3 edition of Early murine immune response to peroral infection with Toxoplasma gondii found in the catalog.
Early murine immune response to peroral infection with Toxoplasma gondii
Brown, Charles Robert
Written in English
|Statement||by Charles Robert Brown.|
|LC Classifications||Microfilm 94/2323 (Q)|
|The Physical Object|
|Pagination||x, 107 leaves|
|Number of Pages||107|
|LC Control Number||94629112|
Immune responses associated with early survival after peroral infection with Toxoplasma gondii.J. Immunol. Role of Gamma Interferon in Cellular Immune Response against Murine Encephalitozoon cuniculiInfection. Imtiaz A. Khan, Magali by: In many countries, Toxoplasma gondii (T. gondii) is a major cause of reproductive disorders and abortions in the sheep industry, and therefore responsible for important financial and economic losses. In addition, undercooked infected lamb is an important risk factor for human toxoplasmosis. In the present study, the initial phase of the infection was investigated: the parasite’s Cited by: 5. Background & Aims: Acute inflammatory ileitis occurs in susceptible (C57BL/6) mice after oral infection with Toxoplasma gondii. Overproduction of interferon (IFN)-γ and synthesis of nitric oxide mediate the inflammation. We evaluated the role of transforming growth factor (TGF)-β produced by intraepithelial lymphocytes (IELs) in this process. Methods: We analyzed the histologic and. Success and virulence in Toxoplasma as the results of sexual recombination between two distinct ancectries. Science , *joint corresponding authors. Kang H, and Suzuki Y. Requirement of non-T cells that produce interferon-gamma for prevention of reactivation of Toxoplasma gondii infection in the brain. Infect Immun
Fc receptors on the surface of Toxoplasma gondii trophozoites: a confounding factor in testing for anti-Toxoplasma antibodies by indirecimmunofluorescence. J. Clin. Microbiol., 27, Page Bülow, R. and Boothroyd, J. C. (). Protection of mice from fatal Toxoplasma gondii infection by immunization with p30 antigen in liposomes. J.
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Innate immune responses to T. gondii. Following challenge with T. gondii, monocytes, neutrophils and dendritic cells (DCs) are recruited to the site of infection, and all of these cell types have been implicated in resistance to this organism [26–32].However, questions remain about their specific roles in controlling infection.
One of the most critical functions of the innate immune response Cited by: Immune response to Toxoplasma gondii. During infection with T.
gondii, ICOS promotes early T cell responses, while in the chronic stage of infection ICOS plays a regulatory role by limiting T. Humoral immune response Infection with T. gondii has been shown to give rise to production of specific antibodies against the parasite in the intestine and blood (reviewed in 25).
Secretory IgA responses against T. gondii can be detected in intestinal secretions and milk (26, 27).Cited by: This chapter reviews our current understanding of the innate immune response to T.
gondii, highlighting prominent questions in the field about how T. gondii is recognized and controlled by the cytokine IFN-γ and advances in our understanding of parasite evasion of innate immunity.
IMMUNE RESPONSE TO TOXOPLASMA GONDII73 The CD8+ TL, activated by the IL-2 secreted by the CD4+ TL, exert a cytotoxic activity against tachyzoites or cells infected with T. gondii[49, 47]. This activity, exerted by IFN-γ, is obviously restricted by class-I MHC and helps to provide the host with resistance during the chronic phase of ToxoplasmaFile Size: KB.
Protective Mucosal Th2 Immune Response against Toxoplasma gondii by Murine Mesenteric Lymph Node Dendritic Cells Article (PDF Available) in Infection and Immunity 71(9) October Toxoplasma gondii is a protozoan parasite of medical and veterinary significance that is able to infect any warm-blooded vertebrate host.
In addition to its importance to public health, several inherent features of the biology of T. gondii have made it an important model organism to study host–pathogen interactions.
One factor is the genetic tractability of the parasite, which allows studies Cited by: Citation: Severance EG, Kannan G, Gressitt KL, Xiao J, Alaedini A, et al.
() Anti-Gluten Immune Response following Toxoplasma gondii Infection in Mice. PLoS PLoS ONE 7(11): e doi Immune Responses to Toxoplasma Gondii in the Gut Immune Responses to Toxoplasma Gondii in the Gut Liesenfeld, Oliver Toxoplasma gondii is an important cause of disease, in pregnant women, newborns and immunocompromised hosts.
Infection with T. gondii naturally occurs through ingestion of raw or undercooked meat containing cysts or through contact with cat feces Author: Liesenfeld, Oliver. Toxoplasma gondii is a universally distributed pathogen that infects over one billion people worldwide.
Host resistance to this protozoan parasite depends on a Th1 immune response with potent production of the cytokines interleukin and interferon γ. Although Toll-like receptor 11 (TLR11) plays a major role in controlling Th1 immunity to this pathogen in mice, this innate immune receptor is Cited by: Interestingly, pcGRA14 coated with nanoparticles led to statistically significant enhancements of cellular and humoral immune responses against Toxoplasma infection (P challenge.
Abstract To investigate early immune responses to the intracellular parasite Toxoplasma gondii, we examined the capacity of nonimmune splenocytes to respond in vitro to intact tachyzoites and soluble tachyzoite antigen (Ag). Both types of stimuli induced high levels of proliferation as well as interferon gamma (IFN-gamma) secretion.
Lymphocyte blastogenic transformation in response to Toxoplasma lysate antigen was markedly impaired in six of eight patients with chronic, latent Toxoplasma gondii infection and treated Hodgkin's. Toxoplasma gondii is an obligate intracellular protozoan parasite that causes various diseases, including lymphadenitis, congenital infection of fetuses and life-threatening toxoplasmic encephalitis in immunocompromised individuals.
Interferon-gamma (IFN-γ)-mediated immune responses are essential for controlling tachyzoite proliferation during both acute acquired infection.
Primary infection with Toxoplasma gondii stimulates production of high levels of interleukin 12 (IL) and interferon γ (IFN-γ) by cells of the innate immune system. These two cytokines are central to resistance to T. gondii. Signaling through the Toll-like receptor (TLR) adaptor protein MyD88 is indispensible for activating early innate immune by: Toxoplasma gondii infection can cause different clinical manifestations and the immune response, both locally and systemically, vary among individuals by their diverse genetic backgrounds and immune status.
In this study, TS and TR mice were showed to be useful models for toxoplasmosis after oral by: 5. High mobility group box 1 (HMGB1) is abundantly expressed in intracellular engaged DNA binding ability. However, more importantly, it is a weapon against infection through proinflammatory response and immune regulation while released to extracellular.
Toxoplasma gondii causes inflammatory pathological changes including ileitis and encephalitis in chronic by: 1. To investigate early immune responses to the intracellular parasite Toxoplasma gondii, we examined the capacity of nonimmune splenocytes to respond in vitro to intact tachyzoites and soluble tachyzoite antigen (Ag).
Both types of stimuli induced high levels of proliferation as well as interferon gamma (IFN-gamma) secretion. Sturge, C.R. & Yarovinsky, F. Complex immune cell interplay in the gamma interferon response during Toxoplasma gondii infection. Infect. Im – ().Cited by: 6. Abstract. A murine model of peroral and congenital infection was developed to study protection against Toxoplasma gondii as infection is naturally acquired.
Immunization with a temperature sensitive mutant (ts4) T. gondii was found to confer protection against peroral and congenital infection using this model.
As it was possible to elicit a protective immune response against infection, immune Cited by: 2. Innate responses to Toxoplasma gondii in mice and humans Reed Pifer and Felix Yarovinsky Department of Immunology, University of Texas Southwestern Medical Center at Dallas, Harry Hines Boulevard, Dallas, TXUSA Primary infection with Toxoplasma gondii stimulates production of high levels of interleukin 12 (IL) and.
This article has been cited by other articles in PMC. Depression of the cellular immune response to Toxoplasma gondii has been reported in both mice and humans.
The present study was undertaken to determine the kinetics and mechanism of the observed downregulation of interleukin 2 (IL-2) production during experimental murine by: Abstract. Toxoplasma gondii is a major opportunistic infection of the central nervous system (CNS) in AIDS patients and increasingly is a problem in other immunocompromised patients.
In these patients clinical disease results from a reactivation of the latent tissue cyst stage in the brain. Tissue cysts contain bradyzoites, a slowly replicating form of the by: 2. Immune responses associated with early survival after peroral infection with Toxoplasma gondii.
McLeod R, Eisenhauer P, Mack D, Brown C, Filice G, Spitalny G. J Immunol, (9), 01 May Cited by: 59 articles | PMID: The activation of a predominant T-helper-cell subset plays a critical role in disease resolution. In the case of Toxoplasma gondii, the available evidence indicates that CD4+protective cells belong to the Th1 subset.
The aim of this study was to determine whether T. gondii antigens (in T. gondii sonicate [TSo]) presented by splenic dendritic cells (DC) were able to induce a specific immune Cited by: Natural infection by Toxoplasma gondii occurs via oral ingestion of tissue cysts that rupture in the small intestine, releasing zoites that infect locally before disseminating throughout the host.
The studies presented here used fluorescent parasites combined with flow cytometry and multiphoton microscopy techniques to understand the events associated with parasite replication in the by: Toxoplasma gondii, an obligate intracellular parasite pathogen which initially invades the intestinal epithelium before disseminating throughout the body, may cause severe sequelae in fetuses and life-threatening neuropathy in immunocompromised protection is usually thought to be performed through a systemic Th1 response; considering the route of parasite entry it is important.
Intestinal immune responses to infection with T. gondii include generation of specific secretory IgA antibodies [ 12, 13 ], early and transient T cell proliferation in mesenteric lymph nodes [ 14 ], and increases in relative percentages of CD8 + αβ intraepithelial lymphocytes that are cytotoxic and produce interferon (IFN)-γ [ 15 ].Cited by: Toxoplasma Modulates Signature Pathways of Human and deconvolution of Toxoplasma gondii brain infection proteins that participate in the regulation of the immune response Cited by: The intracellular apicomplexan parasite Toxoplasma gondii is able to survive and persist in immunocompetent intermediate hosts for the host’s life span.
This is despite the induction of a vigorous humoral and—more importantly—cell-mediated immune response during infection. In order to establish and maintain such chronic infections, however, T. gondii has evolved multiple strategies to Cited by: Abstract.
Clinical manifestations and congenital transmission rates vary markedly among individuals with Toxoplasma infection (reviewed in Boyer and McLeod ; Remington et al.
An influence of host immune response genes on the outcome of congenital infection is supported by observations of concordance of manifestations in monozygotic versus discordance of manifestations in dizygotic Cited by: This effective immune reaction against parasites results in the chronic infection of an immunocompetent individual with T.
gondii usually being contained (12). Immune protection is thought to be performed through a Th1 systemic response (17), but the importance of gut mucosal immunity against infection with T. gondii is less well by: Abstract. Factors which determine the pathogenesis and course of Toxoplasma encephalitis are poorly understood.
In the present study, the influence of genetic factors in congenic B10 and BALB mice of H-2q, H-2k, and H-2b haplotypes was examined following oral infection with a low-virulence strain of Toxoplasma gondii (DX).Cited by: ing infection .
Immune responses elicited by the parasite are influenced by a variety of factors, including the genetic back-ground of the mice, their sex, and the dose and strain of the para-site [6,].
Oral Infection of Mice with T. gondii and the Development of Intestinal Pathology Following peroral infection with cysts of the. Toxoplasma gondii Infections in Chickens (Gallus domesticus): Prevalence, Clinical Disease, Diagnosis and Public Health Signiﬁcance J.
Dubey United States Department of Agriculture, Agricultural Research Service, Animal Parasitic Diseases Laboratory, Animal and Natural Resources T. gondii infection in chickens and to assess the role of.
As mice are very sensitive to Toxoplasma gondii infection, there are problems in challenge experiments, and either a low virulent strain or high virulent strain of Toxoplasma gondii with low dose must be used.
In this study, we used 2×10 3 RH parasites (a virulent Toxoplasma gondii strain) to challenge immunized mice (Yap et al., Cited by: Within seven days following peroral high dose infection with Toxoplasma gondiisusceptible conventionally colonized mice develop acute ileitis due to an underlying T helper cell (Th) -1 type by: As an intracellular parasite, Toxoplasma gondii must avoid a variety of host defences including the host immune response.
Recent studies have demonstrated that T. gondii extensively remodels its host altering host metabolism and gene expression. These events are mediated by parasite products that are secreted into the host cell during and after by: 3. These authors also suggested that the peroral infection can be useful for more in-depth analysis of in vivo immune responses against T.
gondii, as well as for therapeutic studies of candidate drugs for treatment (Meyer et al., ).Author: Miguel J. Bortolini, Miguel J. Bortolini, Murilo V. Silva, Fábio M. Alonso, Luciana A. Medeiro. Lee, Y.-H., Channon, J. Y., Matsuura, T., Schwartzman, J. D., Shin, D.-W., and Kasper, L.
Functional and quantitative analysis of splenic T cell immune responses following oralToxoplasma gondiiinfection in mental Parasitology91,–Immunity toToxoplasma gondiiis mediated primarily by the host T cell gh there is considerable information regarding host Cited by:.
In the first response to infection, toxoplasma-specific IgG has a low affinity for the toxoplasma antigen; in the following weeks and month, IgG affinity for the antigen increases. Based on the IgG avidity test, if the IgG in the infected individual has a high affinity, it means that the infection began three to Causes: Toxoplasma gondii.Recent epidemiologic studies indicate that infectious agents may contribute to some cases of schizophrenia.
In animals, infection with Toxoplasma gondii can alter behavior and neurotransmitter function. In humans, acute infection with T. gondii can produce psychotic symptoms similar to those displayed by persons with schizophrenia. Sincea total of 19 studies of T.
gondii antibodies in.Toxoplasma gondii is an obligate intracellular protozoa parasite that causes the disease toxoplasmosis. It resides within host cells in a parasitophorous vacuole distinct from the host cell endocytic system. T. gondii was used as a model to investigate how obligate intracellular parasites alter their gene expression in response to the host immune response during infection compared to growth in Cited by: 6.