Acute inflammatory response

The migration of phagocytic cells to the site of damage is one of the most fundamental components of the acute inflammatory response, and the key players in this process will be presented next. 

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... 

The very early peak of neutrophil invasion into an inflamed area is followed several hours later by a wave of a second class of phagocytic cells, the macrophages. This biphasic pattern of inflammatory cell movement and accumulation is observed in most acute inflammatory responses. The mononuclear phagocyte in the blood is known as the monocyte and differentiates... 

After 7 days, the acute inflammatory response at the implantation site was evaluated. Bisphenol A resulted in a moderate level of irritation at the implantation site and was clearly the least biocompatible test substance. Tyrosine derivatives containing the benzyloxycar-bonyl group caused a slight inflammatory response, while all other tyrosine derivatives produced no abnormal tissue response at all. These observations indicate that tyrosine dipeptide derivatives, even if fully protected, are more biocompatible than BPA, a synthetic diphenol. ... 

Hepatic reperfusion injury is not a phenomenon connected solely to liver transplantation but also to situations of prolonged hypoperfusion of the host s own liver. Examples of this occurrence are hypovolemic shock and acute cardiovascular injur) (heart attack). As a result of such cessation and then reintroduction of blood flow, the liver is damaged such that centrilobular necrosis occurs and elevated levels of liver enzymes in the serum can be detected. Particularly because of the involvement of other organs, the interpretation of the role of free radicals in ischaemic hepatitis from this clinical data is very difficult. The involvement of free radicals in the overall phenomenon of hypovolemic shock has been discussed recently by Redl et al. (1993). More specifically. Poll (1993) has reported preliminary data on markers of free-radical production during ischaemic hepatitis. These markers mostly concerned indices of lipid peroxidation in the serum and also in the erythrocytes of affected subjects, and a correlation was seen with the extent of liver injury. The mechanisms of free-radical damage in this model will be difficult to determine in the clinical setting, but the similarity to the situation with transplanted liver surest that the above discussion of the role of XO activation, Kupffer cell activation and induction of an acute inflammatory response would be also relevant here. It will be important to establish whether oxidative stress is important in the pathogenesis of ischaemic hepatitis and in the problems of liver transplantation discussed above, since it would surest that antioxidant therapy could be of real benefit. 

In addition to minimizing the acute inflammatory response, rest prevents additional injury to the affected area.13 The properties of the muscle-tendon unit are altered during the acute injury, with limitations on the ability of the muscles and tendons to stretch. Early activity predisposes a patient to further injury, but prolonged inactivity can lengthen recovery times. 

Peritonitis is defined as the acute inflammatory response of the peritoneal lining to microorganisms, chemicals, irradiation, or foreign-body injury. This chapter deals only with peritonitis of infectious origin. 

Immunoglobulin receptors, such as the high affinity receptor for IgE, are present on mast cells and bloodbome basophils. These receptors play an important role in hypersensitivity and the initiation of acute inflammatory responses. 

Weekes J et al. Bovine dilated cardiomyopathy proteomic analysis of an animal model of human dilated cardiomyopathy Electrophoresis 1999 20 898-906. Doherty NS et al. Analysis of changes in acute phase plasma proteins in an acute inflammatory response and in rheumatoid arthritis using two-dimensional gel electrophoresis. Electrophoresis 1998 19 355-363. 

Srikrishna, G., Toomre, D.K., Manzi, A., Panneerselvam, K., Freeze, H.H., Varki, A., and Varki, N.M. (2001) A novel anionic modification of N-glycans on mammalian endothelial cells is recognized by activated neutrophils and modulates acute inflammatory responses./. Immunol. 166, 624-632. 

NiS04 and NiCl2 instilled into rat lungs also produced an inflammatory response (17). However, analysis of bronchoalveolar lavage fluid from rodents exposed to diesel exhaust containing 3.5 mg soot/m3, 7 h/day for 2, 12 or 17 days indicated no influx of inflammatory cells (20). Thus, the diesel soot, at lung burdens of 0.5 mg/g lung, does not produce an acute inflammatory response. 

Dietary copper deficiency increases the acute inflammatory response in rats and other small laboratory animals (Schuschke et al. 1994). The release of inflammatory mediators, such as histamine and serotonin, from mast cells increases the vascular permeability of postcapillary venules and results in edema. In copper-deficient rats, release of histamine from mast cells correlates positively with frequency of the acute inflammatory response. Copper-deficient rats (0.6 mg Cu/kg DW ration for 4 weeks) have more mast cells in muscle than copper-adequate controls given diets containing 6.3 mg Cu/kg DW ration however, histamine content of mast cells is not affected (Schuschke et al. 1994). An early clinical sign of copper deficiency is a reduction in the number of circulating neutrophils the mechanism for copper-deficient neutropenia (leukopenia in which... 

Kerkvliet, N. and Oughton, J., Acute inflammatory response to sheep red blood cell challenge in mice treated with 2,3,7,8-tetrachlordibenzo-p-dioxin Phenotypic and functional analysis of peritoneal exudate cells, Toxicol. Appl. Pharmacol., 119, 248, 1993. 

Gross autopsy findings of pulmonary edema and hemorrhage after acute exposure to ozone have been known for some time. Several studies have shown that edema and an acute inflammatory response occur in several species after brief exposures to ozone. The minimal concentration of ozone... 

Side effects associated with diethylcarbamazine include headache, malaise, weakness, and loss of appetite. More severe reactions (fever, acute inflammatory response) may also occur following diethylcarbamazine use, but these reactions may be caused by the release of antigenic substances from the dying roundworms rather than from the drug itself. 

Figure 1.8 Tissue section at implant site showing the effect of NO evolution on the acute inflammatory response, (a) Sensor with no NO evolution (control) (b) no evolution for about 18h. Reprinted with permission from Ref. 65. Copyright 2005 John Wiley Sons. (See the color version of this figure in Color Plates section.)...

Tang L, Eaton JW. Fibrin(ogen) mediates acute inflammatory responses to biomaterials. Journal of Experimental Medicine 1993, 178, 2147-2156. 

Zdolsek J, Eaton JW, Tang L. Histamine release and fibrinogen adsorption mediate acute inflammatory responses to biomaterial implants in humans. Journal of Translational Medicine 2007, 5, 31. 

Tang L, Jennings TA, Eaton JW. Mast cells mediate acute inflammatory responses to implanted biomaterials. Proceedings of the National Academy of Sciences of the United States of America 1998, 95, 8841-8846. 

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