Abstract
The inflammatory response should be considered a protective immune reaction of the host aimed at the removal of pathogens, sometimes irrespective of negative side-effects. In this review we discuss the differential contribution of macrophages and neutrophilic granulocytes to nitrosative stress in vivo and discuss how the timing and concentration of nitric oxide (NO.) are important factors determining the degree of nitrosative stress during parasite-induced inflammation. Infections of common carp (Cyprinus carpio) with the extracellular protozoan parasite Trypanoplasma borreli provide an excellent example of how adaptation and homeostasis are essential elements of the host-pathogen relationship. On the one hand, host-derived NO. interferes with clearance of IgM from the parasite surface and thus can be considered a protective immune reaction of the host. On the other hand, it is essential that the host limits the risks associated with the production of NO., preventing suppressive effects on lymphocyte proliferation. We review, for both host and parasite, the role of oxygen and nitrogen radicals in the induction of nitrosative stress and the importance of antioxidant compounds for protection against these radicals. Finally, mediators of inflammation such as cytokines, chemokines or alarmins that are involved in the inflammatory response will be discussed in the context of the carp-T. borreli infection model.
Keywords: Nitrosative stress, inflammation, teleost, myeloperoxidase, macrophages, neutrophilic granulocytes, nitric oxide, protozoan parasites
Current Pharmaceutical Design
Title: Nitrosative Stress During Infection-Induced Inflammation in Fish: Lessons From a Host-Parasite Infection Model
Volume: 16 Issue: 38
Author(s): Geert F. Wiegertjes and Maria Forlenza
Affiliation:
Keywords: Nitrosative stress, inflammation, teleost, myeloperoxidase, macrophages, neutrophilic granulocytes, nitric oxide, protozoan parasites
Abstract: The inflammatory response should be considered a protective immune reaction of the host aimed at the removal of pathogens, sometimes irrespective of negative side-effects. In this review we discuss the differential contribution of macrophages and neutrophilic granulocytes to nitrosative stress in vivo and discuss how the timing and concentration of nitric oxide (NO.) are important factors determining the degree of nitrosative stress during parasite-induced inflammation. Infections of common carp (Cyprinus carpio) with the extracellular protozoan parasite Trypanoplasma borreli provide an excellent example of how adaptation and homeostasis are essential elements of the host-pathogen relationship. On the one hand, host-derived NO. interferes with clearance of IgM from the parasite surface and thus can be considered a protective immune reaction of the host. On the other hand, it is essential that the host limits the risks associated with the production of NO., preventing suppressive effects on lymphocyte proliferation. We review, for both host and parasite, the role of oxygen and nitrogen radicals in the induction of nitrosative stress and the importance of antioxidant compounds for protection against these radicals. Finally, mediators of inflammation such as cytokines, chemokines or alarmins that are involved in the inflammatory response will be discussed in the context of the carp-T. borreli infection model.
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Cite this article as:
F. Wiegertjes Geert and Forlenza Maria, Nitrosative Stress During Infection-Induced Inflammation in Fish: Lessons From a Host-Parasite Infection Model, Current Pharmaceutical Design 2010; 16 (38) . https://dx.doi.org/10.2174/138161210794519138
DOI https://dx.doi.org/10.2174/138161210794519138 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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