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Covalent conjugation of allergens to toll-like receptor (TLR) agonists appears to be a powerful strategy for the development of safety compounds for allergen-specific immunomodulatory response toward tolerance in allergy. In this work, we have synthesized two family of ligands, an 8-oxoadenine derivative as a ligand for TLR7 and a pyrimido[5,4-b]indole as a ligand for TLR4, both conjugated with a T-cell peptide of Pru p 3 allergen, the lipid transfer protein (LTP) responsible for LTP-dependent food allergy. These conjugates interact with dendritic cells, inducing their specific maturation, T-cell proliferation, and cytokine production in peach allergic patients. Moreover, they increased the Treg-cell frequencies in these patients and could induce the IL-10 production. These outcomes were remarkable in the case of the TLR7 ligand conjugated with Pru p 3, opening the door for the potential application of these allergen-adjuvant systems in food allergy immunotherapy.

Local respiratory allergy (LRA) is defined by the negativity of atopy tests, a clinical history suggestive of airway allergy and a positive response to the nasal and/or bronchial allergen challenge. The clinical spectrum of LRA is comprised of three conditions: local allergic rhinitis (LAR) and local allergic asthma in non-atopic patients, and dual allergic rhinitis (coexistence of allergic rhinitis and LAR) in atopic individuals. LRA is an independent disease phenotype not progressing to atopy over time, but naturally evolving to the clinical worsening and the onset of comorbidities. Published data suggests that LRA is mediated through the mucosal synthesis of allergen-specific (s)IgE, which binds to FcϵRI on resident mast cells, and in >50% of cases traffics to the blood stream to sensitize circulating basophils. To date, 4 clinical trials have demonstrated the capacity of allergen immunotherapy (AIT) to decrease nasal, conjunctival and bronchial symptoms, to improve quality of life, to increase the threshold dose of allergen eliciting respiratory symptoms, and to induce serum sIgG4 in LRA individuals. Collectively, these data indicate that local allergy is a relevant disease mechanisms in both atopic and non-atopic patients with airway diseases.

Introduction Mild non-immediate reactions (NIRs) to beta-lactams (BLs) are the most frequent manifestation of drug allergy in children. The diagnostic approach is complex as the utility of skin tests (STs) and lymphocyte transformation tests (LTTs) is controversial. Drug provocation test (DPT) is the gold standard, although no standardized protocols exist. We aimed to investigate the utility of DPT in a unique dose without previous STs, and LTTs in the diagnosis of NIRs to BLs in children. Methods We prospectively evaluated children 0-14 years old referred to the Regional University Hospital of Malaga during 2017-2020 reporting NIRs to BLs. We performed a DPT with a unique dose followed by regular treatment at home. If positive, STs and LTTs were done after the reaction had disappeared. Results We included 194 children, having 24 (12.4%) a positive DPT. The main culprit was AX (70.1%) followed by AX-clavulanic acid (CLV) (26.8%) and the main symptoms maculopapular exanthema (MPE) (49.5%) and delayed-urticaria (48.5%). A decrease (p = 0.013) in the interval of days between drug administration and onset of symptoms was observed in positive DPT compared with the original reaction (3.5 vs 6 days), with no differences in the overall percentage of MPE and delayed-appearing urticaria (p = 0.551). No severe reactions occurred during DPT. Moreover, STs were positive in 13.33% and LTTs in 52.9%. Conclusions Single-dose DPT without previous STs is a safe and useful way to assess NIRs to BLs in children. LTT has shown to be useful, confirming a T-cell mechanism involved in these reactions.

House dust mites (HDMs) are the allergenic sources most frequently involved in airway allergy. Nevertheless, not every sensitized patient develops respiratory symptoms upon exposure to HDM, and there is a clinical need to differentiate allergic asthmatics (AAs) from atopic non-allergic asthmatics with HDM sensitization. This differentiation sometimes requires in vivo provocations like the bronchial allergen challenge (BAC). Interestingly, recent data demonstrate that non-atopic patients with asthma can also develop positive BAC results. This novel phenotype has been termed local allergic asthma (LAA). The interest in identifying the allergic triggers of asthma resides in the possibility of administering allergen immunotherapy (AIT). AIT is a disease-modifying intervention, the clinical benefit of which persists after therapy discontinuation. Recently, new modalities of sublingual tablets of HDM immunotherapy registered as pharmaceutical products (HDM-SLIT tablets) have become commercially available. HDM-SLIT tablets have demonstrated a robust effect over critical asthma parameters (dose of inhaled corticosteroids, exacerbations, and safety), thus being recommended by international guidelines for patients with HDM-driven AA. In this review, we will summarize the current knowledge on the phenotype and endotype of HDM-driven AA, and LAA, address the difficulties for BAC implementation in the clinic, and discuss the effects of AIT in AA and LAA.

Background: Patients with peach allergy due to nsLTP sensitisation constitute a heterogeneous group in terms of sensitisation profile and severity. This could be due to the presence of additional allergies to pollens. The aim of this study was to analyse the clinical characteristics, sensitisation profile, and severity of reactions in peach-allergic patients sensitised to nsLTP from two Mediterranean areas with different pollen exposure. Methods: Patients with diagnosis of LTP allergy from the Allergy Unit of Hospital Regional Universitario de Malaga (HRUM) and Hospital Clinic de Barcelona (HCB) were prospectively included and classified into two groups; (a) LTP-monoallergic: those that presented reaction only with peach, and (b) LTP-Allergy: those that presented reaction with peach and at least another plant-food containing LTP. Results: 252 patients were included, 235 (93.2%) had LTP-syndrome and 17 (6.8%) were LTP-monoallergic. We found a higher percentage of anaphylaxis and delayed onset of symptoms in the LTP-monoallergic group (p=0.02 and p=0.04, respectively). Moreover, anaphylaxis was less frequent in patients with profilin sensitisation (p=0.03). The comparison of patients' data from HRUM with data from HCB showed differences in sensitisation to olive tree pollen and profilin (p=0.01 and p=0.001, respectively). Conclusion: This study was undertaken to characterize two large group of subjects from to two regions with differing exposures to pollen. We found that more than 90% of peach-allergic patients in both populations evolved to LTP-Allergy and showed an early onset. Profilin sensitisation could be more useful as a severity biomarker than the number of nsLTP, aeroallergen sensitisations, or sIgE levels. This could provide clues regarding sensitisation and severity patterns that might be relevant in other geographical areas.

Food allergy (FA) is an increasing problem worldwide and, over recent years, its prevalence is rising in developed countries. Nowadays, the immunological and cellular processes that occur in the allergic reactions are not fully understood, which hampers the development of in vitro diagnostic tools and further treatment options. Moreover, allergic diseases could be reinforced by environmental exposure and genetic modifications. Gene expression can be controlled by different epigenetic mechanisms like DNA methylation, histone modifications, and microRNAs. In addition, several environmental factors such as dietary components (vitamin D, butyrate, folic acid) are able to regulate this epigenetic mechanism. All these factors produce modifications in immune genes that could alter the development and function of immune cells, and therefore the etiology of the disease. Furthermore, these epigenetic mechanisms have also an influence on immunomodulation, which could explain sustained responsiveness or unresponsiveness during immunotherapy due to epigenetic modifications in key genes that induce tolerance in several FA. Thus, in this review we focus on the different epigenetic mechanisms that occur in FA and on the influence of several dietary components in these gene modifications.

Food allergy is an increasing problem worldwide, with strict avoidance being classically the only available reliable treatment. The main objective of this review is to cover the latest information about the tools available for the diagnosis and treatment of food allergies. In recent years, many efforts have been made to better understand the humoral and cellular mechanisms involved in food allergy and to improve the strategies for diagnosis and treatment. This review illustrates IgE-mediated food hypersensitivity and provides a current description of the diagnostic strategies and advances in different treatments. Specific immunotherapy, including different routes of administration and new therapeutic approaches, such as hypoallergens and nanoparticles, are discussed in detail. Other treatments, such as biologics and microbiota, are also described. Therefore, we conclude that although important efforts have been made in improving therapies for food allergies, including innovative approaches mainly focusing on efficacy and safety, there is an urgent need to develop a set of basic and clinical results to help in the diagnosis and treatment of food allergies.

Pemphigoid diseases (PDs) are chronic and life-threatening autoimmune diseases of the skin and mucous membranes. PDs are characterized and caused by autoantibodies targeting components of the basement membrane. In the PD epidermolysis bullosa acquisita (EBA), the target autoantigen is type VII collagen. Current treatment options of PD, especially EBA, are limited and are mostly based on systemic immunosuppression. Animal models of PD have greatly advanced our understanding of PD pathogenesis. This has led to the identification of several novel therapeutic targets, including signalling molecules. Herein, the contribution of signalling molecules in the pathogenesis of the PD EBA and the effects of pharmacological targeting of these pathways are reviewed in detail. The p38 MAPK, ERK1/2, AKT, PI3Kβ, Hsp90, RORα, PDE4, Src kinases and CARD9 have been demonstrated to be critically involved in EBA pathogenesis. With the advent of new signal transduction inhibitors, we expect that the so far poor prognosis of EBA and other PD will improve significantly in the future.

Taenia solium is a parasite whose larvae (cysticerci) can locate in the central nervous system of humans and cause neurocysticercosis (NC). The introduction of cysticidal drugs such as albendazole (ABZ) for the treatment of NC has significantly improved its prognosis. However, treatment is not always effective, and the high levels of corticosteroids used to prevent inflammatory complications in this disease could be, partly, the cause of this observation. In this context, this study investigated, using the experimental mouse model of intraperitoneal infection with Taenia crassiceps, the influence of corticosteroid administration on the therapeutic efficacy of ABZ. We evaluated and compared the effects of ABZ, dexamethasone (DXM) and their combination (ABZ + DXM) on cyst viability, both in vitro and in vivo. Serum levels of IL-4, IFN-gamma, IL-6 and IL-10 were evaluated in the in vivo study. Results showed that the treatment with ABZ, in vitro and in vivo, was associated with a high number of parasites deaths. Concomitant treatment with DXM did not alter ABZ in vitro cysticidal activity but reduced its effectiveness significantly in the in vivo experimental model. Cytokine serum levels did not change significantly in treated mice compared to the controls. The results of this study are relevant as they indicate a negative effect of corticosteroids on the efficacy of cysticidal therapy. In human neurocysticercosis, control of inflammation is of great importance to most patients in order to avoid complications. Corticosteroids are generally used for this purpose and the results of this study demonstrate the need to find other therapeutic strategies. Further studies are needed to better understand the mechanisms involved.

Scope: Much of the knowledge about gene expression during anaphylaxis comes from candidate gene studies. Despite their potential role, expression changes in dendritic cells (DCs) have not been studied in this context using high throughput methods. The molecular mechanisms underlying food-antigen-induced anaphylaxis are investigated using DCs from an animal model. Methods and results: RNA sequencing is used to study gene expression in lymph-node-derived DCs from anaphylactic mice sensitized intranasally with the major peach allergen Pru p 3 during the acute reaction phase, induced intraperitoneally. In total, 237 genes changed significantly, 181 showing at least twofold changes. Almost three-quarters of these increase during anaphylaxis. A subset is confirmed using RT-PCR in a second set of samples obtained from a new batch of mice. Enrichment analysis shows an overrepresentation of genes involved in key immune system and inflammatory processes, including TGF-β signaling. Comparison with a study using anaphylactic human subjects show significant overlap. Conclusions: The findings provide a comprehensive overview of the transcriptional changes occurring in DCs during anaphylaxis and help elucidate the mechanisms involved. They add further weight to the putative role of these cells in anaphylaxis and highlight genes that may represent potential therapeutic targets.

In the search of new alternatives for neurocysticercosis treatment , Taenia crassiceps ORF strain cysticerci have been used instead of T. solium for in vitro studies. Up to date, the main criteria for the use of the murine cysticercosis model for drug efficacy evaluation have not been assessed. The aim of the present study was to evaluate the influence of two of the main variables related to the in vivo efficacy: the length of drug treatment and the starting time of treatment after experimental infection, using albendazole (ABZ) and praziquantel (PZQ) as test drugs. Additionally, the relationship between the number of cysts and the parasite weight was assessed. For the study, female BALB/c mice were experimentally infected with T. crassiceps cysts. Three different post-infection periods (10, 20 and 30 days) and three different lengths of treatment with ABZ or PZQ (10, 20 and 30 days) were selected. The efficacy of each treatment was evaluated by comparison with a control group. Our results show that for in vivo efficacy studies, the best time to start the drug treatment is 10 days post-infection and that a minimum of 20 days of treatment is required when ABZ or PZQ are used as positive control. Moreover, in this model the parasite weight can be used as a rapid tool to measure the in vivo drug activity.

cope Sublingual immunotherapy using peach extract enriched in Pru p 3 (Pru p 3-enriched-SLIT) brings a new perspective to treating patients with allergy to lipid transfer proteins. We evaluated the immunological changes induced by Pru p 3-enriched-SLIT during one year. Methods and results Three groups were included: peach allergic patients who received Pru p 3-enriched-SLIT, peach allergic untreated patients and controls. Peripheral blood mononuclear cells were obtained before treatment and different time-points. Monocyte-derived dendritic cells (moDCs) maturation and lymphocyte proliferation were assessed by flow cytometry. Data showed a significant reduction of moDCs maturation status during one year of treatment and an increase in PD-L1. Moreover, we observed a significant decrease of the Pru p 3-specific proliferation of effector cells and an increase in Treg cells with higher PD-L1 expression and IL-10 production. These were observed in patients treated only. Conclusion Successful Pru p 3-enriched-SLIT is linked to an important immunosuppression of allergen-specific effector T cells maybe the increase of allergen-specific Treg cells. These cellular changes are orchestrated by the activity of moDCs promoting the expression PD-L1 that will participate in the regulatory response. These changes may serve as biomarkers during SLIT alongside other features such as IgE/IgG4 ratio. This article is protected by copyright. All rights reserved

Pru p 3 is the major peach allergen in the Mediterranean area. It frequently elicits severe reactions, limiting its study in humans, raising the need for animal models to investigate the immunological mechanisms involved. However, no anaphylaxis model exists for Pru p 3. We aimed to develop a model of peach anaphylaxis by sensitising mice with Pru p 3 in combination with lipopolysaccharide (LPS) as an adjuvant. Four groups of mice were sensitised intranasally: untreated; treated with Pru p 3; treated with LPS; treated with Pru p 3 + LPS. After sensitisation mice were intraperitoneally challenged with Pru p 3 and in vivo and in vitro parameters were evaluated. Only mice in the Pru p 3 + LPS group showed anaphylaxis symptoms, including a decrease in temperature. Determination of in vitro parameters showed a Th2 response with an increase of Pru p 3-specific IgE and IgG1. Moreover, at the cellular level, we found increased levels of IgE and IgG1 secreting Pru p 3-specific cells and a proliferative CD4+ T-cell response. These results demonstrate that Pru p 3-specific anaphylaxis can be generated after nasal sensitisation to Pru p 3 in combination with LPS. This is a promising model for evaluating food allergy immunotherapies

Actin remodelling proteins regulate cytoskeletal cell responses and are important in both innate and adaptive immunity. These responses play a major role in providing a fine balance in a cascade of biological events that results in either protective acute inflammation or chronic inflammation that leads to a host of diseases including autoimmune inflammation mediated epidermolysis bullosa acquisita (EBA). This review describes the role of the actin cytoskeleton and in particular the actin remodelling protein called Flightless I (Flii) in regulating cellular inflammatory responses and its subsequent effect on the autoimmune skin blistering disease EBA. It also outlines the potential of an antibody based therapy for decreasing Flii expression in vivo to ameliorate the symptoms associated with EBA. Refereed/Peer-reviewed

Epidermolysis bullosa acquisita (EBA) is a chronic mucocutaneous autoimmune skin blistering disease, in which generation of autoantibodies to type VII collagen (COL7) is the key factor for pathogenesis. Much of this current understanding of EBA pathogenesis has been obtained through the development and further application of respective model systems. In vitro model systems of EBA duplicate neutrophil activation by immune complexes of COL7 and anti-COL7 antibodies. Blister induction by anti-COL7 antibodies can be reproduced ex vivo by incubation of cryosections of human skin with anti-COL7 antibodies and neutrophils. Furthermore, EBA can be induced in mice by transfer of human or rabbit anti-COL7 IgG into adult mice, or by immunization of susceptible mouse strains with an immunodominant fragment within the non-collagenous 1 domain of COL7. However, our understanding of EBA pathogenesis is largely limited to mechanisms in autoantibody-induced tissue injury. Furthermore, these model systems of EBA have not been used to a large extent to evaluate the potential of novel treatment options. To foster a broader use of these elaborate model systems to specifically address these open issues, this review focuses on a detailed description of model systems for EBA, which should allow for a broad use of these models. This will hopefully lead to a better understanding of EBA pathogenesis, as well to a benefit in patient care.

Epidermolysis bullosa acquisita (EBA) is an autoimmune bullous dermatosis characterized by chronic mucocutaneous blistering caused by autoantibodies directed against type VII collagen. EBA causes a high morbidity and is difficult to treat. Model systems have significantly broadened our understanding of EBA pathogenesis, leading to the identification of numerous therapeutic targets. Of these, so far, a few have been evaluated for their therapeutic potential in preclinical models. In mice, EBA can be induced by transfer of anti-type VII collagen antibodies or by immunization with the protein. The latter model, immunization-induced EBA, is ideal to test drugs for their therapeutic efficacy. Here, mice with already established disease can be treated for prolonged periods. Albeit time consuming, results from immunization-induced EBA will pave the way for clinical application in patients. As the key pathogenic principle, that is, autoantibody-induced, leukocyte-mediated tissue injury and inflammation, is shared by other diseases, these findings may have translational applications beyond EBA.

Objectives: Neurocysticercosis is a common parasitic disease in the CNS in humans caused by the metacestode Taenia solium, with high incidence in developing countries. Albendazole is the drug of choice. However, a wide interindividual variability in the response has been reported. In order to evaluate alternative treatment options, the in vitro efficacy of nitazoxanide, its main metabolite tizoxanide as well as the tizoxanide and albendazole sulphoxide combination was tested against Taenia crassiceps cysts. Methods: T. crassiceps cysts were incubated in culture medium containing different concentrations of nitazoxanide, tizoxanide and albendazole sulphoxide (0.037–0.42 mg/mL). The effect of the tizoxanide and albendazole sulphoxide combination was evaluated in a fixed-concentration ratio (1:1). Isobolographic analyses were used to define the kind of interaction between drugs. Morphological and ultrastructural alterations over the parasite tissue were observed by light and transmission electron microscopy. Results: Nitazoxanide and tizoxanide exhibited cestocidal activity which was time–concentrationdependent. The EC50 values were 0.15, 0.12 and 0.080 mg/mL for nitazoxanide, tizoxanide and albendazole sulphoxide, respectively. No statistical differences between EC50 values were found, indicating that nitazoxanide and tizoxanide are equally potent as albendazole sulphoxide. The effect of the tizoxanide and albendazole sulphoxide combination was faster than that observed with each drug alone. Isobolographic analysis showed that the effect of the combination was additive. Nitazoxanide and tizoxanide had an effect on the germinal layer, where lipid droplets were found. Nitazoxanide and tizoxanide produced less damage than albendazole sulphoxide on the germinal layer. After the tizoxanide and albendazole sulphoxide combination, a high accumulation of lipid droplets within the germinal layer of the parasite was found. Conclusions: Our results suggest that nitazoxanide in combination with albendazole could be useful for treatment of cysticercosis infections. Additional in vivo studies are required to confirm this hypothesis.

Praziquantel and albendazole are currently used for chemotherapeutic treatment of neurocysticercosis. Albendazole has been found to be more effective than praziquantel; however, it is well known that not all patients will show a complete resolution of cysts. Searching for more effective treatments, this study was designed to evaluate the effect of the combination of praziquantel and albendazole sulphoxide in a Taenia crassiceps in vitro model as well as the kind of interaction between both drugs.In order to determine the concentration that produced 50% effect (EC50), T. crassiceps cysts were incubated in culture medium containing praziquantel (0.005-0.04 microg/mL), albendazole sulphoxide (0.021-0.16 microg/mL) or the combination of praziquantel and albendazole sulphoxide in a fixed-dose ratio (1:1). The experimental concentration (EC50Exp) of the combination was determined from the concentration-response curve constructed from the combined drug treatment. Isobolographic analyses were used to define the nature of the interaction between praziquantel and albendazole sulphoxide. Morphological and ultrastuctural alterations after different treatments over the parasite tissue were observed by light and transmission electron microscopy.The changes in ultrastructure were more marked with the praziquantel and albendazole sulphoxide combination. Also the cysticidal effect of the combination was observed earlier than that of each drug alone. When isobolographic analysis was employed, we found that the experimental EC50 value (0.042 microg/mL) was not significantly different from the theoretical EC50 value (0.035 microg/mL), which indicates an additive interaction between praziquantel and albendazole sulphoxide.Our study suggests that the combination of praziquantel and albendazole sulphoxide could potentially improve the current neurocysticercosis treatment.

Although fluoroquinolones (FQs) are generally well-tolerated antibiotics, increasing numbers of hypersensitivity reactions have been reported. These can be evaluated in vitro by basophil activation tests (BATs); however, sensitivity is not optimal. Many factors could influence sensitivity such as basophil activation markers. The objective of this study was to evaluate the influence of 2 different activations markers, CD63 and CD203c, on the sensitivity of BAT to FQ. We studied 17 patients with immediate allergic reactions to FQ. BAT was performed with moxifloxacin and ciprofloxacin using CD193 (CCR3) for basophil selection and CD203c or CD63 as activation markers. Stimulation with ciprofloxacin induced a significantly higher expression of CD63 in ciprofloxacin-allergic patients compared to moxifloxacin-allergic patients (P = 0.002). In patients allergic to moxifloxacin with anaphylactic shock, we have observed an increase in the percentage of cells that upregulate CD203c, whereas patients with anaphylaxis preferentially upregulate CD63. The best sensitivity–specificity was obtained using a cutoff of 3 and the culprit FQ, using CD203c for moxifloxacin-allergic patients (sensitivity = 36.4%; specificity = 94.4%), and CD63 for ciprofloxacin-allergic patients (sensitivity = 83.3%; specificity = 88.9%). A negative correlation was found between the upregulation of CD63 and CD203c and the time interval between the reaction occurrence and the performance of the test (Spearman r = −0.446; P

Objective: Cefepime neurotoxicity usually occurs in patients with renal impairment. The aim of this study was to evaluate the neurotoxicity of cefepime administered by continuous intravenous infusion during treatment of nosocomial infections in neurological patients with normal renal function. Methods: This was an open pilot study of neurological patients with infections caused by cefepime sensitive bacteria. Patients had baseline neurological assessment and electroencephalogram (EEG). Cefepime plasma concentrations were determined 48 hours after infusion was initiated and at end of treatment (EOT). Results: Eleven patients were included. These were diagnosed with a brain tumor (9), cerebrovascular disease (1) and polyneuropathy (1). Infections were surgical site infection in 5, clinically defined nosocomial pneumonia in 4, and bacterial meningitis associated to postoperative CSF fistula in 2. Gram-negative organisms were isolated in 10 patients. Cefepime dose was 2 g/day in 9 patients and 4 g/day in 2. Mean cefepime plasma concentration at 48h was 13.6 ± 2.0 µg/mL (range 4.6 to 24.5 µg/mL), at EOT was 11.9 ± 1.8 µg/mL (range 3.0 to18.9 µg/mL ). EEG interpreted by two experts showed at baseline alpha background rhythm in 5 and theta-alpha rhythm in 6 patients. On EEG at EOT background rhythm was alpha in 4 and theta-alpha in 7, one patient presented isolated sharp and slow wave activity. No mental status changes or seizures occurred and all infections resolved. Conclusion: Significant EEG change was observed in 1of 11 patients. A preserved mental status may correlate with cefepime safety in neurological patients with normal renal function during cefepime treatment.

Tissue-selective recruitment of lymphocytes to peripheral organs, such as the skin, is crucial for spatial compartmentalisation within the immune system as well as immune surveillance under normal conditions. In addition, this process plays a key role for the pathogenesis of various diseases including common inflammatory disorders such as atopic dermatitis or psoriasis, but also malignancies such as cutaneous T cell lymphomas. Recruitment of lymphocytes to the skin is a highly complex process that involves adhesion to the endothelial lining, extravasation, migration through the connective tissue, and, finally, localisation of a subpopulation of lymphocytes to the epithelial compartment, the epidermis. An intertwined network of constitutively expressed and inducible cytokines, chemokines and other mediators provides guidance for lymphocyte migration, and a large number of adhesion receptors mediate sequential steps of cell-cell- and cell-substrate-interactions resulting in tissue-specific localisation of immune cells. Selectively targeting the functions of one or several key molecules involved in this complex cascade promises exciting new therapeutic options for treating inflammatory disorders, but at the same time, bears considerable imponderables which will be discussed in this article.

We investigated the minimum exposure times of prazicuantel (PZQ) and albendazole sulfoxide (ABZSO) required for their activities against Taenia cysts in vitro as well as the 50 and 99% effective concentrations. The results showed that although the effects of both drugs are time and concentration dependent, ABZSO acts much slower and is less potent than PZQ.