Abstract
We have recently described the purification of a 54 kDa acidic protein, identified as macrophage-derived neutrophil chemotactic factor (MNCF). This protein causes in vitro chemotaxis as well as in vivo neutrophil migration even in animals treated with dexamethasone. This in vivo chemotactic activity of MNCF in animals pretreated with dexamethasone is an uncommon characteristic which discriminates MNCF from known chemotactic cytokines. MNCF is released in the supernatant by macrophage monolayers stimulated with lipopolysaccharide (LPS). In the present study, we describe some biological characteristics of homogenous purified MNCF. When assayed in vitro, MNCF gave a bell-shaped dose–response curve. This in vitro activity was shown to be caused by haptotaxis. Unlike N-formyl-methionylleucyl- phenylalanine (FMLP) or interleukin 8 (IL-8), the chemotactic activity of MNCF in vivo and in vitro, was inhibited by preincubation with D-galactose but not with D-mannose. In contrast with IL-8, MNCF did not bind to heparin and antiserum against IL-8 was ineffective in inhibiting its chemotactic activity. These data indicate that MNCF induces neutrophil migration through a carbohydrate recognition property, but by a mechanism different from that of the known chemokines. It is suggested that MNCF may be an important mediator in the recruitment of neutrophils via the formation of a substrate bound chemotactic gradient (haptotaxis) in the inflamed tissues.
Highlights
Emigration of neutrophils from the circulating blood to the site of the injury is a cardinal event during the inflammatory process
The chemotactic activity was shown to result from haptotaxis rather than chemokinesis since the neutrophil chemokinetic migration induced by purified macrophage-derived neutrophil chemotactic factor (MNCF) was similar to that of a negative control
Like the crude macrophage-derived neutrophil chemotactic factor (MNCF), this protein was able to stimulate neutrophil migration in animals pretreated with dexamethasone. 14 21 This in vivo chemotactic activity is an uncommon cytokine characteristic and seems peculiar to MNCF
Summary
Emigration of neutrophils from the circulating blood to the site of the injury is a cardinal event during the inflammatory process. This phenomenon is complex and mediated by various molecules acting in different ways. 8 (IL-1, IL-8), tumour necrosis factor (TNF), and the complement fragments and leukotriene B4 (LTB4) are macrophage products thought to be involved in the migration of neutrophils to the inflamed site, a phenomenon characteristic of the acute phase of the inflammatory process.[2,3,4,5] Some products such as C5a and LTB4 may have a direct chemotactic effect on neutrophils.[6,7,8] Others may act indirectly by mechanisms which depend on the tissue’s resident cells and on the endothelium. In addition to their effects on neutrophils and endothelial cells, where they increase the expression of adhesion molecules, IL-1 and TNF stimulate the release of chemotactic factors by resident macro-
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