However, patients with CE3b cysts, a stage clinically unresponsive to treatments,

had statistically significantly higher median levels of IL4 and percentage of positive samples for IL4. We conclude that the analysis of serum cytokine dosage, at least in its present form, is not useful as a marker of cyst activity. However, our results support recent findings suggesting the chronic activity of CE3b cysts and suggest that this might be partly because of a skewed Th2 response. Human cystic echinococcosis (CE) is a chronic infection caused by the larval stage of the tapeworm Echinococcus granulosus and is an increasingly important public health problem in many Selleck PCI-32765 regions of the world (1). Despite its wide distribution and the heavy economical and sanitary burden imposed on the healthcare systems, funding allotted to this neglected disease is limited (2,3). Moreover,

many aspects of this disease, such as its natural history, the underlying causes of the poor response to treatment CHIR-99021 and chronicization of some cyst stages, are still poorly known, making its clinical management particularly difficult. The diagnosis and the decisions about clinical management of CE are currently based on imaging methods, mostly ultrasound (US), and, to a lesser extent, on serology. Cyst viability (i.e. presence of viable protoscolices in the cystic liquid) would be the optimal parameter to guide clinical decision-making, but at present no easily implementable noninvasive technique is available in this regard. Serology is hampered by several problems, such as lack of standardization, and its diagnostic performance is a function of many variables including prevalence of infection, cross-reactions with other parasites, and location, stage and size of the cyst (4). Moreover, anti-Echinococcus antibodies (Ab) may persist for years, although often at low titres, even after the complete surgical removal of the cysts (5,6), so serology alone is

not a reliable means to assess cyst viability and should always be coupled with US staging. Biological activity also does not necessarily match US appearance of cysts (7). A long-term follow-up of patients is therefore required, as only changes in the US appearance of the cyst and Ab titres can be relied upon to assess cyst progression towards inactivation (stages CE4 and CE5) or IMP dehydrogenase chronicization (stages CE2 and CE3b) (8,9). It has been suggested that chronicization of CE might be favoured by a skewing of the host’s immune response towards a Th2 response. Indeed, persistently high titres of IgG4 and IgE have been associated with the presence of active and not cured cysts (10–12). Moreover, in vitro studies investigating the cytokines production from peripheral blood mononuclear cells of CE patients showed a predominant Th1 response in patients with inactive or cured cysts and a predominant Th2 profile in those with active or not cured cysts (12–14).