute phase response and synthesis of cytokines. Biochim Biophys Acta 1996,1317,84-94. 

In the very early phases of the acute inflammatory response most of the cells invading the damaged area are polymorphonuclear neutrophils, also denoted as PMNs, which serve as initial line of defense and source of proinflammatory cytokines. These cells, which usually live for 4-5 days, circulate in the blood until they are attracted by chemokines into injured tissues. Whereas physical injury does not recruit many neutrophils, infections with bacteria or fungi elicit a striking neutrophil response. The characteristic pus of a bacterial abscess is composed mainly of apoptotic (apoptosis) and necrotic PMNs. Emigration of neutrophils from the blood starts with a process denoted as margination where neutrophils come to lie at the periphery of flowing blood cells and adhere to endothelial cells (Fig. 1). L-Selectin is expressed... 

Lipids A first induce the expression of early inflammatory genes such as tumor necrosis factor- (TNF)-a, EL-1(3, type 2 TNF receptor, IP-10, D3, D8 and D2 genes [34]. Then further genes are activated such as other cytokines and receptors, adhesion molecules, acute-phase proteins, tissue factors, as well as the inducible NOS (NOS II). These cascades of events initiated by lipid A provoke in their target cells complex responses in vivo, whose relevance in the host response to tumor growth is reviewed below. 

Abstract The diet of industrialised countries is usually rich in amino acids, which are partly used as a source of calories. However, metabolic alterations are observed in diseased patients and a preferential retention of Sulphurated Amino Acids (SAA) occurs during the inflammatory response. It has been demonstrated in an acute sepsis phase model in rats that the metabolism of L-Cysteine (Cys) is modified. Glutathione (GSH) concentration is greater in the liver, kidneys and other organs and Cys incorporation into proteins is higher in the spleen and lungs. In the plasma Acute Phase Proteins are released while Albumin is decreased. The pro-inflammatory cytokines such as Interleukin-1, lnterleukin-6 and TNF-a are the main initiators altering protein and amino acid metabolism. 

There are a number of nonspecific laboratory tests that are useful to support the diagnosis of infection. The inflammatory process initiated by an infection sets up a complex of host responses. Activation of complements, such as C3a and C5a, initiates inflammation and sets off a cascade of changes and the subsequent release of mediators, all of which can be measured and monitored. Serum complement concentrations, particularly C3, usually are consumed as part of the host defense mechanism and subsequently are reduced during the early stages of an acute infectious process. Acute-phase reactants, such as the erythrocyte sedimentation rate (ESR) and the C-reactive protein concentration, are elevated in the presence of an inflammatory process but do not confirm the presence of infection because they are often elevated in noninfectious conditions, such as collagen-vascular diseases and arthritis. Large elevations in ESR are associated with infections such as endocarditis, osteomyelitis, and intraabdominal infections. ... 

A. Prodromal Phase. The initial phase of prodromal symptoms is characterized by the relatively rapid onset of nausea, vomiting, and malaise. This is a nonspecific clinical response to acute radiation exposure. It is not diagnostic of the degree of radiation injury however, in the absence of associated trauma and an early onset, it does suggest a large radiation exposure. The duration of this prodromal phase is short, generally a few hours, and the incapacitation should not be severe enough to warrant evacuation of military personnel away from their units. 

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