Inflammation, proteinases

Eosinophils may be increased in some patients, particularly during exacerbations. Activated inflammatory cells release a variety of mediators, most notably leukotriene B4, interleukin-8, and tumor necrosis factor-a (TNF-a). Various proteinases, such as elastase, cathepsin G, and proteinase-3, are secreted by activated neutrophils. These mediators and proteinases are capable of sustaining inflammation and damaging lung structures. 

While the majority of attention has focused on peptides contained within the nervous system, two other important methods for delivering peptides to the vicinity of the mast cell have been established (1) peptides produced and secreted by other cells of inflammation that may affect mast-cell function and (2) the local generation of mast-cell-active peptides by secreted enzymes acting on circulating protein precursors. Examples of the former include several, as yet ill-defined, peptide factors and cationic proteins from other immunocompetent cells [66-69], defined lymphokines such as the interleukin-1 [70] and interleukin-3 [71], and tumour necrosis factor [70], Examples of the latter include bradykinin [72] and a recently identified peptide produced by the action of acid proteinases on albumin [73, 74]. 

Molecular imaging may potentially address not only the pathophysiology of ischemia but also vascular inflammation causing rupture of atherosclerotic plaques before major ischemic events. Initial approaches have used imaging of "indium radiolabeled monocytes [150], upregulated metallo-proteinases [151], and imaging of apoptosis in atherosclerotic lesions [152]. However, none have evolved into clinically useful tests. 

Henson P, Johnston R (1987) Tissue injury in inflammation, oxidants, proteinases and cationic proteins. J Clin Invest 79 669-674... 

The proteolytic load a connective tissue endures during inflammation is a balance between the activity of the proteinases secreted by inflammatory cells and the local specific activity of functional plasma inhibitors. During inflammatory episodes, oxidative inactivation of specific inhibitors may move this delicate balance so that connective tissue macromolecule proteolysis is favoured (see Fig. 2). 

A proteinase inhibitor characteristic of acute-phase inflammation, al-antichymo-trypsin (ACT) has been identified in SP and reported to be elevated in AD patients (283). The level of ACT depended on ApoE genotype and was the highest in e3/e3 homozygotes and correlated with cognitive impairment and duration of the disease. The e4 genotypes have shovm a lower level of ACT and no correlation with impairment or duration. One should keep in mind that the same ACT inhibits Aj3... 

Abnormal accumulation of elastase, a serine proteinase from human neutrophil, causes a number of acute and chronic inflammation diseases (Bernstein et al, 1994, cited in (1)). There is a demand for specific and potent exogenous inhibitors of proteinases, such as HNE, associated with these inflammatory processes (Stemlicht and Werb, 1999, cited in (1)). The serine proteinase inhibitor from tamarind seeds needs to be studies to determine whether it could have such application. Anti-inflammatory properties of tamarind fmit pulp were reported (7). 

A. Janoff, Emphysema proteinase-anti proteinase imbalance. In Inflammation Basic Principles and Clinical Correlates (J. I. Gallin, I. M. Goldstein, and R. Snyderman, eds.). Raven Press, New York, 1988, p. 803. 

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