scholarly journals Defining the Location of T-bet-expressing Myeloid Cells During Acute Intestinal Toxoplasma gondii Infection

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Melody Wickstrom ◽  
Madison Schanz ◽  
Kimberly Larson ◽  
Américo H. López-Yglesias
Keyword(s):  
Toxoplasma Gondii ◽  
Treatment Options ◽  
Foodborne Pathogen ◽  
Myeloid Cells ◽  
Myeloid Cell ◽  
Protozoan Parasite ◽  
The United States ◽  
Parasite Infection ◽  
Toxoplasma Gondii Infection ◽  
Deficient Mice

Background/Objective: The protozoan parasite Toxoplasma gondii is the second leading cause of foodborne pathogen-related deaths in the United States. The transcription factor T-bet is indispensable for host immunity against T. gondii. The absence of T-bet results in rapid susceptibility during parasite infection. T-bet has been considered essential for T-cell-derived IFN-g during T. gondii infection; yet, recent research has shown that T-bet is not required for lymphocyte-derived IFN-g responses. Our preliminary research shows that T-bet-deficient mice succumb to parasite infection significantly quicker than mice lacking lymphocytes. This has led to our hypothesis that T-bet-dependent myeloid cells are critical for host resistance during acute intestinal T. gondii infection. The objective of this project was to define the location of the T-bet-expressing myeloid cells in the medial small intestines (MSI) of naïve and infected mice during acute mucosal parasite infection. Methods: We used immunofluorescence microscopy to determine the location of T-bet-expressing myeloid cells in the MSI of naïve and T. gondii infected mice. Mice were orally infected with 40 cysts of the ME49 strain of T. gondii. On days 0 and 5, one-inch MSI segments were harvested, fixed with 4% paraformaldehyde for at least one hour, and then frozen in OCT compound. Tissues were then cut into 8mm sections and placed onto slides for staining. Sections were stained for nuclei, CD11c, T-bet, and T. gondii. Results: Our results revealed T-bet-expressing CD11c+ cells in both the MSI and spleen on days 0 and 5 of T. gondii infection. Summary: These data indicate that T-bet-expressing myeloid cells are present in the MSI during T. gondii infection. Defining the position of these cells will allow us to determine T-bet’s role in mediating myeloid cell-dependent T. gondii clearance. Due to the limited treatment options for patients suffering from toxoplasmosis it is critical to define new mechanisms for eliminating T. gondii.

scholarly journals Potential linkage between Toxoplasma gondii Infection and physical education scores of College Students

2020 ◽  
Author(s):  
Zhijin Sheng ◽  
Yu Jin ◽  
Yinan Du ◽  
Xinlei Yan ◽  
Yong Yao
Keyword(s):  
College Students ◽  
Physical Education ◽  
Toxoplasma Gondii ◽  
Protozoan Parasite ◽  
Anhui Province ◽  
Behavioral Changes ◽  
Enzyme Linked Immunosorbent Assay ◽  
Serum Samples ◽  
School Students ◽  
Toxoplasma Gondii Infection

ABSTRACTObjectiveToxoplasma gondii is a worldwide protozoan parasite that could infect virtually all warm-blooded animals, including humans. Our study aimed to investigate the prevalence of T. gondii infection in college students at Anhui province, China. Moreover, growing studies demonstrated the association between T. gondii infection and host behavioral changes. We also studied the linkage between T. gondii and scores of college students.Methods2704 serum samples of medical school students attending physical education lessons were collected from September 2017 to September 2019 and evaluated for T. gondii IgG antibodies using an enzyme-linked immunosorbent assay (ELISA). We also analysed PE scores of T. gondii infected students and T. gondii uninfected students.ResultsThe overall seroprevalence of T. gondii was 11.5%. The main risk factors related to T. gondii infections were cat in the household and gardening or agriculture activity. Furthermore, in basketball group and football group, scores of T. gondii seropositive students were significantly higher than that of seronegative students, while in other sports there is no difference between scores of T. gondii infected students and T. gondii uninfected students.ConclusionThis is the first report of T. gondii seroprevalence in college students in Anhui province, China.

scholarly journals Complete Protection against Lethal Toxoplasma gondii Infection in Mice Immunized with a Plasmid Encoding theSAG1 Gene

1999 ◽  
Vol 67 (12) ◽  
pp. 6358-6363 ◽  
Author(s):  
Henrik Vedel Nielsen ◽  
Sanne Lise Lauemøller ◽  
Lone Christiansen ◽  
Søren Buus ◽  
Anders Fomsgaard ◽  
...  
Keyword(s):  
T Cells ◽  
Toxoplasma Gondii ◽  
Cytotoxic T Lymphocyte ◽  
Protozoan Parasite ◽  
Complete Protection ◽  
Effective Protection ◽  
Partial Protection ◽  
Empty Plasmid ◽  
Toxoplasma Gondii Infection ◽  
Best Fit

ABSTRACT Infection with the protozoan parasite Toxoplasma gondiiis transmitted to humans from infected animals by tissue cysts and oocysts excreted by cats. Immunization with inactivated parasites or recombinant proteins has at best shown partial protection. We constructed a plasmid expressing the SAG1 surface antigen of T. gondii, p1tPASAG1, and showed that animals immunized with the plasmid produce anti-SAG1 antibodies which recognize the native SAG1. Mice immunized with p1tPASAG1 showed 80 to 100% protection against challenge with the non-cyst-producing, virulent RH isolate, compared to an 80% mortality in mice immunized with empty plasmid, which is the greatest efficacy of any vaccine against T. gondii produced so far. The SAG1 molecule was analyzed for potential cytotoxic T-lymphocyte (CTL) epitopes, and four peptides with the best fit were synthesized. The ability of the peptides to stimulate gamma interferon production by CD8+ T cells from p1tPASAG1-immunized mice was tested in an ELISPOT assay, and one new CTL epitope was identified. Adoptive transfer of CD8+ T cells from p1tPASAG1-immunized to naı̈ve mice showed partial protection. In conclusion, DNA vaccination with p1tPASAG1 gave effective protection in mice againstT. gondii infection and the protection could be adoptively transferred by purified CD8+ T cells.

Toxoplasmosis Related Uveitis: Clinic, Diagnosis, and Treatment

2019 ◽  
pp. 237-243
Keyword(s):  
Toxoplasma Gondii ◽  
Treatment Options ◽  
Protozoan Parasite ◽  
Posterior Uveitis ◽  
Ocular Toxoplasmosis ◽  
Diagnosis And Treatment ◽  
Frequent Form

Ocular toxoplasmosis (OT) is considered the most frequent form of infectious posterior uveitis and is caused by the protozoan parasite Toxoplasma gondii. Despite large advances in the field of OT, large gaps still exist in our knowledge concerning the epidemiology and pathophysiology of this potentially blinding infectious old disease. In this review, we aimed to investigate the current clinical understanding of OT, diagnosis treatment options.

scholarly journals Seroprevalence and associated risk factors of Toxoplasma gondii infection among pregnant mother in Makassar, Indonesia

PLoS ONE ◽  
2021 ◽  
Vol 16 (6) ◽  
pp. e0245572
Author(s):  
Nurul Fadilah Ali Polanunu ◽  
Sitti Wahyuni ◽  
Firdaus Hamid
Keyword(s):  
Toxoplasma Gondii ◽  
Pregnant Women ◽  
Protozoan Parasite ◽  
Cross Sectional Study ◽  
Igg Antibody ◽  
Cross Sectional ◽  
Antibody Positivity ◽  
Toxoplasma Gondii Infection ◽  
Associated Risk Factors ◽  
Pregnant Mothers

The protozoan parasite, Toxoplasma gondii is estimated to infect one-third of the world’s population. Infection in pregnant women can cause severe conditions for their babies. Until now, there is no data regarding Toxoplasma infection from Makassar pregnant mothers. This study aims to obtain information on Toxoplasma specific antibodies and to measure the risk factor associate with parasite infection. This cross-sectional study conducted in 9 of 47 primary health centres (Puskesmas) in Makassar. Blood samples and questionnaires were collected from 184 pregnant women aged 15–42 years old from September to October 2020. ELISA technique was used to examine the IgG and IgM antibodies. Univariable and multivariable analyses were carried out to measure factors that independently associate with Toxoplasma antibody positivity. Our result showed the range of Toxoplasma IgM and IgG are 0.06–1.01 and 0.09–3.01, respectively. While no one of our participants has an acute Toxoplasma gondii infection (IgM positive), we found 32,6% pregnant mothers are exposed to parasite (positive IgG). Contact with cats [OR(95%CI): 10.45(3.77–28.99)], consume chicken satay [OR(95%CI): 9.72(3.71–25.48)] and consume un-boiled water/ filtered water [OR(95%CI): 5.98(1.77–20.23)] are independently associate with positive Toxoplasma IgG antibody. Based on the result, we conclude that pregnant women in Makassar are exposed to T. gondii and the oocyst and tissue cyst of parasite contaminates food and water in Makassar.

scholarly journals Presence of Toxoplasma gondii tissue cysts in human semen

2021 ◽  
Author(s):  
Wen Han Tong ◽  
Jana Hlaváčová ◽  
Samira Abdulai-Saiku ◽  
Šárka Kaňková ◽  
Jaroslav Flegr ◽  
...  
Keyword(s):  
Toxoplasma Gondii ◽  
Sexual Transmission ◽  
Congenital Toxoplasmosis ◽  
Protozoan Parasite ◽  
Specific Gene ◽  
Human Populations ◽  
Human Semen ◽  
Latently Infected ◽  
Clinically Significant ◽  
Toxoplasma Gondii Infection

Toxoplasma gondii is a widely prevalent protozoan parasite in human populations. This parasite is thought to be primarily transmitted through undercooked meat and contamination by cat feces. Here, we demonstrate that Toxoplasma gondii cysts can be found within human semen, thus suggesting a potential for sexual transmission. We visualized Toxoplasma gondii cysts in ejaculates of immune-competent and latently infected human volunteers. We confirmed the encystment by probing transcription of a bradyzoite-specific gene in these structures. These observations extend previous observations of the parasite in semen of several non-human host species, including rats, dogs, and sheep. Toxoplasma gondii infection is a clinically significant infection, in view of its high prevalence, its purported role in neuropsychiatric disorders such as schizophrenia, as well as in the more serious form of congenital toxoplasmosis. Our demonstration of intact Toxoplasma gondii cysts in the ejaculate supports the possibility of sexual transmission of the parasite and provides an impetus for further investigations.

scholarly journals Investigation of Toxoplasma gondii Infection in Aborted Fetuses of Sheep Using PCR: A Study in North Khorasan Province, Iran

2020 ◽  
Vol 2020 ◽  
pp. 1-5
Author(s):  
Mitra Salehi ◽  
Hosein Nezami ◽  
Hamid Reza Niazkar
Keyword(s):  
Toxoplasma Gondii ◽  
Gestational Age ◽  
Protozoan Parasite ◽  
Abortion Rate ◽  
Obligate Intracellular ◽  
Significant Difference ◽  
Pcr Method ◽  
Toxoplasma Gondii Infection ◽  
Intracellular Protozoan Parasite

Toxoplasma gondii is a zoonotic obligate intracellular protozoan parasite that infects warm-blooded animals as well as humans worldwide. The purpose of this study was to delineate the prevalence of Toxoplasma infection in aborted fetuses of sheep in North Khorasan province, Iran. Three hundred and ninety-nine samples of the liver (133 samples), placenta (133 samples), and brain (133 samples) from 133 aborted fetuses of sheep were collected from 2015 to 2017. The ages of aborted fetuses were higher than 120 days’ gestational age in this study. According to the samples, sixteen out of 133 aborted fetuses of sheep were infected with T. gondii. Toxoplasma DNA was found in the placenta (68.75%) and liver (31.25%) samples of infected fetuses using the PCR method. The highest and lowest rates of Toxoplasma infection were observed during 2016 and 2017, respectively. Shirvan and Faruj provinces were recognized as the two most infected districts among others. There was a significant difference between the year and abortion rate in sheep due to infection by the Toxoplasma parasite (P<0.05). Furthermore, no significant difference between the prevalence of T. gondii infection and aborted fetuses was seen (P>0.05) in different areas. According to the present study, T. gondii infection can be one of the causes of fetus abortion of sheep in North Khorasan province, Iran.

Vitamin A deficiency in mice causes a systemic expansion of myeloid cells

Blood ◽  
2000 ◽  
Vol 95 (11) ◽  
pp. 3349-3356 ◽  
Author(s):  
Takeshi Kuwata ◽  
I-Ming Wang ◽  
Tomohiko Tamura ◽  
Roshini M. Ponnamperuma ◽  
Rachel Levine ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Vitamin A ◽  
Cell Population ◽  
Vitamin A Deficiency ◽  
Myeloid Cells ◽  
Myeloid Cell ◽  
Direct Result ◽  
Essentially Normal ◽  
Deficient Mice

Abstract To examine the role of retinoids in hematopoietic cell growth in vivo, we studied female SENCAR mice made vitamin A deficient by dietary restriction. Deficient mice exhibited a dramatic increase in myeloid cells in bone marrow, spleen, and peripheral blood. The abnormal expansion of myeloid cells was detected from an early stage of vitamin A deficiency and contrasted with essentially normal profiles of T and B lymphocytes. This abnormality was reversed on addition of retinoic acid to the vitamin A–deficient diet, indicating that the myeloid cell expansion is a direct result of retinoic acid deficiency. TUNEL analysis indicated that spontaneous apoptosis, a normal process in the life cycle of myeloid cells, was impaired in vitamin A–deficient mice, which may play a role in the increased myeloid cell population. Quantitative reverse transcriptase-polymerase chain reaction analysis of purified granulocytes showed that expression of not only RAR, but RXRs, 2 nuclear receptors that mediate biologic activities of retinoids, was significantly reduced in cells of deficient mice. This work shows that retinoids critically control the homeostasis of myeloid cell population in vivo and suggests that deficiency in this signaling pathway may contribute to various myeloproliferative disorders.

scholarly journals A Pseudouridine Synthase Homologue Is Critical to Cellular Differentiation in Toxoplasma gondii

2009 ◽  
Vol 8 (3) ◽  
pp. 398-409 ◽  
Author(s):  
Matthew Z. Anderson ◽  
Jeremy Brewer ◽  
Upinder Singh ◽  
John C. Boothroyd
Keyword(s):  
Toxoplasma Gondii ◽  
Chronic Infection ◽  
Insertional Mutagenesis ◽  
Protozoan Parasite ◽  
The United States ◽  
Rna Modification ◽  
Wild Type ◽  
Coding Region ◽  
Pseudouridine Synthase

ABSTRACT Toxoplasma gondii is a haploid protozoan parasite infecting about one in seven people in the United States. Key to the worldwide prevalence of T. gondii is its ability to establish a lifelong, chronic infection by evading the immune system, and central to this is the developmental switch between the two asexual forms, tachyzoites and bradyzoites. A library of mutants defective in tachyzoite-to-bradyzoite differentiation (Tbd−) was created through insertional mutagenesis. This library contains mutants that, compared to the wild type, are between 20% and 74% as efficient at stage conversion. Two mutants, TBD5 and TBD8, with disruptions in a gene encoding a putative pseudouridine synthase, PUS1, were identified. The disruption in TBD8 is in the 5′ end of the PUS1 gene and appears to produce a null allele with a 50% defect in differentiation. This is about the same switch efficiency as obtained with an engineered pus1 deletion mutant (Δpus1). The insertion in TBD5 is within the PUS1 coding region, and this appears to result in a more extreme phenotype of only ∼10% switch efficiency. Complementation of TBD8 with the genomic PUS1 allele restored wild-type differentiation efficiency. Infection of mice with pus1 mutant strains results in increased mortality during the acute phase and higher cyst burdens during the chronic infection, demonstrating an aberrant differentiation phenotype in vivo due to PUS1 disruption. Our results suggest a surprising and important role for RNA modification in this biological process.

Hematopoietic Cells from Gadd45a, Gadd45b Deficent Mice Exhibit Altered Myelopoiesis and Higher Apoptosis after Cytokine Treatment.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 1697-1697
Author(s):  
Shiv K. Gupta ◽  
Mamta Gupta ◽  
Barbara Hoffman ◽  
Dan A. Liebermann
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Cells ◽  
Myeloid Cells ◽  
Methyl Cellulose ◽  
Myeloid Cell ◽  
Cell Maturation ◽  
Wild Type ◽  
Wild Type Littermate ◽  
Deficient Mice ◽  
Marrow Cells

Abstract Growth arrest and DNA damage, Gadd45 gene family members are rapidly induced by genotoxic agents as well as by apoptosis and differentiation inducing cytokines. Their role in hemetopoiesis, wherein proliferation, differentiation and apoptosis integrate to maintain cellular homeostasis, is not clear. Using bone marrow cells from gadd45a or gadd45b deficient and wild type littermate mice we have investigated the role of Gadd45 proteins in cytokine induced myeloid cell differentiation in vitro. Bone marrow cells obtained from either gadd45a or gadd45b deficient mice displayed compromised cytokines (IL3, GM-CSF, M-CSF or G-CSF) induced myelopoiesis, resulting in a quantitatively decreased population of mature myeloid cells. Immuno-phenotyping with antibodies to cell surface molecules associated with myeloid cell maturation confirmed impaired myeloid cell maturation in Gadd45a or b deficient bone marrow cells treated with the above cytokines. Analysis of apoptosis by annexin-V and PI staining followed by FACS analysis showed a substantially higher apoptosis in Gadd45a−/− as well as gadd45b−/− cells compared to wild type cells after treatment with M-CSF or G-CSF. Gadd45a−/− as well as gadd45b−/− bone marrow cells were found to be less clonogenic in methylcellulose medium. Morphologically compact and round colonies consisting of immature myeloid cells prevailed over dispersed- colonies consisting of mature myeloid cells in gadd45- deficient cells cultured in methyl cellulose containing IL-3. Furthermore, colony re-plating assay showed better self-renewal abilities in gadd45a−/− as well as gadd45b−/− progenitors, compared to wild type progenitor cells. Altered myelopoiesis in gadd45 a or b deficient mice was further confirmed in vivo by intra-peritoneal administration of sodium casienate - a known inducer of inflammatory response and myelopoiesis in mice bone marrow. Sodium casienate failed to enhance myelopoiesis in gadd45a or gadd45b deficient mice bone marrow, while wild type littermate mice showed a rapid induction of myelopoiesis. Simultaneously peritoneal exudates collected from gadd45 deficient mice consisted of 2–3 fold less myeloid cells compared to age matched wild type control mice after sodium casienate treatment. Gadd45a−/− or gadd45b−/− mice showed a slow recovery after myelo-suppressive effect of antimetabolite 5-Fluorouracil, which further confirmed that gadd45 deficiency leads to delayed myelopoiesis in mouse. Mechanistic aspects of Gadd45 deficiency, which results in impaired myelopoiesis are under investigation.

Vitamin A deficiency in mice causes a systemic expansion of myeloid cells

Blood ◽  
2000 ◽  
Vol 95 (11) ◽  
pp. 3349-3356 ◽  
Author(s):  
Takeshi Kuwata ◽  
I-Ming Wang ◽  
Tomohiko Tamura ◽  
Roshini M. Ponnamperuma ◽  
Rachel Levine ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Vitamin A ◽  
Cell Population ◽  
Vitamin A Deficiency ◽  
Myeloid Cells ◽  
Myeloid Cell ◽  
Direct Result ◽  
Essentially Normal ◽  
Deficient Mice

To examine the role of retinoids in hematopoietic cell growth in vivo, we studied female SENCAR mice made vitamin A deficient by dietary restriction. Deficient mice exhibited a dramatic increase in myeloid cells in bone marrow, spleen, and peripheral blood. The abnormal expansion of myeloid cells was detected from an early stage of vitamin A deficiency and contrasted with essentially normal profiles of T and B lymphocytes. This abnormality was reversed on addition of retinoic acid to the vitamin A–deficient diet, indicating that the myeloid cell expansion is a direct result of retinoic acid deficiency. TUNEL analysis indicated that spontaneous apoptosis, a normal process in the life cycle of myeloid cells, was impaired in vitamin A–deficient mice, which may play a role in the increased myeloid cell population. Quantitative reverse transcriptase-polymerase chain reaction analysis of purified granulocytes showed that expression of not only RAR, but RXRs, 2 nuclear receptors that mediate biologic activities of retinoids, was significantly reduced in cells of deficient mice. This work shows that retinoids critically control the homeostasis of myeloid cell population in vivo and suggests that deficiency in this signaling pathway may contribute to various myeloproliferative disorders.

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