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PubMed2005

Helicobacter pylori and Schistosoma japonicum co-infection in a Chinese population: helminth infection alters humoral responses to H. pylori and serum pepsinogen I/II ratio.

The effects of helminth infection on humoral IgG responses and clinical outcome of gastric Helicobacter pylori infection are unknown. IgG and IgG subclass responses to H. pylori and serum pepsinogen I/II ratio, a marker of gastric atrophy, were investigated in a Schistosoma japonicum prevalent Chinese population. H. pylori, CagA and IgG subclass responses were assayed by ELISA. Serum pepsinogen I and pepsinogen II were assayed by ELISA and the pepsinogen I/II ratio determined. In 150 subjects, infection with S. japonicum and H. pylori was 55.3% and 51.3%, respectively. H. pylori IgG titres and CagA seropositivity were significantly lower (P<0.05) in co-infected subjects, and differences in H. pylori IgG isotype responses were evident. In H. pylori positives, a significantly higher (P<0.05) pepsinogen I/II ratio was observed in co-infected subjects. The difference between S. japonicum positive and negative subjects was only evident in H. pylori CagA seronegative subjects. In conclusion, S. japonicum co-infection with H. pylori is associated with alterations in IgG responses to H. pylori and less gastric atrophy.

Adolescent↗

PubMed2004

Helminth infection modulates the development of allergen-induced airway inflammation.

It has been proposed that infections with helminths can protect from the development of allergic diseases. However, epidemiological and experimental studies have yielded conflicting results. Therefore we investigated if an infection with Nippostrongylus brasiliensis influenced the development of allergen-induced Th2 cell responses in mice. We found a decrease in allergen-induced airway eosinophilia and Eotaxin levels in the airways when mice were infected with the helminths 8 weeks, and especially 4 weeks, but not 1 or 2 weeks before ovalbumin (OVA)-airway challenge. While OVA-specific IgG1 and IgE serum levels and cutaneous hypersensitivity reactions were not reduced by the helminth infection, there was a reduction in OVA-specific IgG1 and IgE levels in bronchoalveolar lavage fluid of mice. Suppression of allergen-induced airway eosinophilia and reduction of Eotaxin production was not observed in IL-10 deficient mice. In addition, we found that helminth-induced airway eosinophilia and Eotaxin production was strongly increased in IL-10 deficient mice infected with the helminths in comparison to control mice. Taken together, these results show that infection with N. brasiliensis suppresses the development of allergen-induced airway eosinophilia and that this effect may be mediated by IL-10. Our results support the view that helminth infections can contribute to the suppression of allergies in humans.

Allergens↗

PubMed2005

Immunologic responses to common antigens in helminthic infections and allergic disease.

PURPOSE OF REVIEW: It is estimated that over 1 billion individuals are infected with helminth parasites worldwide. Epidemiologic studies have pointed to a protective role of helminthic infections in the development of allergy and asthma; however, evidence for this inverse association has not been consistently established. The focus of this review is to discuss the potential role of shared antigens between parasites and environmental allergens in modulating allergic immune responses, specifically tropomyosin. RECENT FINDINGS: Tropomyosin has been identified as a highly conserved molecule in invertebrates. In populations exposed concomitantly to mites, cockroach, Ascaris, and shrimp and other crustaceans and mollusks, IgE antibody responses to tropomyosin are found in over 50% of individuals. Evidence suggests that IgE cross-reactivity to tropomyosin has clinical relevance. SUMMARY: Mechanisms underlying the immunomodulatory effects of parasites in allergy and asthma remain poorly understood. Identification of molecules in intestinal parasites, particularly Schistosoma mansoni and Ascaris lumbricoides, associated with protection from or promotion of allergy and asthma, could provide the basis for novel forms of treatment or prevention of these diseases. Prospective studies will be necessary to clarify the role of tropomyosin and other parasite antigens shared with inhalant or food allergens in the development of allergic diseases.

Ancylostomatoidea↗

PubMed1986

Mast cell responses to helminth infection.

Mast cells have been suggested to be major effector cells in the immune response to infection with helminths. It is now clear, however, that mast cells are heterogeneous and have a diversity of important functions. In this review, Timothy Lee, Mark Swieter and Dean Befus point out that much of the confusion about the role of mast cells in immunity stems from methods and interpretations which are inadequate for the diversity of roles played by these cells in host responses to parasites. Classical histochemistry may fail to reveal active mast cells, and studies using chemical antagonists are difficult to interpret until we know more about the action of the drugs. The authors show that current research is extending our knowledge of mast cell heterogeneity, and helping to define the powerful array of mediators that they can use to orchestrate the immune response to helminth infections.

Journal Article↗

PubMed1982

Generation of mucosal mast cells is stimulated in vitro by factors derived from T cells of helminth-infected rats.

The connective tissue of rats, and several other species of mammals, contains two distinct types of mast cells that differ in morphology, histochemical staining properties and location1. One type, frequently called the normal connective tissue mast cell, can be obtained in nearly homogeneous preparation from a mixed cell population in the peritoneal cavity and forms the basis of our knowledge of mast cells. The other type is referred to as the mucosal mast cell because in normal rats it has been observed only in mucosal tissue. Infection with helminth parasites induces an exteNsive accumulation of mast cells and eosinophils in the tissues, and parasites of mucous surfaces, in particular, stimulate a rapid hyperplasia of mucosal mast cells. However, the origin of mucosal mast cells, and their relationship to the connective tissue mast cells is uncertain. We now slow that lymphocytes of helminth-infected rats, on in vitro stimulation with specific antigen, release factors causing pronounced mucosal mastocytosis in normal rat bone marrow cultures.

Animals↗

PubMed1993

Diarrhea in helminthic infections.

Enteric helminths are among the most prevalent parasites of humankind, yet only scanty information exists about their effects on the gastrointestinal tract of their hosts. Specifically, there is little agreement on which worms definitely cause diarrhea. The available evidence suggests that five helminthic parasites are associated with human diarrheal disease: Trichinella spiralis (early phases of infection), Trichuris trichiura, Strongyloides stercoralis, Capillaria philippinensis, and Schistosoma (particularly Schistosoma mansoni). All these parasites have an invasive phase during which adult worms, their eggs, or their larvae establish intimate contact with the host's intestinal mucosa and elicit strong local inflammatory responses resulting in various structural and functional alterations of the gut. In contrast, strictly intraluminal worms do not seem to interfere with their hosts' intestinal structure and function to a degree sufficient to cause diarrhea.

Animals↗

PubMed1993

Immunity and immunoregulation in helminth infections.

Parasitic helminths continue to be a major cause of morbidity in human populations, particularly in the tropics and subtropics. The need for effective vaccines that minimize worm burdens, thus reducing associated pathology, is evident. With this goal in mind, an intense research effort is in progress to characterize immune responses to helminths, especially in the context of recent developments in our understanding of the cytokine network. The growing realization that the parasites can themselves subvert host immune responses to their own advantage makes the task of vaccine development that much harder.

Animals↗

PubMedDate not supplied

Associations between helminth infection and CD4+ T cell count, viral load and cytokine responses in HIV-1-infected Ugandan adults.

It has been proposed that helminth infection may exacerbate HIV progression by promoting activation of 'type 2' immune responses. To examine this hypothesis, we investigated helminth infection in a cohort of HIV-1-seropositive adults in Entebbe, Uganda, during November 1999 to January 2000. Individuals with helminths were treated. At enroLlment, after 5 weeks and after 4 months, CD4+ and CD8+ T cell counts and viral load were measured. Cytokine responses (interferon [IFN]-gamma, interleukin [IL]-2, IL-4 and IL-5) to Schistosoma mansoni adult worm antigen (SWA), Mycobacterium tuberculosis culture filtrate proteins (CFPs) and phytohaemagglutinin (PHA) were measured in a whole blood assay. At baseline, CD4+ T cell counts and CD4+: CD8+ ratios were higher in individuals with helminths than in those without (median CD4+ T cell counts 467/microL and 268/microL, respectively, P = 0.005). Viral load was lower among those with helminths but this was not statistically significant. During follow-up, CD4+ T cell counts and cytokine responses to PHA fell among individuals without helminths. Among those treated for helminths, CD4+ counts remained stable. Viral loads showed a transient increase at 5 weeks, which was more marked among those treated for helminths, but the levels at 4 months were similar to baseline in both groups. Among those with schistosomiasis, IFN-gamma and IL-2 responses to CFP, and IL-2 and IL-4 responses to PHA declined but there was a sustained increase in cytokine responses to SWA following treatment. These data do not support the hypothesis that helminth infection exacerbates HIV infection. The possibility that chronic helminth infection may suppress HIV replication and that effects on HIV replication may vary during helminth infection and treatment should be considered.

Adult↗

PubMed2005

Can worms defend our hearts? Chronic helminthic infections may attenuate the development of cardiovascular diseases.

The established risk factors for atherosclerosis fail to fully explain the extent and severity of coronary artery diseases in 50% of the patients. Thus, the causative agents and processes, which may be involved in the pathogenesis of atherosclerosis, are being sought. Notoriously, atherosclerosis and cardiovascular event rates are much lower in developing countries. Clinically, severe infections by intracellular pathogens are widespread mostly in developing countries with poor sanitation, nutrition and massive worm infections. A link between atherosclerosis and helminth infections has never been examined. Based on the present knowledge of immune and infectious mechanisms related to atherosclerosis, it is proposed that chronic helminthic infections can have a significant bearing on the epidemiology of cardiovascular diseases. How can helminthic infections affect the cardiovascular risk? (1) Helminths evade or suppress host immune responses, by producing anti-inflammatory and other immunomodulatory molecules. (2) Helminths induce chronic Th2 activation, which can modify cytokine profiles and immunological responses to heat shock proteins, Chlamydia pneumoniae and cytomegalovirus. (3) The chronic Th2 profile may modulate monocyte activation and chemotaxis to inflammatory sites (atherosclerotic plaques). (4) Chronic Th2 activation may lead to a cytokine profile that could be beneficial for attenuation of atherosclerosis development (upregulation of IL-4, IL-10 and IL-13 and downregulation of proinflammatory cytokines). (5) Helminthic infections may reduce plasma LDL level not only by affecting the host nutrition, but also via modulation of naturally occurring antibodies to cholesterol. Studies are needed to clarify these suggestions. If the hypothesis that helminthic infections impact atherosclerosis is correct, it should be taken into consideration in atherosclerosis immunomodulation therapy and especially in the design of vaccines and vaccine trials.

Animals↗

PubMed2003

Estimating the number of helminthic infections in the Republic of Cameroon from data on infection prevalence in schoolchildren.

INTRODUCTION: The prevalence of infection with helminths is markedly dependent on age, yet estimates of the total number of infections are typically based on data only from school-aged children. Such estimates, although useful for advocacy, provide inadequate information for planning control programmes and for quantifying the burden of disease. Using readily available data on the prevalence of infection in schoolchildren, the relation between the prevalence of infection in school-aged children and prevalence in the wider community can be adequately described using species-specific models. This paper explores the reliability of this approach to predict the prevalence infection in the community and provides a model for estimating the total number of people infected in the Republic of Cameroon. METHODS: Using data on the prevalence of helminthic infection in school-aged children in Cameroon, the prevalence of infection in pre-school children and adults was estimated from species-specific linear and logistic regression models developed previously. The model predictions were then used to estimate the number of people infected in each district in each age group in Cameroon. RESULTS: For Cameroon, if only the prevalence of infection in schoolchildren is used, the number of people infected with each helminthic species will be overestimated by up to 32% when compared with the estimates provided by the species-specific models. The calculation of confidence intervals supports the statistical reliability of the model since a narrow range of parameter estimates is evident. Furthermore, this work suggests that estimation of national prevalence of infection and the number infected will be enhanced if data are stratified by age; this model represents a useful planning tool for obtaining more accurate estimates. Estimates based on data aggregated from three geographical levels (district, regional, and national) show that summarizing prevalence data at the national level will result in biases of up to 19%. Such biases reflect differences in the geographical distribution for the prevalence of each species. DISCUSSION: Developing more accurate estimates requires a better understanding of the differences in the spatial heterogeneity of each species and also better methods of incorporating this information when making estimates.

Adolescent↗

PubMedDate not supplied

The epidemiological implications of a multiple-infection approach to the control of human helminth infections.

It has been suggested that there is economic advantage in using a single community therapy programme to deliver multiple treatments against several parasitic infections. This preliminary study estimates the occurrence of concurrent helminth infection in Africa and Brazil to determine whether such an approach is justified epidemiologically. The results indicate that the occurrence of geohelminthiasis with schistosomiasis is sufficiently frequent in some areas of both Africa and Brazil for a combined approach to control to be appropriate, but that the relatively low frequency of occurrence of onchocerciasis with other infections would justify a multi-infection approach to control at specific foci only.

Africa↗

PubMed1993

IgE and IgG subclass regulation by IL-4 and IFN-gamma in human helminth infections. Assessment by B cell precursor frequencies.

Helminth infections, like atopic disorders, show characteristic elevations of serum IgE and IgG4. To examine the mechanisms underlying the regulation of these two isotypes and of the other IgG subclasses, the frequency (Fo) of isotype-specific B lymphocytes (Bc) from 11 patients with helminth infections was compared by filter-spot ELISA using fresh peripheral blood-derived lymphocytes after 14-day Ag stimulation in vitro. The role of IL-4 and IFN-gamma in the generation and regulation of Ag-driven isotype responses was determined. The Fo of freshly obtained lymphocytes (expressed/10(5) Bc) secreting polyclonal Ig for the following isotypes was: IgE (geometric mean = 0.72; range, 0 to 17.7); IgG4 (geometric mean = 4.9; range, 1.8 to 24.4); IgG1 (geometric mean = 134.3; range, 16.7 to 318). The Fo of IgE correlated with IgG4-secreting Bc among study subjects (r = 0.8, p < 0.01), however there was no association with the other isotypes. Parasite Ag added to cultured lymphocytes induced significant expansion in the number of Ig-secreting Bc for IgE and all IgG subclasses. In contrast, addition of a nonparasite Ag, tetanus toxoid, generated increased Fo of Ig-secreting Bc for IgG1, IgG2, and IgG3, and no expansion of IgG4 or IgE. The essential role of IL-4 in the expansion of IgE- and IgG4-secreting B cells in response to filarial Ag was demonstrated when simultaneous addition of neutralizing anti-IL-4 antibodies completely inhibited this response in all 11 patients studied. Neutralizing anti-IL-4 had no effect on either filarial or tetanus toxoid-driven expansion of IgG1-, IgG2-, or IgG3-secreting Bc. An inhibitory role of endogenously produced IFN-gamma was also shown when addition of neutralizing anti-IFN-gamma to cultures significantly augmented Ag-driven expansion of Bc-secreting IgE and all IgG subclasses; IgE, 0.4- to 9-fold; IgG4, 1.4- to 12-fold; IgG1, 1.6- to 13-fold; IgG2, 1.9- to 5-fold; and IgG3, 2.7- to 6-fold. This study demonstrates that parasite Ag stimulates Bc expansion in helminth-infected patients. Although this response for all five isotypes studied is down-regulated by IFN-gamma, the generation of only the IgE and IgG4 responses appears to be mediated selectively by IL-4. These findings support the concept that IgE and IgG4 production are linked and related to the quantities of IL-4 and IFN-gamma induced by Ag-specific T cells.

Antigens, Helminth↗

PubMed2006

Basophils, basophilia and helminth infections.

A growing body of evidence suggests basophils are important components of the human immune response to helminth infections. Basophil numbers are increased in several animal models of helminth infection, and basophils have been shown to release both histamine and IL-4 in response to helminths. Helminth infections typically provoke type 2 immune responses characterized by eosinophilia, elevated levels of Ag-specific and polyclonal IgE, and T cell production of type 2 cytokines such as IL-4, IL-5, and IL-13. IL-4 plays a central role in this type 2 response. As basophils are the only peripheral blood mononuclear cells with the ability to release IL-4 rapidly in response to appropriate stimuli, releasing large quantities of preformed IL-4 within minutes of surface IgE cross-linking, it appears likely that basophils play an important role in amplifying ongoing type 2 immune responses to helminth infections once Ag-specific IgE is present. Basophils may also function to initiate type 2 responses upon first exposure to helminths and to potentially re-establish these responses upon re-exposure. This article reviews basic basophil biology and physiology, evaluates the evidence for the presence of basophilia in helminth infections, and then focuses on the possible roles basophils serve in the immune response to helminth infections.

Allergens↗

PubMed2006

Helminth infection suppresses T-cell immune response to HIV-DNA-based vaccine in mice.

A number of HIV-1 vaccines are in various phases of clinical trials and many more are in the developmental pipeline. Vaccines are especially needed for developing countries where morbidity and mortality due to HIV/AIDS is most severe, the prevalence of HIV infection is highest, and its incidence is often still rising dramatically. Individuals living in these regions are often infected with one or more helminth parasites which systemically bias the immune system towards Th2-type as well as drive immune anergy. The goal of this study was to develop a multi-T-cell epitope DNA-based vaccine for HIV-1 subtype C and to determine the impact of helminth infection on the immune response to this vaccine. We found that vaccination of naïve mice with the multi-epitope vaccine, designated TD158, induced a strong HIV-1C-specific T-cell immune response, and that the addition of the Igkappa leader sequence to the TD158 vaccine construct significantly increased the frequencies of IFN-gamma secreting CD8+ T cells. However, the TD158 vaccine specific response of mice infected with the human helminth Schistosoma mansoni was significantly suppressed. The impact of schistosome infection on suppressing the virus-specific immune response was the same whether mice were vaccinated with the TD158 vaccine or with the Igkappa enhanced TD158. The results of this study suggest that helminth infection may pose a serious problem for vaccination with the DNA-based HIV-1 vaccine in developing country populations, and that the prevalence of helminth infections in the vaccine cohorts should be taken into account for HIV-1 vaccine trial design.

AIDS Vaccines↗

PubMed2002

An enteric helminth infection protects against an allergic response to dietary antigen.

Although helminths induce a polarized Th2 response they have been shown, in clinical studies, to confer protection against allergies. To elucidate the basis for this paradox, we have examined the influence of an enteric helminth infection on a model of food allergy. Upon Ag challenge, mice fed peanut (PN) extract plus the mucosal adjuvant cholera toxin (CT) produced PN-specific IgE that correlated with systemic anaphylactic symptoms and elevated plasma histamine. PN-specific IgE was not induced in helminth-infected mice fed PN without CT. Moreover, when PN plus CT was fed to helminth-infected mice, both PN-specific IgE and anaphylactic symptoms were greatly diminished. The down-regulation of PN-specific IgE was associated with a marked reduction in the secretion of IL-13 by PN-specific T cells. When helminth-infected PN plus CT-sensitized mice were treated with neutralizing Abs to IL-10, the PN-specific IgE response and anaphylactic symptoms were similar to, or greater than, those seen in mice that receive PN and CT alone. Taken together, these results suggest that helminth-dependent protection against allergic disease involves immunoregulatory mechanisms that block production of allergen-specific IgE.

Administration, Oral↗

PubMedDate not supplied

Eradication of helminthic infections.

The eradication of helminthic infections described by models of the Nåsell-Hirsch type is investigated. Simple criteria are proposed for comparing the efficiency of different modes of eradication.

Helminthiasis↗

PubMed2000

Eosinophilia and helminthic infections.

Among microbial agents, helminths are the most common cause of eosinophilia. An approach to the evaluation of a patient with eosinophilia is outlined, with particular emphasis on clues in the history, examination and routine laboratory data that can help with the diagnosis. Multiple helminthic infections have been associated with eosinophilia, and the characteristic modes of spread, clinical manifestations, diagnostic tests and therapeutic considerations of these infections are discussed.

Animals↗

PubMed2001

Treatment vs non-treatment of helminth infections in cattle: defining the threshold.

Helminth infections are an important cause of lost productivity in livestock world-wide, often necessitating anthelmintic treatment. However, a large part of the anthelmintics are used indiscriminately because the parasite levels are too low to justify treatment or because the treatments are not correctly programmed, resulting in undertreatment or overtreatment. The objective of this paper is to discuss possible thresholds for anthelmintic treatment of some of the more important helminth infections in livestock, i.e. gastrointestinal nematodes, lungworms and liver fluke, to promote a more appropriate use of anthelmintics. When possible, a distinction is made between therapeutic thresholds, production-based thresholds and preventive thresholds. A "therapeutic threshold" is intended to identify (an) animal(s) with parasite levels that necessitate immediate treatment. The therapeutic threshold is basically the diagnosis of clinical disease, and can be determined relatively easily for the parasites discussed in this paper. A "production-based threshold" is intended to measure the effects of sub-clinical parasitism on productivity parameters, such as weight gain and milk yield, before clinical disease occurs. Finally, a "preventive threshold" is meant to predict future infection levels, to enable the application of appropriate control measures.

Animals↗