Background IgE characterizes the humoral response of allergic sensitization but less is known about what modulates its function and why some patients present clinical symptoms for a given IgE level and others do not. An IgE response also occurs during helminth diseases, independently of allergic symptoms. This response could be a model of non-functional IgE. Objective To study the IgE response against environmental allergens induced during natural helminth infection. Methods In 28 non allergic subjects from the periphery of Ho Chi Minh city with (H+, n = 18) and without helminth infection (H-, n = 10), we measured IgE and IgG4 against several components of Dermatophagoïdes pteronyssinus (Dpt) and Ascaris (a marker of immunization against nematodes), and determined the IgE component sensitization profile using microarray ISAC biochips. The functional ability of IgE to induce degranulation of cultured mast cells was evaluated in the presence of Dpt. Results Non allergic H+ subjects exhibited higher levels of IgE against Dpt compared to H- subjects. Dpt IgE were not functional in vitro and did not recognize usual Dpt major allergens. IgE recognized other component allergens that belong to different protein families, and most were glycosylated. Depletion of IgE recognizing carbohydrate cross-reactive determinant (CCD) did not induce a reduction in Dpt IgE. The Dpt IgG4 were not significantly different. Conclusion Helminth infections induced IgE against allergens such as Dpt and molecular components that belong to different sources as well as against CCD (such as β-1,2-xylose and/or ⍺-1,3-fucose substituted N-glycans). Dpt IgE were not able to induce degranulation of mast cells and were not explained by sensitization to usual major allergens or N-glycans.

BackgroundAnthelmintics are one of the more commonly available classes of drugs to treat infections by parasitic helminths (especially nematodes) in the human intestinal tract. As a result of their cost-effectiveness, mass school-based deworming programs are becoming routine practice in developing countries. However, experimental and clinical evidence suggests that anthelmintic treatments may increase susceptibility to other gastrointestinal infections caused by bacteria, viruses, or protozoa. Hypothesizing that anthelmintics may increase diarrheal infections in treated children, we aim to evaluate the impact of anthelmintics on the incidence of diarrheal disease caused by viral and bacterial pathogens in school children in southern Vietnam.Methods/designThis is a randomized, double-blinded, placebo-controlled trial to investigate the effects of albendazole treatment versus placebo on the incidence of viral- and bacterial-induced diarrhea in 350 helminth-infected and 350 helminth-uninfected Vietnamese school children aged 6–15 years. Four hundred milligrams of albendazole, or placebo treatment will be administered once every 3 months for 12 months. At the end of 12 months, all participants will receive albendazole treatment. The primary endpoint of this study is the incidence of diarrheal disease assessed by 12 months of weekly active and passive case surveillance. Secondary endpoints include the prevalence and intensities of helminth, viral, and bacterial infections, alterations in host immunity and the gut microbiota with helminth and pathogen clearance, changes in mean z scores of body weight indices over time, and the number and severity of adverse events.DiscussionIn order to reduce helminth burdens, anthelmintics are being routinely administered to children in developing countries. However, the effects of anthelmintic treatment on susceptibility to other diseases, including diarrheal pathogens, remain unknown. It is important to monitor for unintended consequences of drug treatments in co-infected populations. In this trial, we will examine how anthelmintic treatment impacts host susceptibility to diarrheal infections, with the aim of informing deworming programs of any indirect effects of mass anthelmintic administrations on co-infecting enteric pathogens.Trial registrationClinicalTrials.gov: NCT02597556. Registered on 3 November 2015.Electronic supplementary materialThe online version of this article (doi:10.1186/s13063-016-1406-1) contains supplementary material, which is available to authorized users.

Background Like other helminths, hookworms (HW) induce a regulatory immune response able to modulate and dampen reactivity of the host to antigens. No data about the evolution of the immune response after treatment are available. We aim to phenotype the regulatory immune response during natural HW infection and its evolution after treatment. Methodology Twenty hookworm infected (HW+) and 14 non-infected subjects HW–from endemic area in the periphery of Ho Chi Minh City were included. Blood and feces samples were obtained before, 2 and 4 weeks after treatment with Albendazole 400mg. Additional samples were obtained at 3 and 12 months in the HW+ group. Hematological parameters, Treg (CD4+CD25hiFoxP3hi) and surface molecules (CD39, CD62L, ICOS, PD-1, CD45RA) were measured as well as inflammatory and lymphocytes differentiation cytokines such as IL-1β, IL-6, IFNγ, IL-4, IL-17, IL-10, IL-2 and TGFβ. Results HW+ subjects showed higher Treg, TregICOS+, Treg PD1-, TregCD62L+ and CD45RA+FoxP3lo resting Treg (rTreg). CD45RA-FoxP3lo non-suppressive Treg cells were also increased. No preferential Th1/Th2 orientation was observed, nor difference for IL-10 between two groups. After treatment, Treg, TregICOS+, TregCD62L+, Treg PD1- and rTreg decreased while IL-4 and IL-6 cytokines increased. Conclusion During HW infection, Treg are increased and characterized by a heterogeneous population: a highly suppressive as well as a non-suppressive T cells phenotype. After treatment, Treg with immune-suppressive phenotype exhibited a decrease parallel to an inflammatory Th2 response.

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Objectives: Prolonged fever is a challenge for clinician in managing patients with HIV/AIDS. Their TCD4 counts can be helpful in the diagnosis and treatment. Our goal was to determinethe most common etiologies of prolonged fever and their distribution in different TCD4 count levels in HIV/AIDS patients. Subjects and method: A cross - sectional descriptive study was conducted on 195 HIV/AIDS patients with fever of unknown origin admitted to our hospital from January 2016 to June 2019. We recorded clinical parameters, immune status and etiologies for each patient. Patient immune status based on TCD4 counts was stratified into three levels: < 50 cells/mm3; 50 - 100 cells/mm3 and > 100 cells/mm3. We determined the prolonged fever etiologies in HIV infected patients and compared the distributionof these etiologies in different TCD4 count levels. Results: Among 195 HIV - infected cases with fever of unknown origin, opportunistic infections accounted for 93.3%, non - infectious etiologies took 3.6% and 3.1% were not identified causes. M. tuberculosis was the most common opportunistic infection (46.7%), followed by Talaromycosis (29.2%) and Pneumocytisjiroveci (20.5%), Bacterial pneumonia (11.3%), sepsis (10.3%), CMV (10.3%), Toxoplasma (5.6%), Cryptococcus (2.6%) and MAC (1.0%). Tuberculosis was predominant in all stratified CD4 levels. Most of cases with Talaromycosis had CD4 counts below 50cells/mm3. Besides, CD4 count below 50cells/mm3 was reported in all cases with either Cryptococcus infection or MAC infection. Infections with CMV and toxoplasma were not seen in patients with CD4 count over 100cells/mm3. -7 out of 195 cases were non - infectious etiologies including 4 cases (2.1%) with hemophagocytic lymphohistiocytosis (HLH) syndrome and 3 cases (1.5%) with non - Hodgkin lymphoma. -53.8% of cases were infected by one pathogen while 38% of patients were co - infected by two different pathogens. Co - infection of three pathogens was recognized in 8.2% of study patients.There is no difference between the number of concurrent etiologies and TCD4 levels. Conclusion: Opportunistic infections, especially M. tuberculosis is still the leading cause of prolonged fever in HIV/AIDS patients. T. marnefei should be screened in patients with CD4 < 50cells/mm3. It is important to note that there may be many concurrent etiologies of prolonged fevers in HIV/AIDS patients.