Abstract
The expression of the inducible nitric oxide synthase (iNOS) is one of the direct consequences of an inflammatory process. Early studies have focused on the potential toxicity of the ensuing high-output NO-synthesis serving as a means to eliminate pathogens or tumor cells but also contributing to local tissue destruction during chronic inflammation. More recently, however, data are accumulating on a protective effect of high-output NO synthesis and - equally important - on a generegulatory function that helps to mount a protective stress response and simultaneously aids in downregulating the proinflammatory response. These findings appear to contrast to the often observed sustained iNOS-expression during chronic inflammatory diseases, as for instance in Psoriasis vulgaris and other conditions with a chronic Th1-like reactivity. We here pose the question as to whether the iNOS is really active in these diseases. We review the data accumulated on iNOS expression in chronic diseases. We also report on the various factors that potentially interfere with proper NO formation by the expressed enzyme. We also highlight the recent findings of how, why and where evidences emerge that impeded NO formation contributes to chronic disease processes and finally present details on our current understanding of such abnormally low NO synthesis and its contribution to the pathophysiological processes of the human proinflammatory skin disease Psoriasis vulgaris.
Keywords: proinflammatory disease, reverse transcriptase-polymerase chain reaction, cytokines, inos-expression, disease, cofactors
Current Molecular Medicine
Title: The Role of iNOS in Chronic Inflammatory Processes In Vivo: Is it Damage-Promoting, Protective, or Active at all?
Volume: 4 Issue: 7
Author(s): Christoph V. Suschek, Oliver Schnorr and Victoria Kolb-Bachofen
Affiliation:
Keywords: proinflammatory disease, reverse transcriptase-polymerase chain reaction, cytokines, inos-expression, disease, cofactors
Abstract: The expression of the inducible nitric oxide synthase (iNOS) is one of the direct consequences of an inflammatory process. Early studies have focused on the potential toxicity of the ensuing high-output NO-synthesis serving as a means to eliminate pathogens or tumor cells but also contributing to local tissue destruction during chronic inflammation. More recently, however, data are accumulating on a protective effect of high-output NO synthesis and - equally important - on a generegulatory function that helps to mount a protective stress response and simultaneously aids in downregulating the proinflammatory response. These findings appear to contrast to the often observed sustained iNOS-expression during chronic inflammatory diseases, as for instance in Psoriasis vulgaris and other conditions with a chronic Th1-like reactivity. We here pose the question as to whether the iNOS is really active in these diseases. We review the data accumulated on iNOS expression in chronic diseases. We also report on the various factors that potentially interfere with proper NO formation by the expressed enzyme. We also highlight the recent findings of how, why and where evidences emerge that impeded NO formation contributes to chronic disease processes and finally present details on our current understanding of such abnormally low NO synthesis and its contribution to the pathophysiological processes of the human proinflammatory skin disease Psoriasis vulgaris.
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Cite this article as:
Suschek V. Christoph, Schnorr Oliver and Kolb-Bachofen Victoria, The Role of iNOS in Chronic Inflammatory Processes In Vivo: Is it Damage-Promoting, Protective, or Active at all?, Current Molecular Medicine 2004; 4 (7) . https://dx.doi.org/10.2174/1566524043359908
DOI https://dx.doi.org/10.2174/1566524043359908 |
Print ISSN 1566-5240 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5666 |

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