Cargando…
Trichinella inflammatory myopathy: host or parasite strategy?
The parasitic nematode Trichinella has a special relation with muscle, because of its unique intracellular localization in the skeletal muscle cell, completely devoted in morphology and biochemistry to become the parasite protective niche, otherwise called the nurse cell. The long-lasting muscle inf...
Autores principales: | , |
---|---|
Formato: | Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2011
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3079684/ https://www.ncbi.nlm.nih.gov/pubmed/21429196 http://dx.doi.org/10.1186/1756-3305-4-42 |
_version_ | 1782202045159178240 |
---|---|
author | Bruschi, Fabrizo Chiumiento, Lorena |
author_facet | Bruschi, Fabrizo Chiumiento, Lorena |
author_sort | Bruschi, Fabrizo |
collection | PubMed |
description | The parasitic nematode Trichinella has a special relation with muscle, because of its unique intracellular localization in the skeletal muscle cell, completely devoted in morphology and biochemistry to become the parasite protective niche, otherwise called the nurse cell. The long-lasting muscle infection of Trichinella exhibits a strong interplay with the host immune response, mainly characterized by a Th2 phenotype. The aim of this review is to illustrate the role of the Th2 host immune response at the muscle level during trichinellosis in different experimental models, such as knock-out or immuno-modulated mice. In particular, in knock-out mice a crucial role of IL-10 is evident for the regulation of inflammation intensity. The muscular host immune response to Trichinella is partially regulated by the intestinal phase of the parasite which emphasizes the intensity of the following muscle inflammation compared with animals infected by synchronized injections of newborn larvae. In eosinophil-ablated mice such as PHIL and GATA-- animals it was observed that there was an increased NOS2 expression in macrophages, driven by higher IFN-γ release, thus responsible for muscle larva damage. Besides modulation of the intestinal stage of the infection, using recombinant IL-12, increases the muscular parasite burden delaying adult worm expulsion from the intestine. Furthermore, a Th1 adjuvant of bacterial origin called Helicobacter pylori neutrophil activating protein (HP-NAP), administered during the intestinal phase of trichinellosis, alters the Th2 dependent response at muscle level. All these data from the literature delineate then a mutual adaptation between parasite and host immune response in order to achieve a strategic compromise between two evolutionary forces pointed towards the survival of both species. |
format | Text |
id | pubmed-3079684 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-30796842011-04-20 Trichinella inflammatory myopathy: host or parasite strategy? Bruschi, Fabrizo Chiumiento, Lorena Parasit Vectors Review The parasitic nematode Trichinella has a special relation with muscle, because of its unique intracellular localization in the skeletal muscle cell, completely devoted in morphology and biochemistry to become the parasite protective niche, otherwise called the nurse cell. The long-lasting muscle infection of Trichinella exhibits a strong interplay with the host immune response, mainly characterized by a Th2 phenotype. The aim of this review is to illustrate the role of the Th2 host immune response at the muscle level during trichinellosis in different experimental models, such as knock-out or immuno-modulated mice. In particular, in knock-out mice a crucial role of IL-10 is evident for the regulation of inflammation intensity. The muscular host immune response to Trichinella is partially regulated by the intestinal phase of the parasite which emphasizes the intensity of the following muscle inflammation compared with animals infected by synchronized injections of newborn larvae. In eosinophil-ablated mice such as PHIL and GATA-- animals it was observed that there was an increased NOS2 expression in macrophages, driven by higher IFN-γ release, thus responsible for muscle larva damage. Besides modulation of the intestinal stage of the infection, using recombinant IL-12, increases the muscular parasite burden delaying adult worm expulsion from the intestine. Furthermore, a Th1 adjuvant of bacterial origin called Helicobacter pylori neutrophil activating protein (HP-NAP), administered during the intestinal phase of trichinellosis, alters the Th2 dependent response at muscle level. All these data from the literature delineate then a mutual adaptation between parasite and host immune response in order to achieve a strategic compromise between two evolutionary forces pointed towards the survival of both species. BioMed Central 2011-03-23 /pmc/articles/PMC3079684/ /pubmed/21429196 http://dx.doi.org/10.1186/1756-3305-4-42 Text en Copyright ©2011 Bruschi and Chiumiento; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Bruschi, Fabrizo Chiumiento, Lorena Trichinella inflammatory myopathy: host or parasite strategy? |
title | Trichinella inflammatory myopathy: host or parasite strategy? |
title_full | Trichinella inflammatory myopathy: host or parasite strategy? |
title_fullStr | Trichinella inflammatory myopathy: host or parasite strategy? |
title_full_unstemmed | Trichinella inflammatory myopathy: host or parasite strategy? |
title_short | Trichinella inflammatory myopathy: host or parasite strategy? |
title_sort | trichinella inflammatory myopathy: host or parasite strategy? |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3079684/ https://www.ncbi.nlm.nih.gov/pubmed/21429196 http://dx.doi.org/10.1186/1756-3305-4-42 |
work_keys_str_mv | AT bruschifabrizo trichinellainflammatorymyopathyhostorparasitestrategy AT chiumientolorena trichinellainflammatorymyopathyhostorparasitestrategy |