Parasitic helminths have a coexistence with mammalian hosts whereby they survive for several years in known hostile conditions of their hosts. Many explanations exist describing how these parasitic helminths are able to survive. In the last years, a lot of studies have focused on both enzymatic and non-

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.

This review describes different aspects of the host immune response to Trichinella. The role of antibodies, T cells, mast cells, eosinophils and neutrophils in immune reaction to this nematode is considered, in the light of the recent data derived from experimental models, both in in vivo and in vitro. The knowledge of immune response mechanisms against Trichinella is fundamental to understand how the parasite can escape such mechanisms. The principal evasion mechanisms of host immune response occurring in trichinellosis are described, some of which are shared by other parasites, some others are peculiar of this parasite, but particular attention is focused on immunomodulation and the possibilities to exploit this parasite ability to verify the effects on immuno-mediated diseases. In conclusion, some considerations on the actual ability to escape the host immune response by the parasite are discussed, taking into account the recent data that shows that the parasite might rather drive immune system of the host towards a less dangerous response.

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This survey aimed to estimate the prevalence of anti-Toxoplasma IgG and IgM antibodies in people living in north west Tuscany (central Italy) and to investigate the adherence to antenatal screening programs and access to the Toxo-test as well. Sera from a large sample of individuals suspected to have acute infection or from pregnant women (10,352 subjects) aged between 1 day and over 70 years were analysed for both IgG and IgM anti-Toxoplasma antibodies using an immunoenzymatic method or a chemo-luminescent immunoassay. Overall, the seroprevalence of IgG antibodies was 21.4% (95% CI 20.62-22.20). A positive trend according to age was found, with low positivity observed in younger age groups. Among women of reproductive age the prevalence of IgG antibodies was 19.4% (95% CI 18.64-20.26). The overall IgM seroprevalence was 1.07% (95% CI 0.87-1.27). A low IgM prevalence was also observed in women of reproductive age (0.8%; 95% CI 0.65-1.03). Our study seems to indicate that primary prevention is widespread among women. However, an epidemiological surveillance system for toxoplasmosis should be implemented, to assess the risk of congenital toxoplasmosis and to determine the true burden of disease in adults.

Diagnostic methods for parasite infections still highly depend on the identification of the parasites by direct methods such as microscopic examination of blood, stool and tissue biopsies. Serodiagnosis is often carried out to complement the direct methods, however few synthetic antigens with sufficient sensitivity and specificity are available. Here we evaluated a glycan microarray approach to select for synthetic glycan antigens that could be used for serodiagnosis of parasitic infections. Using a glycan array containing over 250 different glycan antigens, we identified GalNAcβ1-4(Fucα1-3)GlcNAc-R (LDNF) as a glycan antigen that is recognized by antibodies from Trichinella-infected individuals. We synthesized a neoglycoconjugate, consisting of 5 LDNF molecules covalently coupled to bovine serum albumin (BSA), and used this neoglycoconjugate as an antigen to develop a highly sensitive total-Ig ELISA for serological screening of trichinellosis. The results indicate that glycan microarrays constitute a promising technology for fast and specific identification of parasite glycan antigens to improve serodiagnosis of different parasitic infections, either using an ELISA format, or parasite-specific glycan-arrays.

Th2 responses seem to play an important role in defence against Trichinella spiralis (Ts), The Neutrophil Activating Protein of Helicobacter pylori (HP-NAP), that induces IL-12, and IL-23 expression and shifts to Thl allergen-specific Th2 cells in vitro was used as an anti-Th2 agent in BALB/c mice infected with T. spiralis. The muscle larvae (ML) burden was lower (p < 0.02) in untreated infected animals than those infected treated with HP-NAP. In both groups there was an inverse relationship between ML burden of each animal and total IgE level (controls: r -0.617,p = 0.0013 and HP-NAP-treated: r -O.678,p =0.0001) or eosinophil count, evaluated in the same mouse on day 42 (r -0.390,p = 0.0592 and r -O.803,p =0.0001, respectively). Inflammatory response around the nurse cell-parasite complex was significantly higher in HP-NAP-treated infected animals than in those untreated infected, on the contrary the number of eosinophils, counted around each complex was significantly lower in the first animal group. This study provides evidence of a powerful anti-Th2 activity in vivo by HP-NAP and for the partial protective effect of Th2 responses in T. spiralis infection.Trichinellosis is caused by the parasitic nematode Trichinella, after ingestion of raw or undercooked meat by the host. This parasite has the peculiarity of having an intracellular localization both at intestinal and muscle level where the L] larvae live and grow in a modified skeletal muscle fibre cell , called 'nurse cell ' that induces, in encapsulating Trichinella specie s, the form ation of a collagen capsule which protects the parasite from effector cells of the immune system (1). The immune response of the host at muscle level has recei ved increasing attention in recent years (2).IgE and eosinophils derived from the activation ofTh2 cells have been considered protecti ve against helminths for some time although, to date , in vivo results have provided controversial results (3-4).T helper type 2 (Th2) cells producing cytokines such as interleukin (IL)-4, IL-5, IL-9, IL-lO and IL-13 (2, 5), are not only involved in helminth infections but also in the development ofpathological conditions such as atopy and asthma (6-8).A role of the above cytokines in experimental trichinellosis has been shown; in fact IL-4 plays an important role in the development of protective responses to this parasite (9). lL-4 deficiency or lL-4 blockade delayed expulsion of Trichinella spiralis from the small intestine (7, 10-11). Like IL-4, lL-13 is an important factor during Th2 responses, mediating mechanisms similar to those induced by lL-4, such as stimulating B cell proliferation, antibody class switching to IgE and,.After binding of both IL-4 and IL-13 to IL-4 receptor a chain (lL-4Ra) signal transducer and activator of transcription factor 6 (Stat6) are phosphorylated and activated. The transcription factor Stat6, triggered by GATA3, is necessary in vivo for the expulsion of T. spiralis and for the development of eosinophilia (14).Other Th2-derived cytokines are important ...

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