Toxoplasma gondii in stranded marine mammals from the North Sea and Eastern Atlantic Ocean: Findings and diagnostic difficulties

Vet Parasitol. 2016 Oct 30;230:25-32. doi: 10.1016/j.vetpar.2016.10.021. Epub 2016 Oct 24.

van de Velde N¹, Devleesschauwer B², Leopold M³, Begeman L⁴, IJsseldijk L⁵, Hiemstra S⁵, IJzer J⁵, Brownlow A⁶, Davison N⁶, Haelters J⁷, Jauniaux T⁸, Siebert U⁹, Dorny P¹⁰, De Craeye S¹¹.

Author information

Abstract

The occurrence of the zoonotic protozoan parasite Toxoplasma gondii in marine mammals remains a poorly understood phenomenon. In this study, samples from 589 marine mammal species and 34 European otters (Lutra lutra), stranded on the coasts of Scotland, Belgium, France, The Netherlands and Germany, were tested for the presence of T. gondii. Brain samples were analysed by polymerase chain reaction (PCR) for detection of parasite DNA. Blood and muscle fluid samples were tested for specific antibodies using a modified agglutination test (MAT), a commercial multi-species enzyme-linked immunosorbent assay (ELISA) and an immunofluorescence assay (IFA). Out of 193 animals tested by PCR, only two harbour porpoise (Phocoena phocoena) cerebrum samples, obtained from animals stranded on the Dutch coast, tested positive. The serological results showed a wide variation depending on the test used. Using a cut-off value of 1/40 dilution in MAT, 141 out of 292 animals (41%) were positive. Using IFA, 30 out of 244 tested samples (12%) were positive at a 1/50 dilution. The commercial ELISA yielded 7% positives with a cut-off of the sample-to-positive (S/P) ratio≥50; and 12% when the cut-off was set at S/P ratio≥20. The high number of positives in MAT may be an overestimation due to the high degree of haemolysis of the samples and/or the presence of lipids. The ELISA results could be an underestimation due to the use of a multispecies conjugate. Our results confirm the presence of T. gondii in marine mammals in The Netherlands and show exposure to the parasite in both the North Sea and the Eastern Atlantic Ocean. We also highlight the limitations of the tests used to diagnose T. gondii in stranded marine mammals.

Copyright © 2016 Elsevier B.V. All rights reserved.

KEYWORDS:

ELISA; IFA; MAT; Marine mammals; PCR; Seroprevalence; Toxoplasma gondii

PMID:

 

27884438

 

DOI:

 

10.1016/j.vetpar.2016.10.021

Relationship between Toxoplasma gondii Seropositivity and Acoustic Startle Response in an Inner-City Population

Brain Behav Immun. 2016 Nov 21. pii: S0889-1591(16)30523-2. doi: 10.1016/j.bbi.2016.11.021. [Epub ahead of print]

Massa NM¹, Duncan E², Jovanovic T³, Kerley K³, Weng L⁴, Gensler L³, Lee SS³, Norrholm S², Powers A³, Almli LM³, Gillespie CF³, Ressler K⁵, Pearce BD⁶.

Author information

Abstract

Toxoplasma gondii (TOXO) is a neuroinvasive protozoan parasite that induces the formation of persistent cysts in mammalian brains. It infects approximately 1.1 million people in the United States annually. Latent TOXO infection is implicated in the etiology of psychiatric disorders, especially schizophrenia (Scz), and has been correlated with modestly impaired cognition. The acoustic startle response (ASR) is a reflex seen in all mammals. It is mediated by a simple subcortical circuit, and provides an indicator of neural function. We previously reported the association of TOXO with slowed acoustic startle latency, an index of neural processing speed, in a sample of schizophrenia and healthy control subjects. The alterations in neurobiology with TOXO latent infection may not be specific to schizophrenia. Therefore we examined TOXO in relation to acoustic startle in an urban, predominately African American, population with mixed psychiatric diagnoses, and healthy controls. Physiological and diagnostic data along with blood samples were collected from 364 outpatients treated at an inner-city hospital. TOXO status was determined with an ELISA assay for TOXO-specific IgG. A discrete titer was calculated based on standard cut-points as an indicator of seropositivity, and the TOXO-specific IgG concentration served as serointensity. A series of linear regression models were used to assess the association of TOXO seropositivity and serointensity with ASR magnitude and latency in models adjusting for demographics and psychiatric diagnoses (PTSD, major depression, schizophrenia, psychosis, substance abuse). ASR magnitude was 11.5% higher in TOXO seropositive subjects compared to seronegative individuals (p=0.01). This effect was more pronounced in models with TOXO serointensity that adjusted for sociodemographic covariates (F=7.41, p=.0068; F=10.05, p=0.0017), and remained significant when psychiatric diagnoses were stepped into the models. TOXO showed no association with startle latency (t=0.49, p=0.63) in an unadjusted model, nor was TOXO associated with latency in models that included demographic factors. After stepping in individual psychiatric disorders, we found a significant association of latency with a diagnosis of PTSD (F=5.15, p=0.024), but no other psychiatric diagnoses, such that subjects with PTSD had longer startle latency. The mechanism by which TOXO infection is associated with high startle magnitude is not known, but possible mechanisms include TOXO cyst burden in the brain, parasite recrudescence, or molecular mimicry of a host epitope by TOXO. Future studies will focus on the neurobiology underlying the effects of latent TOXO infection as a potential inroad to the development of novel treatment targets for psychiatric disease.

Copyright © 2016. Published by Elsevier Inc.

KEYWORDS:

Acoustic Startle Response; Infection; Mental Health; PTSD; Schizophrenia; Substance Use Disorder; Toxoplasma gondii

PMID:

 

27884623

 

DOI:

 

10.1016/j.bbi.2016.11.021

Activity of Fluorine-Containing Analogues of WC-9 and Structurally Related Analogues against Two Intracellular Parasites: Trypanosoma cruzi and Toxoplasma gondii

ChemMedChem. 2016 Nov 25. doi: 10.1002/cmdc.201600505. [Epub ahead of print]

Chao MN¹, Li C², Storey M², Falcone BN¹, Szajnman SH¹, Bonesi SM³, Docampo R², Moreno SN², Rodriguez JB¹.

Author information

Abstract

Two obligate intracellular parasites, Trypanosoma cruzi, the agent of Chagas disease, and Toxoplasma gondii, an agent of toxoplasmosis, upregulate the mevalonate pathway of their host cells upon infection, which suggests that this host pathway could be a potential drug target. In this work, a number of compounds structurally related to WC-9 (4-phenoxyphenoxyethyl thiocyanate), a known squalene synthase inhibitor, were designed, synthesized, and evaluated for their effect on T. cruzi and T. gondii growth in tissue culture cells. Two fluorine-containing derivatives, the 3-(3-fluorophenoxy)- and 3-(4-fluorophenoxy)phenoxyethyl thiocyanates, exhibited half-maximal effective concentration (EC₅₀ ) values of 1.6 and 4.9 μm, respectively, against tachyzoites of T. gondii, whereas they showed similar potency to WC-9 against intracellular T. cruzi (EC₅₀ values of 5.4 and 5.7 μm, respectively). In addition, 2-[3- (phenoxy)phenoxyethylthio]ethyl-1,1-bisphosphonate, which is a hybrid inhibitor containing 3-phenoxyphenoxy and bisphosphonate groups, has activity against T. gondii proliferation at sub-micromolar levels (EC₅₀ =0.7 μm), which suggests a combined inhibitory effect of the two functional groups.

© 2016 Wiley-VCH Verlag GmbH & Co. KGaA, Weinheim.

KEYWORDS:

antiprotozoal agents; drug discovery; enzymes; fluorine; inhibitors

PMID:

 

27886451

 

DOI:

 

10.1002/cmdc.201600505

Toxoplasma gondii immune mapped protein 1 is anchored to the inner leaflet of the plasma membrane and adopts a novel protein fold

Biochim Biophys Acta. 2016 Nov 22. pii: S1570-9639(16)30247-3. doi: 10.1016/j.bbapap.2016.11.010. [Epub ahead of print]

Jia Y¹, Benjamin S², Liu Q³, Xu Y², Dogga SK¹, Liu J³, Matthews S⁴, Soldati-Favre D⁵.

Author information

Abstract

The immune mapped protein 1 (IMP1) was first identified as a protective antigen in Eimeria maxima and described as vaccine candidate and invasion factor in Toxoplasma gondii. We show here that TgIMP1 localizes to the inner leaflet of plasma membrane (PM) via dual acylation. Mutations either in the N-terminal myristoylation or palmitoylation sites (G2 and C5) cause relocalization of TgIMP1 to the cytosol. The first 11 amino acids are sufficient for PM targeting and the presence of lysine (K7) is critical. Disruption of TgIMP1 gene by double homologous recombination revealed no invasion defect or any measurable alteration in the lytic cycle of tachyzoites. Following immunization with TgIMP1 DNA vaccine, mice challenged with either wild type or IMP1-ko parasites showed no significant difference in protection. The sequence analysis identified a structured C-terminal domain that is present in a broader family of IMP1-like proteins conserved across the members of Apicomplexa. We present the solution structure of this domain determined from NMR data and describe a new protein fold not seen before.

Copyright © 2016. Published by Elsevier B.V.

KEYWORDS:

Acylation; Invasion; NMR; Protein structure; Toxoplasma gondii; Vaccine

PMID:

 

27888074

 

DOI:

 

10.1016/j.bbapap.2016.11.010

Is there any association between Toxoplasma gondii infection and bipolar disorder? A systematic review and meta-analysis

J Affect Disord. 2016 Nov 17;209:59-65. doi: 10.1016/j.jad.2016.11.016. [Epub ahead of print]

de Barros JL¹, Barbosa IG², Salem H³, Rocha NP⁴, Kummer A², Okusaga OO³, Soares JC³, Teixeira AL⁵.

Author information

Abstract

BACKGROUND:

The relationship between Toxoplasma gondii infection and the development of bipolar disorder (BD) has long been investigated, yet to date it is still poorly understood and documented. The aim of this review is to derive a summary estimate of the strength of the association between infection with T. gondii and BD from the available published studies.

METHODS:

A systematic review was performed using PubMed, LILACS, PsycINFO, and Embase databases. Studies which included a proportion of seropositive BD patients and controls were further examined in a meta-analysis.

RESULTS:

One hundred eighteen citations were initially retrieved. Thirteen studies were included in our systematic review. Eight out of these thirteen studies were included in our meta-analysis. Statistical analyses showed that T. gondii infection is associated with with BD (OR=1.26).

LIMITATIONS:

Small sample size was the major limitation among the studies that carried out serological analyses. In addition, the available studies did not have enough information on disease status/severity or type of bipolar disorder. Also, it was not possible to analyze pregnancy status or perinatal infection. Future studies addressing the aforementioned topics are clearly needed.

CONCLUSIONS:

Despite heterogeneous results, patients with BD are more likely to be infected by T. gondii than controls. Early T. gondii infection might predispose the development of BD. T.gondii infection is becoming clinically relevant in psychiatric disorders and future mechanistic studies are required to elucidate the underlying pathophysiological mechanisms.

Copyright © 2016 Elsevier B.V. All rights reserved.

KEYWORDS:

Bipolar disorder; Immunology; Inflammation; Toxoplasma gondii

PMID:

 

27889597

 

DOI:

 

10.1016/j.jad.2016.11.016

K63-Linked Ubiquitination Targets Toxoplasma gondii for Endo-lysosomal Destruction in IFNγ-Stimulated Human Cells

PLoS Pathog. 2016 Nov 22;12(11):e1006027. doi: 10.1371/journal.ppat.1006027. eCollection 2016.

Clough B1, Wright JD1, Pereira PM2, Hirst EM1, Johnston AC1, Henriques R2, Frickel EM1.

Author information

Abstract

Toxoplasma gondii is the most common protozoan parasitic infection in man. Gamma interferon (IFNγ) activates haematopoietic and non-haematopoietic cells to kill the parasite and mediate host resistance. IFNγ-driven host resistance pathways and parasitic virulence factors are well described in mice, but a detailed understanding of pathways that kill Toxoplasma in human cells is lacking. Here we show, that contrary to the widely held belief that the Toxoplasma vacuole is non-fusogenic, in an immune-stimulated environment, the vacuole of type II Toxoplasma in human cells is able to fuse with the host endo-lysosomal machinery leading to parasite death by acidification. Similar to murine cells, we find that type II, but not type I Toxoplasma vacuoles are targeted by K63-linked ubiquitin in an IFNγ-dependent manner in non-haematopoetic primary-like human endothelial cells. Host defence proteins p62 and NDP52 are subsequently recruited to the type II vacuole in distinct, overlapping microdomains with a loss of IFNγ-dependent restriction in p62 knocked down cells. Autophagy proteins Atg16L1, GABARAP and LC3B are recruited to 10% of parasite vacuoles and show no parasite strain preference, which is consistent with inhibition and enhancement of autophagy showing no effect on parasite replication. We demonstrate that this differs from HeLa human epithelial cells, where type II Toxoplasma are restricted by non-canonical autophagy leading to growth stunting that is independent of lysosomal acidification. In contrast to mouse cells, human vacuoles do not break. In HUVEC, the ubiquitinated vacuoles are targeted for destruction in acidified LAMP1-positive endo-lysosomal compartments. Consequently, parasite death can be prevented by inhibiting host ubiquitination and endosomal acidification. Thus, K63-linked ubiquitin recognition leading to vacuolar endo-lysosomal fusion and acidification is an important, novel virulence-driven Toxoplasma human host defence pathway.

PMID:

 

27875583

 

DOI:

 

10.1371/journal.ppat.1006027

Ocular toxoplasmosis: susceptibility in respect to the genes encoding the KIR receptors and their HLA class I ligands

Sci Rep. 2016 Nov 9;6:36632. doi: 10.1038/srep36632.

Ayo CM^1,2, Frederico FB^2,3, Siqueira RC¹, Brandão de Mattos CC^1,2, Previato M^1,2, Barbosa AP³, Murata FH^1,2, Silveira-Carvalho AP¹, de Mattos LC^1,2.

The objective of this study was to investigate the influence of the genes encoding the KIR receptors and their HLA ligands in the susceptibility of ocular toxoplasmosis. A total of 297 patients serologically-diagnosed with toxoplasmosis were selected and stratified according to the presence (n = 148) or absence (n = 149) of ocular scars/lesions due to toxoplasmosis. The group of patients with scars/lesions was further subdivided into two groups according to the type of ocular manifestation observed: primary (n = 120) or recurrent (n = 28). Genotyping was performed by PCR-SSOP. Statistical analyses were conducted using the Chi-square test, and odds ratio with a 95% confidence interval was also calculated to evaluate the risk association. The activating KIR3DS1 gene was associated with increased susceptibility for ocular toxoplasmosis. The activating KIR together with their HLA ligands (KIR3DS1-Bw4-80Ile and KIR2DS1⁺/C2⁺⁺ KIR3DS1⁺/Bw4-80Ile⁺) were associated with increased susceptibility for ocular toxoplasmosis and its clinical manifestations. KIR-HLA inhibitory pairs -KIR2DL3/2DL3-C1/C1 and KIR2DL3/2DL3-C1- were associated with decreased susceptibility for ocular toxoplasmosis and its clinical forms, while the KIR3DS1^-/KIR3DL1⁺/Bw4-80Ile⁺ combination was associated as a protective factor against the development of ocular toxoplasmosis and, in particular, against recurrent manifestations. Our data demonstrate that activating and inhibitory KIR genes may influence the development of ocular toxoplasmosis.

PMID:

27827450

PMCID:

PMC5101474

DOI:

10.1038/srep36632

Membrane skeletal association and post-translational allosteric regulation of Toxoplasma gondii GAPDH1

Mol Microbiol. 2016 Nov 17. doi: 10.1111/mmi.13577. [Epub ahead of print]

Dubey R¹, Staker BL^2,3, Foe IT⁴, Bogyo M⁴, Myler PJ^2,3,5, Ngô HM^6,7, Gubbels MJ¹.

When Toxoplasma gondii egresses from the host cell, glyceraldehyde-3-phosphate dehydrogenase 1 (GAPDH1), which is primary a glycolysis enzyme but actually a quintessential multifunctional protein, translocates to the unique cortical membrane skeleton. Here we report the 2.25Å resolution crystal structure of the GAPDH1 holoenzyme in a quaternary complex providing the basis for the molecular dissection of GAPDH1 structure-function relationships Knockdown of GAPDH1 expression and catalytic site disruption validate the essentiality of GAPDH1 in intracellular replication but we confirmed that glycolysis is not strictly essential. We identify, for the first time, S-loop phosphorylation as a novel, critical regulator of enzymatic activity that is consistent with the notion that the S-loop is critical for cofactor binding, allosteric activation and oligomerization. We show that neither enzymatic activity nor phosphorylation state correlate with the ability to translocate to the cortex. However, we demonstrate that association of GAPDH1 with the cortex is mediated by the N-terminus, likely palmitoylation. Overall, glycolysis and cortical translocation are functionally decoupled by post-translational modifications. This article is protected by copyright. All rights reserved.

© 2016 John Wiley & Sons Ltd.

PMID:

27859784

DOI:

10.1111/mmi.13577

[PubMed - as supplied by publisher]

Systemic toxoplasma infection triggers a long-term defect in the generation and function of naive T lymphocytes

J Exp Med. 2016 Nov 14. pii: jem.20151636. [Epub ahead of print]

Kugler DG¹, Flomerfelt FA², Costa DL¹, Laky K³, Kamenyeva O⁴, Mittelstadt PR⁵, Gress RE², Rosshart SP⁶, Rehermann B⁶, Ashwell JD⁵, Sher A⁷, Jankovic D⁷.

Because antigen-stimulated naive T cells either die as effectors or enter the activated/memory pool, continuous egress of new T lymphocytes from thymus is essential for maintenance of peripheral immune homeostasis. Unexpectedly, we found that systemic infection with the protozoan Toxoplasma gondii triggers not only a transient increase in activated CD4⁺ Th1 cells but also a persistent decrease in the size of the naive CD4⁺ T lymphocyte pool. This immune defect is associated with decreased thymic output and parasite-induced destruction of the thymic epithelium, as well as disruption of the overall architecture of that primary lymphoid organ. Importantly, the resulting quantitative and qualitative deficiency in naive CD4⁺ T cells leads to an immunocompromised state that both promotes chronic toxoplasma infection and leads to decreased resistance to challenge with an unrelated pathogen. These findings reveal that systemic infectious agents, such as T. gondii, can induce long-term immune alterations associated with impaired thymic function. When accumulated during the lifetime of the host, such events, even when occurring at low magnitude, could be a contributing factor in immunological senescence.

PMID:

27849554

DOI:

10.1084/jem.20151636

[PubMed - as supplied by publisher]

STAT1 Signaling in Astrocytes Is Essential for Control of Infection in the Central Nervous System

MBio. 2016 Nov 8;7(6). pii: e01881-16. doi: 10.1128/mBio.01881-16.

Hidano S^1,2, Randall LM³, Dawson L¹, Dietrich HK⁴, Konradt C¹, Klover PJ⁵, John B¹, Harris TH⁶, Fang Q¹, Turek B¹, Kobayashi T², Hennighausen L⁵, Beiting DP¹, Koshy AA⁴, Hunter CA⁷.

The local production of gamma interferon (IFN-γ) is important to control Toxoplasma gondii in the brain, but the basis for these protective effects is not fully understood. The studies presented here reveal that the ability of IFN-γ to inhibit parasite replication in astrocytes in vitro is dependent on signal transducer and activator of transcription 1 (STAT1) and that mice that specifically lack STAT1 in astrocytes are unable to limit parasite replication in the central nervous system (CNS). This susceptibility is associated with a loss of antimicrobial pathways and increased cyst formation in astrocytes. These results identify a critical role for astrocytes in limiting the replication of an important opportunistic pathogen.

IMPORTANCE:

Astrocytes are the most numerous cell type in the brain, and they are activated in response to many types of neuroinflammation, but their function in the control of CNS-specific infection is unclear. The parasite Toxoplasma gondii is one of the few clinically relevant microorganisms that naturally infects astrocytes, and the studies presented here establish that the ability of astrocytes to inhibit parasite replication is essential for the local control of this opportunistic pathogen. Together, these studies establish a key role for astrocytes as effector cells and in the coordination of many aspects of the protective immune response that operates in the brain.

Copyright © 2016 Hidano et al.

PMID:

27834206

PMCID:

PMC5101356

DOI:

10.1128/mBio.01881-16

PKA and Apicomplexan Parasite Diseases

Horm Metab Res. 2016 Nov 11. [Epub ahead of print]

Haidar M¹, Ramdani G¹, Kennedy EJ², Langsley G¹.

The cAMP-dependent protein kinase PKA is a well-characterized member of the serine-threonine protein AGC kinase family and is the effector kinase of cAMP signaling. As such, PKA is involved in the control of a wide variety of cellular processes including metabolism, cell growth, gene expression and apoptosis. cAMP-dependent PKA signaling pathways play important roles during infection and virulence of various pathogens. Since fluxes in cAMP are involved in multiple intracellular functions, a variety of different pathological infectious processes can be affected by PKA signaling pathways. Here, we highlight some features of cAMP-PKA signaling that are relevant to Plasmodium falciparum-infection of erythrocytes and present an update on AKAP targeting of PKA in PGE2 signaling via EP4 in Theileria annulata-infection of leukocytes and discuss cAMP-PKA signling in Toxoplasma.

© Georg Thieme Verlag KG Stuttgart · New York.

PMID:

27835919

DOI:

10.1055/s-0042-118459

[PubMed - as supplied by publisher]

Genetic impairment of parasite myosin motors uncovers the contribution of host cell membrane dynamics to Toxoplasma invasion forces

BMC Biol. 2016 Nov 9;14(1):97.

Bichet M^1,2,3,4, Touquet B^1,2,3, Gonzalez V⁴, Florent I⁵, Meissner M⁶, Tardieux I^7,8,9,10.

BACKGROUND:

The several-micrometer-sized Toxoplasma gondii protozoan parasite invades virtually any type of nucleated cell from a warm-blooded animal within seconds. Toxoplasma initiates the formation of a tight ring-like junction bridging its apical pole with the host cell membrane. The parasite then actively moves through the junction into a host cell plasma membrane invagination that delineates a nascent vacuole. Recent high resolution imaging and kinematics analysis showed that the host cell cortical actin dynamics occurs at the site of entry while gene silencing approaches allowed motor-deficient parasites to be generated, and suggested that the host cell could contribute energetically to invasion. In this study we further investigate this possibility by analyzing the behavior of parasites genetically impaired in different motor components, and discuss how the uncovered mechanisms illuminate our current understanding of the invasion process by motor-competent parasites.

RESULTS:

By simultaneously tracking host cell membrane and cortex dynamics at the site of interaction with myosin A-deficient Toxoplasma, the junction assembly step could be decoupled from the engagement of the Toxoplasma invasive force. Kinematics combined with functional analysis revealed that myosin A-deficient Toxoplasma had a distinct host cell-dependent mode of entry when compared to wild-type or myosin B/C-deficient Toxoplasma. Following the junction assembly step, the host cell formed actin-driven membrane protrusions that surrounded the myosin A-deficient mutant and drove it through the junction into a typical vacuole. However, this parasite-entry mode appeared suboptimal, with about 40 % abortive events for which the host cell membrane expansions failed to cover the parasite body and instead could apply deleterious compressive forces on the apical pole of the zoite.

CONCLUSIONS:

This study not only clarifies the key contribution of T. gondii tachyzoite myosin A to the invasive force, but it also highlights a new mode of entry for intracellular microbes that shares early features of macropinocytosis. Given the harmful potential of the host cell compressive forces, we propose to consider host cell invasion by zoites as a balanced combination between host cell membrane dynamics and the Toxoplasma motor function. In this light, evolutionary shaping of myosin A with fast motor activity could have contributed to optimize the invasive potential of Toxoplasma tachyzoites and thereby their fitness.

KEYWORDS:

Cell invasion; Cortical actin dynamics; Forces; Macropinocytosis; Membrane dynamics; Myosins; Protozoan parasite; Toxoplasma

PMID:

27829452

DOI:

10.1186/s12915-016-0316-8

Sex Steroids Mediate Bidirectional Interactions Between Hosts and Microbes

Horm Behav. 2016 Nov 2. pii: S0018-506X(16)30391-9. doi: 10.1016/j.yhbeh.2016.10.016. [Epub ahead of print]

Steeg LG1, Klein SL2.

Author information

Abstract

The outcome of microbial infections in mammals, including humans, is affected by the age, sex, and reproductive status of the host suggesting a role for sex steroid hormones. Testosterone, estradiol, and progesterone, signaling through their respective steroid receptors, affect the functioning of immune cells to cause differential susceptibility to parasitic, bacterial, and viral infections. Microbes, including fungi, bacteria, parasites, and viruses, can also use sex steroid hormones and manipulate sex steroid receptor signaling mechanisms to increase their own survival and replication rate. The multifaceted use of sex steroid hormones by both microbes and hosts during infection forms the basis of this review. In the arms race between microbes and hosts, both hosts and microbes have evolved to utilize sex steroid hormone signaling mechanisms for survival.

Copyright © 2016. Published by Elsevier Inc.

KEYWORDS: 

estrogen; influenza; malaria; parasites; progesterone; testosterone; toxoplasma

PMID:

 

27816626

 

DOI:

 

10.1016/j.yhbeh.2016.10.016

[PubMed - as supplied by publisher]

Monitoring of dynamin during the Toxoplasma gondii cell cycle

Pathog Dis. 2016 Nov 2. pii: ftw108. [Epub ahead of print]

Caldas LA1, Soares LL2,3, Seabra S4, Attias M5, de Souza W.

Author information

Abstract

The obligate intracellular protozoan parasite Toxoplasma gondii actively invades virtually all warm-blooded nucleated cells. This process results in a non-fusogenic vacuole, inside which the parasites replicate continuously until egress signaling is triggered. In this work, we investigated the role of the large GTPase dynamin in the interaction of T. gondii with the host cell by using laser and electron microscopy during three key stages: invasion, development and egress. The detection of dynamin during invasion indicates the occurrence of endocytosis, while T. gondii egress appeared to be independent of dynamin participation. However, the presence of dynamin during T. gondii development suggests that this molecule plays undescribed roles in the tachyzoite's cell cycle.

© FEMS 2016. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

PMID:

 

27811048

 

DOI:

 

10.1093/femspd/ftw108

[PubMed - as supplied by publisher]