Protective Effect of Intestinal Helminthiasis Against Tuberculosis Progression Is Abrogated by Intermittent Food Deprivation.

Background: Tuberculosis (TB) is still a major challenge for humankind. Because regions with the highest incidence also have a high prevalence of helminthiasis and nutritional scarcity, we wanted to understand the impact of these on TB progression. Methods: We have developed an experimental murine model for active TB in C3HeB/FeJ, coinfected with Trichuris muris and Heligmosomoides polygyrus nematodes, and exposed to an environmental mycobacterium (M. manresensis) and intermittent fasting. Cause-effect relationships among these factors were explored with Partial Least Squares Path modelling (PLSPM). Results: Previous parasitization had a major anti-inflammatory effect and reduced systemic levels of ADA, haptoglobin, local pulmonary levels of IL-1ß, IL-6, TNF-α, CXCL-1, CXCL-5 and IL-10. Oral administration of heat-killed M. manresensis resulted in a similar outcome. Both interventions diminished pulmonary pathology and bacillary load, but intermittent food deprivation reduced this protective effect increasing stress and inflammation. The PLSPM revealed nematodes might have protective effects against TB progression. Conclusions: Significantly higher cortisol levels in food-deprivation groups showed it is a stressful condition, which might explain its deleterious effect. This highlights the impact of food security on TB eradication policies and the need to prioritize food supply over deworming activities.

Malaria and intestinal parasite co-infection and its association with anaemia among people living with HIV in Buea, Southwest Cameroon: A community-based retrospective cohort study.

BACKGROUND: Both malaria and intestinal parasites are endemic in Cameroon, and their co-infection can be of great impact on anaemia among people living with HIV (PLWH). This community-based retrospective cohort study determined the prevalence and association of infections with anaemia in PLWH and HIV-negative individuals in Buea, Cameroon from March to August 2019. METHODS: The study population comprised of 190 PLWH and 216 consenting HIV-negative individuals from the Buea community. Participants were examined clinically, the collected blood sample was used for malaria parasite (MP) detection, HIV diagnosis and haemoglobin (Hb) measurement while stool samples were examined for the detection of intestinal parasites (IPs). Proportions were compared using Pearson's Chi-square test and association of anaemia with independent variables was evaluated using logistic regression analysis. RESULTS: Out of the 406 participants, MP, IPs and MP/IP co-infection prevalences were 15.5%, 13.0% and 3.0% respectively. PLWH had a higher prevalence of MP (16.3%, P = 0.17), IPs (23.7%, P ˂ 0.001) and MP/IPs co-infection (3.7%, P = 0.04) when compared with HIV-negative participants. Similarly, PLWH had significantly lower mean haemoglobin value (11.10 ± 1.54 g/dL) than their HIV-negative counterparts (12.45 ± 2.06 g/dL). Also, PLWH co-infected with MP and IPs were observed to have a significantly lower mean haemoglobin value (10.6 ± 1.21 g/dL). PLWH had a significantly (P ˂ 0.001) higher prevalence of mild (56.8%), moderate (18.4%) and severe (1.6%) anaemia when compared with HIV-negative counterparts. The significant risk factors associated with anaemia included being febrile (P = 0.03), MP-infected only (P = 0.001), HIV-infected only (P < 0.001), having dual (P < 0.001) or triple-infections (P = 0.03). CONCLUSION: Malaria and intestinal parasites remain public health concerns among PLWH and anaemia as a serious haematological abnormality gets exacerbated even with the viral load suppression. Hence, routine medical check-ups among PLWH are recommended.

Gut CD4+ T cell phenotypes are a continuum molded by microbes, not by TH archetypes.

CD4+ effector lymphocytes (Teff) are traditionally classified by the cytokines they produce. To determine the states that Teff cells actually adopt in frontline tissues in vivo, we applied single-cell transcriptome and chromatin analyses to colonic Teff cells in germ-free or conventional mice or in mice after challenge with a range of phenotypically biasing microbes. Unexpected subsets were marked by the expression of the interferon (IFN) signature or myeloid-specific transcripts, but transcriptome or chromatin structure could not resolve discrete clusters fitting classic helper T cell (TH) subsets. At baseline or at different times of infection, transcripts encoding cytokines or proteins commonly used as TH markers were distributed in a polarized continuum, which was functionally validated. Clones derived from single progenitors gave rise to both IFN-γ- and interleukin (IL)-17-producing cells. Most of the transcriptional variance was tied to the infecting agent, independent of the cytokines produced, and chromatin variance primarily reflected activities of activator protein (AP)-1 and IFN-regulatory factor (IRF) transcription factor (TF) families, not the canonical subset master regulators T-bet, GATA3 or RORγ.

Changes in the severity of gastric mucosal inflammation associated with Helicobacter pylori in humans coinfected with intestinal helminths.

BACKGROUND: Though a few studies in animal models suggest that intestinal helminths (IH) favorably affect evolution of gastritis associated with Helicobacter pylori (H. pylori) the studies supporting this concept in humans are only a few and are based on serological data. METHODS: To evaluate the possible influence of IH on the human gastric mucosa, three groups of Venezuelan adults with gastropathy (endoscopically diagnosed) were studied: H. pylori-/IH- (n = 17), H. pylori+/IH- (n = 18), and H. pylori+/IH+ (n = 11). Histological analysis (hematoxylin-eosin) and immunohistochemical staining (peroxidase) for cytokines interleukin-1beta (IL-1ß), tumor necrosis factor alpha (TNF-α), gamma interferon (IFN-γ), and interleukin 4 (IL-4) were undertaken in gastric antral biopsies. RESULTS: Expression of the four cytokines was detected in all individuals in varying degrees, but proinflammatory cytokines were expressed in a higher degree in the H. pylori+/IH- group, mainly IL-1ß (Th1-dominant immune response), associated with a higher degree of both histological inflammation and gastric cancer risk index (GCRI), as compared to the H. pylori-/IH- group. In contrast, an increased expression of IL-4 and a reduced expression of proinflammatory cytokines (Th2-dominant response), plus the tendency to a lower degree of mononuclear infiltration, mucosal atrophy in gastric corpus, and GCRI, were evidenced in the coinfected group. CONCLUSIONS: The findings of the present study is perhaps the first histological evidence of a possible modulatory effect of IH on the gastric mucosal inflammatory response due to H. pylori infection in humans.

The influence of selected gastrointestinal parasites on apoptosis in intestinal epithelial cells.

Studies on the parasite-host interaction may provide valuable information concerning the modulation of molecular mechanisms as well as of the host immune system during infection. To date, it has been demonstrated that intestinal parasites may affect, among others, the processes of digestion in the gastrointestinal system of the host, thus limiting the elimination of the parasite, the immune response as well as inflammation. However, the most recent studies suggest that intestinal parasites may also affect modulation of the apoptosis pathway of the host. The present paper presents the latest scientific information on the influence of intestinal parasite species (Blastocystis sp., Giardia sp., Cryptosporidium sp., Trichuris sp., Entamoeba histolytica, Nippostrongylus brasiliensis, Heligmosomoides polygyrus) on the molecular mechanisms of apoptosis in intestinal epithelial cells. This paper stresses that the interdependency between the intestinal parasite and the host results from the direct effect of the parasite and the host's defense reactions, which lead to modulation of the apoptosis pathways (intrinsic and extrinsic). Moreover, the present paper presents the role of proteins involved in the mechanisms of apoptosis as well as the physiological role of apoptosis in the host's intestinal epithelial cells.

Helminths and microbes within the vertebrate gut - not all studies are created equal.

The multifaceted interactions occurring between gastrointestinal (GI) parasitic helminths and the host gut microbiota are emerging as a key area of study within the broader research domain of host-pathogen relationships. Over the past few years, a wealth of investigations has demonstrated that GI helminths interact with the host gut flora, and that such interactions result in modifications of the host immune and metabolic statuses. Nevertheless, whilst selected changes in gut microbial composition are consistently observed in response to GI helminth infections across several host-parasite systems, research in this area to date is largely characterised by inconsistent findings. These discrepancies are particularly evident when data from studies of GI helminth-microbiota interactions conducted in humans from parasite-endemic regions are compared. In this review, we provide an overview of the main sources of variance that affect investigations on helminth-gut microbiota interactions in humans, and propose a series of methodological approaches that, whilst accounting for the inevitable constraints of fieldwork, are aimed at minimising confounding factors and draw biologically meaningful interpretations from highly variable datasets.

The major secreted protein of the whipworm parasite tethers to matrix and inhibits interleukin-13 function.

Infection by soil transmitted parasitic helminths, such as Trichuris spp, are ubiquitous in humans and animals but the mechanisms determining persistence of chronic infections are poorly understood. Here we show that p43, the single most abundant protein in T. muris excretions/secretions, is non-immunogenic during infection and has an unusual sequence and structure containing subdomain homology to thrombospondin type 1 and interleukin (IL)-13 receptor (R) α2. Binding of p43 to IL-13, the key effector cytokine responsible for T. muris expulsion, inhibits IL-13 function both in vitro and in vivo. Tethering of p43 to matrix proteoglycans presents a bound source of p43 to facilitate interaction with IL-13, which may underpin chronic intestinal infection. Our results suggest that exploiting the biology of p43 may open up new approaches to modulating IL-13 function and control of Trichuris infections.

ILC2s-Trailblazers in the Host Response Against Intestinal Helminths.

Group 2 innate lymphoid cells (ILC2s) were first discovered in experimental studies of intestinal helminth infection-and much of our current knowledge of ILC2 activation and function is based on the use of these models. It is perhaps not surprising therefore that these cells have also been found to play a key role in mediating protection against these large multicellular parasites. ILC2s have been intensively studied over the last decade, and are known to respond quickly and robustly to the presence of helminths-both by increasing in number and producing type 2 cytokines. These mediators function to activate and repair epithelial barriers, to recruit other innate cells such as eosinophils, and to help activate T helper 2 cells. More recent investigations have focused on the mechanisms by which the host senses helminth parasites to activate ILC2s. Such studies have identified novel stromal cell types as being involved in this process-including intestinal tuft cells and enteric neurons, which respond to the presence of helminths and activate ILC2s by producing IL-25 and Neuromedin, respectively. In the current review, we will outline the latest insights into ILC2 activation and discuss the requirement for-or redundancy of-ILC2s in providing protective immunity against intestinal helminth parasites.

Effects of breeding center, age and parasite burden on fecal triiodothyronine levels in forest musk deer.

The objective of this study was to evaluate the effects of sex, breeding center and age on fecal triiodothyronine levels in captive forest musk deer Moschus berezovskii, and to explore the age-intensity model of gastrointestinal parasites. Furthermore, the association between fecal triiodothyronine levels and parasite egg shedding was also analyzed. We collected musk deer fecal samples from two breeding centers located in Shaanxi and Sichuan province, China. Enzyme-linked immunosorbent assays were utilized to estimate the fecal triiodothyronine concentrations and profiles, and fecal parasite eggs or oocysts were counted using the McMaster technique. Female deer from both breeding centers consistently showed higher triiodothyronine concentrations than those observed in males, which indicates that a distinct physiology pattern occurs by sex. The triiodothyronine concentration in Sichuan breeding center was significantly higher than that in Shaanxi center for both sexes, suggesting that differences in environment, diet and management practices are likely to affect the metabolism. In addition, a negative relationship between triiodothyronine concentrations and age was found (r = - 0.75, p < 0.001), and parasite egg shedding was also negatively associated with age (r = - 0.51, p < 0.001), by which we can infer that older animals evolves a more developed immune system. Finally, a positive association between parasite egg shedding and triiodothyronine levels was found, which could be explained by the additional energy metabolism resulting from parasitic infection. Results from this study might suggest metabolic and immunological adaptations in forest musk deer. These baseline data could be used to unveil metabolic status and establish parasite control strategies, which has great potential in captive population management as well as their general health evaluations.

Mast Cells and Serotonin Synthesis Modulate Chagas Disease in the Colon: Clinical and Experimental Evidence.

BACKGROUND: Trypanosoma cruzi (T. cruzi) infects millions of Latin Americans each year and can induce chagasic megacolon. Little is known about how serotonin (5-HT) modulates this condition. Aim We investigated whether 5-HT synthesis alters T. cruzi infection in the colon. MATERIALS AND METHODS: Forty-eight paraffin-embedded samples from normal colon and chagasic megacolon were histopathologically analyzed (173/2009). Tryptophan hydroxylase 1 (Tph1) knockout (KO) mice and c-KitW-sh mice underwent T. cruzi infection together with their wild-type counterparts. Also, mice underwent different drug treatments (16.1.1064.60.3). RESULTS: In both humans and experimental mouse models, the serotonergic system was activated by T. cruzi infection (p < 0.05). While treating Tph1KO mice with 5-HT did not significantly increase parasitemia in the colon (p > 0.05), rescuing its synthesis promoted trypanosomiasis (p < 0.01). T. cruzi-related 5-HT release (p < 0.05) seemed not only to increase inflammatory signaling, but also to enlarge the pericryptal macrophage and mast cell populations (p < 0.01). Knocking out mast cells reduced trypanosomiasis (p < 0.01), although it did not further alter the neuroendocrine cell number and Tph1 expression (p > 0.05). Further experimentation revealed that pharmacologically inhibiting mast cell activity reduced colonic infection (p < 0.01). A similar finding was achieved when 5-HT synthesis was blocked in c-KitW-sh mice (p > 0.05). However, inhibiting mast cell activity in Tph1KO mice increased colonic trypanosomiasis (p < 0.01). CONCLUSION: We show that mast cells may modulate the T. cruzi-related increase of 5-HT synthesis in the intestinal colon.

Experimental Chagas disease-induced perturbations of the fecal microbiome and metabolome.

Trypanosoma cruzi parasites are the causative agents of Chagas disease. These parasites infect cardiac and gastrointestinal tissues, leading to local inflammation and tissue damage. Digestive Chagas disease is associated with perturbations in food absorption, intestinal traffic and defecation. However, the impact of T. cruzi infection on the gut microbiota and metabolome have yet to be characterized. In this study, we applied mass spectrometry-based metabolomics and 16S rRNA sequencing to profile infection-associated alterations in fecal bacterial composition and fecal metabolome through the acute-stage and into the chronic stage of infection, in a murine model of Chagas disease. We observed joint microbial and chemical perturbations associated with T. cruzi infection. These included alterations in conjugated linoleic acid (CLA) derivatives and in specific members of families Ruminococcaceae and Lachnospiraceae, as well as alterations in secondary bile acids and members of order Clostridiales. These results highlight the importance of multi-'omics' and poly-microbial studies in understanding parasitic diseases in general, and Chagas disease in particular.

The Immune and Non-Immune Pathways That Drive Chronic Gastrointestinal Helminth Burdens in the Wild.

Parasitic helminths are extremely resilient in their ability to maintain chronic infection burdens despite (or maybe because of) their hosts' immune response. Explaining how parasites maintain these lifelong infections, identifying the protective immune mechanisms that regulate helminth infection burdens, and designing prophylactics and therapeutics that combat helminth infection, while preserving host health requires a far better understanding of how the immune system functions in natural habitats than we have at present. It is, therefore, necessary to complement mechanistic laboratory-based studies with studies on wild populations and their natural parasite communities. Unfortunately, the relative paucity of immunological tools for non-model species has held these types of studies back. Thankfully, recent progress in high-throughput 'omics platforms provide powerful and increasingly practical means for immunologists to move beyond traditional lab-based model organisms. Yet, assigning both metabolic and immune function to genes, transcripts, and proteins in novel species and assessing how they interact with other physiological and environmental factors requires identifying quantitative relationships between their expression and infection. Here, we used supervised machine learning to identify gene networks robustly associated with burdens of the gastrointestinal nematode Heligmosomoides polygyrus in its natural host, the wild wood mice Apodemus sylvaticus. Across 34 mice spanning two wild populations and across two different seasons, we found 17,639 transcripts that clustered in 131 weighted gene networks. These clusters robustly predicted H. polygyrus burden and included well-known effector and regulatory immune genes, but also revealed a number of genes associated with the maintenance of tissue homeostasis and hematopoiesis that have so far received little attention. We then tested the effect of experimentally reducing helminth burdens through drug treatment on those putatively protective immune factors. Despite the near elimination of H. polygyrus worms, the treatment had surprisingly little effect on gene expression. Taken together, these results suggest that hosts balance tissue homeostasis and protective immunity, resulting in relatively stable immune and, consequently, parasitological profiles. In the future, applying our approach to larger numbers of samples from additional populations will help further increase our ability to detect the immune pathways that determine chronic gastrointestinal helminth burdens in the wild.

Helminths in the gastrointestinal tract as modulators of immunity and pathology.

Helminth parasites are highly prevalent in many low- and middle-income countries, in which inflammatory bowel disease and other immunopathologies are less frequent than in the developed world. Many of the most common helminths establish themselves in the gastrointestinal tract and can exert counter-inflammatory influences on the host immune system. For these reasons, interest has arisen as to how parasites may ameliorate intestinal inflammation and whether these organisms, or products they release, could offer future therapies for immune disorders. In this review, we discuss interactions between helminth parasites and the mucosal immune system, as well as the progress being made toward identifying mechanisms and molecular mediators through which it may be possible to attenuate pathology in the intestinal tract.

IgE and mast cells in host defense against parasites and venoms.

IgE-dependent mast cell activation is a major effector mechanism underlying the pathology associated with allergic disorders. The most dramatic of these IgE-associated disorders is the fatal anaphylaxis which can occur in some people who have developed IgE antibodies to otherwise innocuous antigens, such as those contained in certain foods and medicines. Why would such a highly "maladaptive" immune response develop in evolution and be retained to the present day? Host defense against parasites has long been considered the only beneficial function that might be conferred by IgE and mast cells. However, recent studies have provided evidence that, in addition to participating in host resistance to certain parasites, mast cells and IgE are critical components of innate (mast cells) and adaptive (mast cells and IgE) immune responses that can enhance host defense against the toxicity of certain arthropod and animal venoms, including enhancing the survival of mice injected with such venoms. Yet, in some people, developing IgE antibodies to insect or snake venoms puts them at risk for having a potentially fatal anaphylactic reaction upon subsequent exposure to such venoms. Delineating the mechanisms underlying beneficial versus detrimental innate and adaptive immune responses associated with mast cell activation and IgE is likely to enhance our ability to identify potential therapeutic targets in such settings, not only for reducing the pathology associated with allergic disorders but perhaps also for enhancing immune protection against pathogens and animal venoms.

Interleukin-13 Receptor α1-Dependent Responses in the Intestine Are Critical to Parasite Clearance.

Nematode infection upregulates interleukin-4 (IL-4) and IL-13 and induces STAT6-dependent changes in gut function that promote worm clearance. IL-4 and IL-13 activate the type 2 IL-4 receptor (IL-4R), which contains the IL-13Rα1 and IL-4Rα chains. We used mice deficient in IL-13Rα1 (IL-13Rα1(-/-)) to examine the contribution of IL-13 acting at the type 2 IL-4R to immune and functional responses to primary (Hb1) and secondary (Hb2) infections with the gastrointestinal nematode parasite Heligmosomoides bakeri There were differences between strains in the IL-4 and IL-13 expression responses to Hb1 but not Hb2 infection. Following Hb2 infection, deficient mice had impaired worm expulsion and higher worm fecundity despite normal production of Th2-derived cytokines. The upregulation of IL-25 and IL-13Rα2 in Hb1- and Hb2-infected wild-type (WT) mice was absent in IL-13Rα1(-/-)mice. Goblet cell numbers and resistin-like molecule beta (RELM-ß) expression were attenuated significantly in IL-13Rα1(-/-)mice following Hb2 infections. IL-13Rα1 contributes to the development of alternatively activated macrophages, but the type 1 IL-4R is also important. Hb1 infection had no effects on smooth muscle function or epithelial permeability in either strain, while the enhanced mucosal permeability and changes in smooth muscle function and morphology observed in response to Hb2 infection in WT mice were absent in IL-13Rα1(-/-)mice. Notably, the contribution of claudin-2, which has been linked to IL-13, does not mediate the increased mucosal permeability following Hb2 infection. These results show that activation of IL-13Rα1 is critical for key aspects of the immune and functional responses to Hb2 infection that facilitate expulsion.

Expression of growth-related genes in the mouse placenta is influenced by interactions between intestinal nematode (Heligmosomoides bakeri) infection and dietary protein deficiency.

Intestinal nematode infection and dietary protein deficiency are common during pregnancy and both have been shown to impair fetal growth in humans, livestock and laboratory animals. The placenta has been linked to fetal growth but its role in mediating the response to maternal infection and protein deficiency is not understood. We used microarrays to test the hypothesis that maternal intestinal nematode infection and protein deficiency alter the expression of placental genes related to fetal growth. Placentas were obtained on day 18 of pregnancy from CD-1 mice fed protein sufficient (24%) or protein deficiency (6%) isoenergetic diets and either uninfected or infected with Heligmosomoides bakeri. Gene expression was analysed using the Affymetrix GeneChip 2.0 ST mouse array (n=3/experimental group). Differentially expressed genes were identified using two-way ANOVA (P<0.02, fold-change >1.25) and pathway analyses were performed using DAVID software. Expression changes for selected genes were confirmed using qPCR. Heligmosomoides bakeri infection down-regulated 109 transcripts, including genes related to oxidative phosphorylation, and up-regulated 214 transcripts, including genes involved in ATP binding and hemopoiesis. Up-regulation of hemopoiesis genes may explain increased placental mass previously reported in H. bakeri-infected mice. Protein deficiency down-regulated 141 annotated transcripts, including genes involved in cell motility and endopeptidase activity, and up-regulated 131 annotated transcripts, including genes related to hemopoiesis. A statistical interaction was detected for 248 transcripts, including several genes with known functions in fetal growth. Notably, expression of the gene Irs1 (insulin receptor substrate) was lower in infected dams but only when they were fed a protein sufficient diet. Also, expression of several genes, including Igf1r (insulin-like growth factor-1 receptor) and Prl (prolactin) was up-regulated by infection in protein deficiency dams and down-regulated by protein deficiency in uninfected dams. Our results highlight that expression of placental genes involved in fetal growth is influenced by the interaction between protein deficiency and H. bakeri infection.

Cas 2015.3. Lactant de 9 mesos amb lesió perianal / No disponible

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Determinants of Iron Deficiency Anemia in a Cohort of Children Aged 6-71 Months Living in the Northeast of Minas Gerais, Brazil.

Iron deficiency anemia is one of the most common nutritional disorders worldwide. The aim was to identify the prevalence and incidence of anemia in children and to identify predictors of this condition, including intestinal parasites, social, nutritional and environmental factors, and comorbidities. A population-based cohort study was conducted in a sample of 414 children aged 6-71 months living in Novo Cruzeiro in the Minas Gerais State. Data were collected in 2008 and 2009 by interview and included socio-economic and demographic information about the children and their families. Blood samples were collected for testing of hemoglobin, ferritin and C-reactive protein. Anthropometric measurements and parasitological analyses of fecal samples were performed. To identify risk factors associated with anemia multivariate analyses were performed using the generalized estimating equations (GEE). In 2008 and 2009, respectively, the prevalence rates of anemia were 35.9% (95%CI 31.2-40.8) and 9.8% (95%CI 7.2-12.9), the prevalence rates of iron deficiency were 18.4% (95%CI 14.7-22.6) and 21.8% (95%CI 17.8-26.2), and the incidence rates of anemia and iron deficiency were 3.2% and 21.8%. The following risk factors associated with anemia were: iron deficiency (OR = 3.2; 95%CI 2.0-.5.3), parasitic infections (OR = 1.9; 95%CI 1.2-2.8), being of risk of or being a low length/height-for-age (OR = 2.1; 95%CI 1.4-3.2), and lower retinol intake (OR = 1.7; 95%CI 1.1-2.7), adjusted over time. Nutritional factors, parasitic infections and chronic malnutrition were identified as risk factors for anemia. These factors can be verified in a chronic process and have been classically described as risk factors for these conditions.

Host-parasite relationships as determinants of heavy metal concentrations in perch (Perca fluviatilis) and its intestinal parasite infection.

The concentrations of As, Cd, Cr, Cu, Hg, Mn, Ni, Pb, and Zn and their bioconcentration factors (BCFs) were determined in two intestinal parasites, an acanthocephalan, Acanthocephalus lucii, a tapeworm, Proteocephalus percae, present in the same host, the European perch (Perca fluviatilis, L.), in the heavily polluted Ruzín reservoir in eastern Slovakia. The bioaccumulation of heavy metals in the fish organs and parasites was studied for acanthocephalan and tapeworm monoinfections or mixed infections by the two parasites and for the size of their parasitic infrapopulations. Bioconcentration factors (c[parasite]/c[muscle tissue]) showed that the concentrations of As, Ni, Pb and Zn were higher in mixed infections than in monoinfections. Negative correlations between heavy metal concentrations in perch organs and the parasites were found. For example, higher concentrations of Ni and Zn in both parasite species corresponded with lower metal concentrations in perch and hard roe. Likewise, significant negative relationships between metal concentrations in fish organs and number of parasites were noticed with lower levels of Pb in fish harbouring higher numbers of tapeworms. Similarly, in both parasite species the concentrations of some essential elements (Cr, Mn) were lower at high infection intensities compared to low intensities. Our study revealed that the differential concentration of heavy metals in perch organs was affected by the type of infection (mono- or mixed-infection), and needs to be considered in field ecotoxicological and parasitological studies as a potentially important factor influencing the pollutant concentrations in fish.

Sex-determined susceptibility and differential MUC2 mRNA expression during the course of murine intestinal eimeriosis.

Parasitic diseases differ in prevalence, course, and severity between males and females. The study was designed to compare males with females for the susceptibility to Eimeria papillata infection as well as the expression of the mucin gene, MUC2. Oocysts output was detected to be more in the feces of male mice (3.5 × 10(4) ± 4000 oocysts/g feces) than in females (2 × 10(4) ± 2000 oocysts/g feces). In addition, infected males showed a significant higher number of meronts, gamonts, and developing oocysts compared to infected female mice. Moreover, E. papillata induced a marked goblet cell hypoplasia where the jejuna of infected male mice contained lower numbers of goblet cells per ten villus-crypt units compared to infected females. Also, the expression of MUC2 mRNA is found to be more expressed in infected females than males. In addition, testosterone, nitric oxide, and inducible nitric oxide synthase activities were found to be higher in infected male mice than in infected females. In general, male Swiss albino mice have been shown to be relatively more susceptible to infection with E. papilaata when compared with female mice.