Ability Of Parasite Research Articles

Potential benefits of male diploidy and female triploidy for parasitoid wasps used as biological control agents: A case study in Nasonia

Parasitoid wasps are haplodiploid insects, but polyploidy (diploid males, triploid females) occurs for many species. In biological control, polyploidy may have beneficial effects on desirable biological related traits. However, this is only possible in species for which polyploidy does not impair essential biological functions, as in for instance species with Complementary Sex Determination (CSD), where inbreeding drives sterile diploid male production and extinction risk. Notably, while CSD polyploidy is better studied, most biological agents are non-CSD species. This includes model Nasonia vitripennis, a blowfly parasitoid that can be purposefully made polyploid and then produces a high number of reproductive polyploid individuals. To test baseline non-CSD polyploid utility, an outbred polyploid N. vitripennis transformer knockdown line (tKDL) was established and assayed for relevant traits for considering polyploids as biological agents. Male diploidy and female triploidy increased head width, a body size proxy. Polyploidy increased unmated lifespan in diploid males, but decreased it in triploid females. In first matings, haploid and diploid males had equal fecundity, but sperm depletion assays revealed reduced diploid male fitness overall. Triploid females had a reduction in parasitization ability. This reduced male fecundity and female parasitization in tKDL suggest that polyploid Nasonia parasitoids have limited direct use in biological control, particularly in this outbred background. They are possibly more suitable for preparative applications, such as retaining alleles with sex-specific benefits.

Duffy Binding Protein Ligand (PvDBP) gene duplication in Indian P. Vivax Malaria isolates: implication for malaria research.

Plasmodium vivax malaria poses a major global health challenge, fueled by the parasite's ability to establish chronic infections via dormant liver hypnozoites that enable immune evasion and show transmission resilience. A key virulence determinant of P. vivax blood-stage infection is the ligand-receptor interaction of infected erythrocytes mediated by the Duffy Binding Protein (PvDBP) ligand. Gene duplication events leading to increased PvDBP copy numbers have been documented in parasite populations in Cambodia, Brazil, and Sudan, but whether such changes exist in Indian isolates is not known. India shoulders a disproportionately high P. vivax burden in the world. DNA extracted from malaria-positive samples from a multisite survey was subjected to diagnostic PCR to evaluate PvDBP duplication. We identified PvDBP duplication at 18.6% frequency across various regions in India via diagnostic PCR. Both 'Cambodian-type' and 'Malagasy-type' duplication patterns were detected. PvDBP copy number variations associated with specific Duffy antigen receptor genotypes were correlated in the patient cohort. While PvDBP duplication was widespread, its geographic distribution varied, occurring most prevalently in northeastern regions of India. The presence of Duffy binding protein gene duplication in nearly one-fifth of P. vivax isolates in India may have significant epidemiological and clinical implications. This genetic variation could potentially impact, parasite fitness and invasion efficiency, possibly leading to higher parasitemia levels and immune evasion capabilities, which may affect the efficacy of natural immunity and vaccine development efforts and / or transmission dynamics if the duplication confers any advantage in mosquito stages. To fully understand these implications, we propose longitudinal studies tracking patients with and without PvDBP duplications, comparing clinical outcomes, parasitemia levels, and transmission rates. Additionally, spatial and temporal analyses of duplication frequency across India could reveal patterns of spread and potential selective pressures driving this genetic change.

Detection of DNA of Leishmania infantum in the brains of dogs without neurological signs in an endemic region for leishmaniasis in the state of Rio Grande do Sul, Brazil.

Canine visceral leishmaniasis (CVL) is a parasitic disease caused by the protozoan Leishmania infantum. Neurological infection occurs due to the parasite's ability to cross the blood-brain barrier. It is known that dogs can remain infected with a subclinical infection for life, potentially acting as reservoirs for L. infantum when bitten by sandflies. In this context, the objective of this study was to evaluate the occurrence of Leishmania spp. in the brains of dogs from the metropolitan region of Rio Grande do Sul, Brazil, without a history of neurological disease but residing in an endemic area for L. infantum. A total of 200 samples, from 2022 to 2023, were evaluated using conventional Polymerase Chain Reaction (PCR) with the primers Leishmini-F GGKAGGGGCGTTCTGC and Leishmini-R STATWTTACACCAACCCC, aiming to amplify a product of 120 base pairs for Leishmania spp. To identify the species, a multiplex PCR was used, differentiating L. braziliensis (127bp), L. amazonensis (100bp), and L. infantum (60bp), with the molecular target being the conserved region of the kinetoplast DNA (kDNA) minicircle, specific to Leishmania spp. Of the 200 samples evaluated, 26.5% (53/200) tested positive in the conventional PCR reaction for Leishmania spp., with the PCR multiplex the only species detected was Leishmania infantum. The average age of the positive animals was 5.08years, with 47.2% being females and 52.8% being males; among these, mixed-breed dogs were the most predominant, representing 43.4% of the total. Clinical signs varied: hepatomegaly in two dogs, pronounced neutrophilic hepatitis in one, splenomegaly in one with lymphoid hyperplasia, and glomerulonephritis and nephritis in two animals. Mild anemia and thrombocytopenia were found in eight, with pale mucous membranes in three, and diffuse alveolar edema in one case. Notable pathological findings included suspected distemper in one animal and lymphoplasmacytic meningitis in another. Histopathological findings revealed alveolar edema and acute renal failure. A third dog exhibited bilateral hydrocephalus and diffuse edema in the brain. Additional changes, such as mild inflammatory infiltrate and slight vacuolar degeneration, were observed in 11.3% of the analyzed brains. There was no clinical suspicion of leishmaniasis in any of the studied cases. Therefore, the detection of L. infantum DNA in the brains of dogs suggests that animals with subclinical infection may play a crucial role in the spread of leishmaniasis, and infection by Leishmania spp. should be considered as a differential diagnosis for neurological disease in endemic areas for the protozoan.

Identification of new inhibitors of Plasmodium falciparum hypoxanthine–guanine–xanthine Phosphoribosyltransferase (HG(X)PRT): An outlook towards the treatment of malaria

Plasmodium, a protozoan parasite responsible for causing malaria relies on the purine salvage pathway to synthesize purine as they are incapable of synthesizing them de novo. This pathway is crucial for the survival of the parasite and hence enzymes of this pathway can serve as antimalarial drug targets. One of the enzymes of this pathway is hypoxanthine guanine (xanthine) phosphoribosyltransferase [HG(X)PRT] that serves as novel target, potentially less prone to existing resistance mechanisms seen with the use of traditional antimalarial drugs. HGXPRT inhibition disrupts the parasite's ability to synthesize nucleotides, essential for its growth and replication. In this regard, the current study was designed to identify the inhibitors of HGXPRT. For this purpose, the enzyme was produced through recombinant technology and purified with 10 mg/ L yield. Followed this, UV-based enzyme inhibition assay was optimized and >200 fully characterized compounds were evaluated for their HGXPRT inhibitory activity. Out of them fourteen compounds 1–14 showed significant to weak inhibition of HGXPRT enzyme with IC50 values in the range of 15.7 to 229.6 μM, as compared to the standard inhibitor i.e. 9-deazaguanine (IC50 = 12 ± 1.0 μM). In- silico and biophysical studies were further performed on active compounds to get structural insights into enzyme-inhibitor complex at the atomic level. Docking studies predicted that these inhibitors accommodate the purine binding site of enzyme and interacted with critical residues such as Asp148, Phe197, and Val198. Biophysical studies showed that these identified inhibitors interacted with HGXPRT enzyme in a non-ambiguous manner. Furthermore, these inhibitors were found to be non-cytotoxic against human fibroblast cell lines (BJ). Hence, this study identified 14 hits that could lead to further research towards anti-malarial drug design and development.

Toxoplasma gondii sustains survival by regulating cholesterol biosynthesis and uptake via SREBP2 activation

Toxoplasma gondii (T. gondii) is an obligate intracellular parasite that cannot biosynthesize cholesterol via the mevalonate pathway, it sources this lipid from its host. We discovered that T. gondii infection upregulated the expression of host cholesterol synthesis-related genes HMG-CoA reductase(HMGCR), squalene epoxidase (SQLE), and dehydrocholesterol reductase-7 (DHCR7), and increased the uptake pathway gene low-density lipoprotein receptor (LDLR). We found a protein, sterol regulatory element binding protein 2 (SREBP2), which is the key protein regulating the host cholesterol synthesis and uptake during T. gondii infection. T. gondii induced a dose-dependent nuclear translocation of SREBP2. Knockdown SREBP2 reduced T. gondii-induced cholesterol biosynthesis and uptake. Consequently, the parasite's ability to acquire cholesterol was significantly diminished, impairing its invasion, replication, and bradyzoites development. Interfering cholesterol metabolism using AY9944 effectively inhibited T. gondii replication. In summary, SREBP2 played an important role in T. gondii infection in vitro, serving as a potential target for regulating T. gondii-induced cholesterol metabolism, offering insights into the prevention and treatment of toxoplasmosis.

Frequency of chloroquine-resistant haplotype of Plasmodium falciparum (CVIET) in Ibadan, Southwest Nigeria 17 years post-chloroquine withdrawal

The replacement of chloroquine with artemisinin-based combination therapies (ACTs) for over a decade has had varying impacts on the ability of the malaria parasite to sustain its chloroquine resistance prowess in different malaria-endemic regions. We evaluated the frequency of Plasmodium falciparum chloroquine resistance transporter (PfCRT) mutations in Ibadan, Nigeria 17 years after the replacement of chloroquine with ACTs for malaria treatment. Fragments of PfCRT gene from genomic DNA of microscopically confirmed P. falciparum-infected patients were amplified and sequenced. There were 19% CVIET mutant and 81% CVMNK wild-type haplotypes on residues 72–76. A220S change were found in 16.7% of samples occurring concurrently with the CVIET haplotype, while a Q271E mutation occurred in a PfCRT wild-type isolate. The reduced prevalence of the PfCRT mutant alleles in this study compared to previous reports suggests a gradual disappearance of chloroquine-resistant malaria parasites following reduced drug pressure. It may also be a result of fitness demand on the parasites in attempts to evolve resistance against the current first-line regimen. However, evaluating the prevalence of other chloroquine resistance markers such as Plasmodium falciparum multidrug resistance 1 gene mutations in this population, and a more robust sample size will help to consolidate these findings.

The emerging role of Toxoplasma gondii in periodontal diseases and underlying mechanisms.

Toxoplasma gondii (T. gondii), an obligate intracellular protozoan parasite, is increasingly recognized for its role in various human diseases, including periodontal diseases. Periodontal diseases comprise a wide range of inflammatory conditions that not only affect the supporting structures of the teeth and oral health but also contribute to systemic diseases. The parasite's ability to modulate the host's immune response and induce chronic inflammation within the periodontium is a key factor in periodontal tissue damage. Through its virulence factors, T. gondii disrupts the balance of inflammatory cytokines, leading to dysregulated immune responses, and exacerbates oxidative stress in periodontal tissues. And T. gondii invasion could affect specific proteins in host cells including HSP70, BAGs, MICs, ROPs, SAGs, and GRAs leading to periodontal tissue damage. The indirect role of the host immune response to T. gondii via natural killer cells, monocytes, macrophages, neutrophils, dendritic cells, T cells, and B cells also contributes to periodontal diseases. Understanding these complex interactions of T. gondii with host cells could unravel disease mechanisms and therapeutic targets for periodontal diseases. This review delves into the pathogenic mechanisms of T. gondii in periodontal diseases, offering a detailed exploration of both direct and indirect pathways of its impact on periodontal health.

Microbial artists: the role of parasite microbiomes in explaining colour polymorphism among amphipods and potential link to host manipulation.

Parasite infections are increasingly reported to change the microbiome of the parasitised hosts, while parasites bring their own microbes to what can be a multi-dimensional interaction. For instance, a recent hypothesis suggests that the microbial communities harboured by parasites may play a role in the well-documented ability of many parasites to manipulate host phenotype, and explain why the degree to which host phenotype is altered varies among conspecific parasites. Here, we explored whether the microbiomes of both hosts and parasites are associated with variation in host manipulation by parasites. Using colour quantification methods applied to digital images, we investigated colour variation among uninfected Transorchestia serrulata amphipods, as well as amphipods infected with Plagiorhynchus allisonae acanthocephalans and with a dilepidid cestode. We then characterised the bacteriota of amphipod hosts and of their parasites, looking for correlations between host phenotype and the bacterial taxa associated with hosts and parasites. We found large variation in amphipod colours, and weak support for a direct impact of parasites on the colour of their hosts. Conversely, and most interestingly, the parasite's bacteriota was more strongly correlated with colour variation among their amphipod hosts, with potential impact of amphipod-associated bacteria as well. Some bacterial taxa found associated with amphipods and parasites may have the ability to synthesise pigments, and we propose they may interact with colour determination in the amphipods. This study provides correlational support for an association between the parasite's microbiome and the evolution of host manipulation by parasites and host-parasite interactions more generally.

Orthologs of Plasmodium ICM1 are dispensable for Ca2+ mobilization in Toxoplasma gondii.

Apicomplexan parasites mobilize ionic calcium (Ca2+) from intracellular stores to promote microneme secretion and facilitate motile processes including gliding motility, invasion, and egress. Recently, a multipass transmembrane protein, ICM1, was found to be important for calcium mobilization in Plasmodium falciparum and P. berghei. Comparative genomics and phylogenetics have revealed putative ICM orthologs in Toxoplasma gondii and other apicomplexans. T. gondii possesses two ICM-like proteins, which we have named TgICM1-L (TGGT1_305470) and TgICM2-L (TGGT1_309910). TgICM1-L and TgICM2-L localized to undefined puncta within the parasite cytosol. TgICM1-L and TgICM2-L are individually dispensable in tachyzoites, suggesting a potential compensatory relationship between the two proteins may exist. Surprisingly, mutants lacking both TgICM1-L and TgICM2-L are fully viable, exhibiting no obvious defects in growth, microneme secretion, invasion, or egress. Furthermore, loss of TgICM1-L, TgICM2-L, or both does not impair the parasite's ability to mobilize Ca2+. These findings suggest that additional proteins may participate in Ca2+ mobilization or import in Apicomplexa, reducing the dependence on ICM-like proteins in T. gondii. Collectively, these results highlight similar yet distinct mechanisms of Ca2+ mobilization between T. gondii and Plasmodium.IMPORTANCECa2+ signaling plays a crucial role in governing apicomplexan motility; yet, the mechanisms underlying Ca2+ mobilization from intracellular stores in these parasites remain unclear. In Plasmodium, the necessity of ICM1 for Ca2+ mobilization raises the question of whether this mechanism is conserved in other apicomplexans. Investigation into the orthologs of Plasmodium ICM1 in T. gondii revealed a differing requirement for ICM proteins between the two parasites. This study suggests that T. gondii employs ICM-independent mechanisms to regulate Ca2+ homeostasis and mobilization. Proteins involved in Ca2+ signaling in apicomplexans represent promising targets for therapeutic development.

Calcium-binding protein TgpCaBP regulates calcium storage of the zoonotic parasite Toxoplasma gondii.

Toxoplasma gondii, the causative parasite of toxoplasmosis, is an apicomplexan parasite that infects warm-blooded mammals. The ability of the calcium-binding proteins (CBPs) to transport large amounts of Ca2+ appears to be critical for the biological activity of T. gondii. However, the functions of some members of the CBP family have not yet been deciphered. Here, we characterized a putative CBP of T. gondii, TgpCaBP (TGME49_229480), which is composed of four EF-hand motifs with Ca2+-binding capability. TgpCaBP was localized in the cytosol and ER of T. gondii, and parasites lacking the TgpCaBP gene exhibited diminished abilities in cell invasion, intracellular growth, egress, and motility. These phenomena were due to the abnormalities in intracellular Ca2+ efflux and ER Ca2+ storage, and the reduction in motility was associated with a decrease in the discharge of secretory proteins. Therefore, we propose that TgpCaBP is a Ca2+ transporter and signaling molecule involved in Ca2+ regulation and parasitization in the hosts.IMPORTANCECa2+ signaling is essential in the development of T. gondii. In this study, we identified a calcium-binding protein in T. gondii, named TgpCaBP, which actively regulates intracellular Ca2+ levels in the parasite. Deletion of the gene coding for TgpCaBP caused serious deficits in the parasite's ability to maintain a stable intracellular calcium environment, which also impaired the secretory protein discharged from the parasite, and its capacity of gliding motility, cell invasion, intracellular growth, and egress from host cells. In summary, we have identified a novel calcium-binding protein, TgpCaBP, in the zoonotic parasite T. gondii, which is a potential therapeutic target for toxoplasmosis.

Extrinsic and Intrinsic Competition between Chouioa cunea Yang and Tetrastichus septentrionalis (Hymenoptera: Eulophidae), Two Pupal Parasitoids of the Fall Webworm, Hyphantria cunea (Lepidoptera: Erebidae).

The endoparasitoids Chouioa cunea Yang and Tetrastichus septentrionalis Yang (Hymenoptera: Eulophidae) are both gregarious pupal parasitoids of the fall webworm, Hyphantria cunea (Drury) (Lepidoptera: Erebidae). In order to analyze the competitive interactions between both parasitoids exploiting H. cunea, we assessed both extrinsic and intrinsic competition. The search time, oviposition duration, and oviposition frequency were used as evaluation criteria for extrinsic competition. The number of survival days, female ratio, and number of parasitoids emerging from the host were used as evaluation criteria for intrinsic competition. The results indicated that both parasitoid species were able to parasitize hosts that were already parasitized by competitors. The first released species consistently emerged as the superior competitor in multiparasitized hosts. Both parasitoid release orders and time intervals between oviposition affect the competition of parasitoids and the parasitic efficiency. The results emphasize the parasitic abilities of both parasitoid species and provide a basis for future research on competition mechanisms and biological control of H. cunea.

Effects of injudicious use of spirotetramat on Encarsia formosa's ability to control Bemisia tabaci

The excessive and frequent use of insecticides has led to serious problems with insecticide residues, impacting nontarget organisms such as the parasitoid Encarsia formosa. This study examined the growth, development, and enzyme activity of E. formosa exposed to spirotetramat at LC10, LC30, and LC50. The regression equation for the toxicity of spirotetramat toward E. formosa was Y = 5.25X–11.07. After exposure to spirotetramat, the survival rates of E. formosa sharply decreased, which occurred earlier than those in the control batch. Although the maximum daily parasitism quantity of E. formosa increased and the average parasitism number, enumerated from the 1st to the 5th day, was 53.97 after being exposed to spirotetramat at LC10, the life span of its F1 generation adults was only 8.47 days, which was significantly shorter than that in the control batch. After being exposed to spirotetramat at LC50, the average parasitism number of E. formosa was 63.30, and the developmental time of its F1 generation, enumerated from the 1st to the 5th day after exposure to spirotetramat, was significantly longer than that of the control batch. The activities of mixed function oxidase, acetylcholinesterase, carboxylesterase, and catalase increased significantly, and the rate of increase in enzyme activity was directly proportional to the increase in the concentration of spirotetramat. These results revealed that the parasitic ability of E. formosa decreased after exposure to spirotetramat at LC10, LC30, and LC50. This leads to a change in parasitoid control of pests, revealing the potential environmental threat of insecticide residues to nontarget organisms.

Improved Molecular Packing of Self-Assembled Monolayer Charge Injectors for Perovskite Light-Emitting Diodes.

Self-assembled monolayers (SAMs) have shown great potential as hole injection materials for perovskite light-emitting diodes due to their low parasitic absorption and ability to adjust energy level alignment. However, the head and anchoring groups on SAM molecules with significant differences in polarity can lead to the formation of micelles in the commonly used alcoholic processing solvent, inhibiting the formation of an intact SAM. In this work, the introduction of methyl groups on carbazole in the phosphonic-acid-based SAM materials is found to facilitate energy level alignment and promote the formation of compact SAMs. The alternative molecular structure also enhances the solvent resistance of poly(9-vinylcarbazole), suppressing interfacial defect densities and nonradiative recombination processes in the emissive perovskites. PeLEDs based on the methyl-containing SAMs exhibit ∼30% enhancement in efficiency. These findings contribute to a better understanding of the design of SAM materials for PeLED applications.

The multispeciesstinkbug iflavirus Halyomorpha halys virus detected in themultispeciesstinkbug egg parasitoid microwasp,Telenomus podisi(Ashmead) (Hymenoptera: Platygastridae).

Wasps are important parasitoids of stinkbugs and frequently exposed to various types of microorganisms through environmental contact and fecal-oral transmission route. Many parasitize stinkbug eggs and are commercially used in the field to control insect population. The parasitoid T. podisi is known for its high parasitism capacity and ability to target multiple species of stinkbugs. In this study we asked whether T. podisi exposed to eggs infected by a multispecies asymptomatic stinkbug virus, the Halyomorpha halys virus (HhV) would get infected. HhV is a geographically distributed multispecies iflavirus previously found to infect four stinkbug hosts, including three Brazilian species, Chinavia ubica, Euschistus heros and Diceraeus melacanthus, and T. posidi can parasitize all of them. As results, RT-PCR screening revealed positive samples for the HhV genome in two out of four tested pools of T. podisi, whereas the antigenome, indicative of replicative activity, was not detected. The wasps were raised in E. heros eggs that presented both the genome and the antigenome forms of the HhV genome. Subsequent RNA-deep sequencing of HhV positive T. podisi RNA pools yielded a complete genome of HhV with high coverage. Phylogenetic analysis positioned the isolate HhV-Tp (isolate Telenomus podisi) alongside with the stinkbug HhV. Analysis of transcriptomes from several hymenopteran species revealed HhV-Tp reads in four species. However, the transmission mechanism and the ecological significance of HhV remain elusive, warranting further studies to illuminate both the transmission process and its capacity for environmental propagation using T. podisi as a potential vector.

Immunomodulatory effects of hydatid antigens on mesenchymal stem cells: gene expression alterations and functional consequences.

Cystic echinococcosis, caused by the larval stage of Echinococcus granulosus, remains a global health challenge. Mesenchymal stem cells (MSCs) are renowned for their regenerative and immunomodulatory properties. Given the parasite's mode of establishment, we postulate that MSCs likely play a pivotal role in the interaction between the parasite and the host. This study aims to explore the response of MSCs to antigens derived from Echinococcus granulosus, the etiological agent of hydatid disease, with the hypothesis that exposure to these antigens may alter MSC function and impact the host's immune response to the parasite. MSCs were isolated from mouse bone marrow and co-cultured with ESPs, HCF, or pLL antigens. We conducted high-throughput sequencing to examine changes in the MSCs' mRNA expression profile. Additionally, cell cycle, migration, and secretory functions were assessed using various assays, including CCK8, flow cytometry, real-time PCR, Western blot, and ELISA. Our analysis revealed that hydatid antigens significantly modulate the mRNA expression of genes related to cytokine and chemokine activity, impacting MSC proliferation, migration, and cytokine secretion. Specifically, there was a downregulation of chemokines (MCP-1, CXCL1) and pro-inflammatory cytokines (IL-6, NOS2/NO), alongside an upregulation of anti-inflammatory mediators (COX2/PGE2). Furthermore, all antigens reduced MSC migration, and significant alterations in cellular metabolism-related pathways were observed. Hydatid disease antigens induce a distinct immunomodulatory response in MSCs, characterized by a shift towards an anti-inflammatory phenotype and reduced cell migration. These changes may contribute to the parasite's ability to evade host defenses and persist within the host, highlighting the complex interplay between MSCs and hydatid disease antigens. This study provides valuable insights into the pathophysiology of hydatid disease and may inform the development of novel therapeutic strategies.

Impact of Nutritional Supplements on the Fitness of the Parasitoid Binodoxys communis (Gahan).

Alterative nutritional foods consumed by adult parasitoids play an important role in their fitness and ability to control pests because of food scarcity in many crops. While adult parasitoids feed on various sugars, they vary in their nutritional value for parasitoids. We assessed the effects of seven sugars (fructose, glucose, sucrose, trehalose, maltose, melezitose, and sorbitol) on the longevity, parasitism ability, parasitism behavior, and flight ability of B. communis, an important parasitoid of cotton aphids. We found that access to glucose, sucrose, or fructose, increased B. communis adult longevity more than the other sugars offered. All sugars except trehalose increased the parasitism rate to more than 50% compared to the starved control (only provided with water). We then compared parasitoid behaviors of wasps fed glucose, sucrose, or fructose to that of the starved control (with access only to water) and found that those fed B. communis spent more time either examining or attacking aphids than parasitoids in the control group, which spent more time walking or resting. Also, consumption of glucose, sucrose, or fructose also significantly improved the flight ability (the total flight distance, flight time, and average flight speed) of B. communis.

Sexual Dimorphism in the Physiopathology and Immune Response during Acute Toxocara canis Infection.

Toxocara canis (T. canis) is a helminth parasite of zoonotic and veterinary health significance that causes the disease known as Toxocariasis. This disease has been associated with conditions of poverty, especially in tropical climate zones throughout the world. Although it rarely causes important clinical manifestations, T. canis can lead to blindness, meningoencephalitis, or other nervous manifestations in humans. Moreover, some studies show its importance in the development of tumor growth, which have been associated with the parasite's ability to modulate the host's immune response. While different studies have evaluated the immune response during this disease, currently, there are no studies where the infection is analyzed from the perspective of sexual dimorphism. To evaluate sex differences in susceptibility, we analyzed lesions and parasite loads in lung and liver at 7 days post-infection. In addition, immune cell subpopulations were analyzed in spleen, mesenteric and peripheral lymph nodes. Finally, the production of cytokines and specific antibodies were determined in the serum. Statical analyses were performed using a Two-way ANOVA and a post-hoc Bonferroni multiple comparison test. Female rats had a higher number of larvae in the liver, while male rats had them in the lungs. The percentages of immune cells were evaluated, and in most cases, no significant differences were observed. Regarding the cytokines production, infection can generate a decrease in Th1 such as IL-1β in both sexes and IL-6 only in females. In the case of Th2, IL-4 increases only in infected males and IL-5 increases in males while decreasing in females due to the effect of infection. IL-10 also decreases in both sexes as a consequence of the infection, and TGF-β only in females. Finally, the infection generates the production of antibodies against the parasite, however, their quantity is lower in females. This study demonstrates that T. canis infection is dimorphic and affects females more than males. This is due to a polarization of the inadequate immune response, which is reflected as a higher parasite load in this sex.

Integrated Transcriptome and Proteome Analysis Reveals That Cell Wall Activity Affects Phelipanche aegyptiaca Parasitism.

Phelipanche aegyptiaca can infect many crops, causing large agricultural production losses. It is important to study the parasitism mechanism of P. aegyptiaca to control its harm. In this experiment, the P. aegyptiaca HY13M and TE9M from Tacheng Prefecture and Hami City in Xinjiang, respectively, were used to analyze the parasitical mechanism of P. aegyptiaca by means of transcriptome and proteome analyses. The parasitic capacity of TE9M was significantly stronger than that of HY13M in Citrullus lanatus. The results showed that the DEGs and DEPs were prominently enriched in the cell wall metabolism pathways, including "cell wall organization or biogenesis", "cell wall organization", and "cell wall". Moreover, the functions of the pectinesterase enzyme gene (TR138070_c0_g), which is involved in the cell wall metabolism of P. aegyptiaca in its parasitism, were studied by means HIGS. The number and weight of P. aegyptiaca were significantly reduced when TR138070_c0_g1, which encodes a cell-wall-degrading protease, was silenced, indicating that it positively regulates P. aegyptiaca parasitism. Thus, these results suggest that the cell wall metabolism pathway is involved in P. aegyptiaca differentiation of the parasitic ability and that the TR138070_c0_g1 gene plays an important role in P. aegyptiaca's parasitism.

Unlocking the mystery of the feeder organelle and versatile energy metabolism in Cryptosporidium parvum

Xu and colleagues recently revealed the critical role of Cryptosporidium's feeder organelle in nutrient uptake, showcasing the parasite's ability to harness glucose and glucose-6-phosphate from host cells. This illuminates the sophisticated energy metabolism and survival strategies of the parasite, highlighting potential therapeutic targets.

Antiparasitic activity of the iron-containing milk protein lactoferrin and its potential derivatives against human intestinal and blood parasites

An iron-containing milk protein named lactoferrin (Lf) has demonstrated antiparasitic and immunomodulatory properties against a variety of human parasites. This protein has shown its capability to bind and transport iron molecules in the vicinity of the host–pathogen environment. The ability of parasites to sequester the iron molecule and to increase their pathogenicity and survival depends on the availability of iron sources. Lf protein has suggested a iron chelating effect on parasites iron and, hence, has shown its antiparasitic effect. Since the parasites have a complex life cycle and have developed drug resistance, vaccines and other treatments are a handful. Therefore, therapeutic research focusing on natural treatment regimens that target the parasite and are non-toxic to host cells is urgently needed. The antiparasitic efficacy of Lf protein has been extensively studied over the past 40 years using both in vitro and in vivo studies. This review article highlighted past important studies on Lf protein that revealed its potential antiparasitic activity against various intracellular and extracellular intestinal or blood-borne human parasites. This review article structures the role of Lf protein in its various forms, such as native, peptide, and nanoformulation, laying the groundwork for its function as an antiparasitic agent and its possible known mechanisms of action.