Cell, animal neutrophils

Tumour necrosis factor (TNF) was originally described as a factor produced following exposure of Bacille-Calmette-Guerin-treated animals to bacterial endotoxin. It was so named because it possessed the ability to necrotise tumours. This factor is now named TNF-a to distinguish it from another, related cytokine lymphotoxin, which is sometimes referred to as TNF-/J Alternative names for TNF-a include cachectin and cytotoxin. Its primary cellular source in the body is the activated macrophage, but some other cell types (e.g. NK cells, astrocytes, some lymphocytes, fibroblasts, many tumour cells, endothelial cells and neutrophils) have also been shown to synthesise this cytokine. 

In an animal model, acute lung injury was inhibited by pretreatment with clarithromycin or roxithromycin, which significantly ameliorated bleomycin-induced increases in the total cell and neutrophil counts in bronchoalveolar lavage fluids and wet lung weight (25). Pretreatment with clarithromycin or roxithromycin also suppressed inflammatory cell infiltration and interstitial lung edema. Pretreatment with azithromycin was much less effective. 

Eicosapentaenoic add (Table 6) is easily incorporated into the cell membrane-bound phospholipids. It is a poor substrate for the cyclooxygenase/hydroper-oxidase enzymatic system, and only very small amounts of endproducts with three double bonds will be formed when compared with the relative effectiveness of arachidonate metabolism. In contrast, dcosapentaenoic add is a preferred substrate for product generation by the S-lipoxygenase in subcellular fractions of human and animal neutrophils [66,87], whereas docosahexaenoic add is also a markedly inferior substrate for leukotriene synthesis. Eicosapentaenoic acid appears to inhibit phospholipase activity, resulting in a decrease of aradiidonic acid release ([67] Fig. 4). Moreover, simultaneously with thromboxane A3 and prostaglandin I3 generation from eicosapentaenoic add, the synthesis of thromboxane A2 and prostacyclin (PGIj) from aradiidonic acid [47] decreases, mainly due to inhibitory effects on PGH synthase activity (Fig. 4). 

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... 

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