Trichinella inflammatory myopathy: host or parasite strategy?

Fabrizo Bruschi,Lorena Chiumiento

doi:10.1186/1756-3305-4-42

Fabrizo Bruschi, Lorena Chiumiento

Open Access

https://doi.org/10.1186/1756-3305-4-42

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Journal: Parasites & Vectors	Publication Date: Mar 23, 2011
Citations: 90	License type: CC BY 2.0

Affiliation: University of Pisa

Abstract

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.

Highlights

The inflammatory myopathies are a group of muscle diseases characterised by inflammation of the muscles or associated tissues, such as for example the blood vessels that supply the muscles themselves
The chronic inflammatory process is sustained by the “invading” cells of the immune system of the host, such as neutrophils, eosinophils, activated macrophages and T-lymphocytes that lead to the destruction of muscle tissue, accompanied by weakness and sometimes pain; over time, there could be loss of muscle bulk
For the function of eosinophil peroxidase gene (PHIL mice) and for that of IL-10, a dramatic reduction in the larval burden (93%) compared with mice deficient only in IL-10 was observed. When these animals were treated with the NOS 2 inhibitor, in both IL-10-/- or IL-10-/-/PHIL mice the lymph node cell produced lower amounts of NO in cultures and in parallel larval survival increased. These results show that muscle larvae are damaged by an immune response driven by T helper 1 (Th1) cells which seem to be downregulated by eosinophils

Summary

Introduction

The inflammatory myopathies (pathological abnormalities of the muscles) are a group of muscle diseases characterised by inflammation of the muscles or associated tissues, such as for example the blood vessels that supply the muscles themselves. Muscle inflammation may be caused by an allergic reaction, cancer or rheumatoid conditions, or following environmental exposure to xenobiotics or drugs, or infection with viruses (influenza, Coxsackie viruses, arboviruses), bacteria (i.e. Lyme disease-related Borrelia species) and parasites (Toxoplasma gondii, Trypanosoma cruzi, Sarcocystis spp. among protozoa and Taenia solium and Trichinella among helminths). All these infectious agents fight part of their combat survival in the muscles.

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