Chitosan induces different L-arginine metabolic pathways in resting and inflammatory macrophages

C. PORPORATTO; I.D. BIANCO; C.M. RIERA; S.G. CORREA

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS

Elsevier

Año: 2003 vol. 304 p. 266 - 272

0006-291X

Chitosan is a linear polymer of N-acetyl-D-glucosamine and deacetylated glucosamine widely used as a wound-healing accelerator in clinical and veterinary medicine. Chitosan enhances the functions of inflammatory cells such as macrophages (M/), inducing the production of cytokines as well as the expression of activation markers, Fc receptors and mannose receptor. In this work we studied the effects of chitosan on the arginine metabolic pathways of both resident and inflammatory (proteose–peptone elicited) rat M/. Our results show that low molecular weight (LMW) chitosan activated moderately both the inducible nitric oxide synthase (iNOS) and arginase pathways in residentM/. In inflammatory M/ treated with chitosan instead, the arginase activity was strongly enhanced. Supernatants of chitosan-stimulated M/ enhanced the proliferation of the rat cell line C6. These findings suggest that the healing activity of chitosan could rely on the enhanced arginase activity observed in a wound-associated inflammatory milieu.N-acetyl-D-glucosamine and deacetylated glucosamine widely used as a wound-healing accelerator in clinical and veterinary medicine. Chitosan enhances the functions of inflammatory cells such as macrophages (M/), inducing the production of cytokines as well as the expression of activation markers, Fc receptors and mannose receptor. In this work we studied the effects of chitosan on the arginine metabolic pathways of both resident and inflammatory (proteose–peptone elicited) rat M/. Our results show that low molecular weight (LMW) chitosan activated moderately both the inducible nitric oxide synthase (iNOS) and arginase pathways in residentM/. In inflammatory M/ treated with chitosan instead, the arginase activity was strongly enhanced. Supernatants of chitosan-stimulated M/ enhanced the proliferation of the rat cell line C6. These findings suggest that the healing activity of chitosan could rely on the enhanced arginase activity observed in a wound-associated inflammatory milieu./), inducing the production of cytokines as well as the expression of activation markers, Fc receptors and mannose receptor. In this work we studied the effects of chitosan on the arginine metabolic pathways of both resident and inflammatory (proteose–peptone elicited) rat M/. Our results show that low molecular weight (LMW) chitosan activated moderately both the inducible nitric oxide synthase (iNOS) and arginase pathways in residentM/. In inflammatory M/ treated with chitosan instead, the arginase activity was strongly enhanced. Supernatants of chitosan-stimulated M/ enhanced the proliferation of the rat cell line C6. These findings suggest that the healing activity of chitosan could rely on the enhanced arginase activity observed in a wound-associated inflammatory milieu./. Our results show that low molecular weight (LMW) chitosan activated moderately both the inducible nitric oxide synthase (iNOS) and arginase pathways in residentM/. In inflammatory M/ treated with chitosan instead, the arginase activity was strongly enhanced. Supernatants of chitosan-stimulated M/ enhanced the proliferation of the rat cell line C6. These findings suggest that the healing activity of chitosan could rely on the enhanced arginase activity observed in a wound-associated inflammatory milieu./. In inflammatory M/ treated with chitosan instead, the arginase activity was strongly enhanced. Supernatants of chitosan-stimulated M/ enhanced the proliferation of the rat cell line C6. These findings suggest that the healing activity of chitosan could rely on the enhanced arginase activity observed in a wound-associated inflammatory milieu./ enhanced the proliferation of the rat cell line C6. These findings suggest that the healing activity of chitosan could rely on the enhanced arginase activity observed in a wound-associated inflammatory milieu.