2 edition of Interferon-induced effector mechanisms in murine Chlamydia psittaci infection found in the catalog.
Interferon-induced effector mechanisms in murine Chlamydia psittaci infection
Angela R Currier
Written in English
|Statement||by Angela R. Currier|
|The Physical Object|
|Pagination||vii, 112 leaves :|
|Number of Pages||112|
Recent studies have revealed remarkable species specificity of the Toll-like receptors (TLRs) TLR11 and TLR12 and the immunity-related GTPase (IRG) proteins that are essential elements for detection and immune control of Toxoplasma gondii in mice, but not in humans. The biological and evolutionary implications of these findings for the T. gondii host-pathogen relationship and for human disease. Chlamydia psittaci is a zoonotic pathogen that is distinct in disease spectrum and biology, especially by its propensity to cause severe systemic infections and sepsis. C. psittaci is generally acquired from inhalation of aerosolized fecal material of infected birds and causes an acute disease called psittacosis.
Chlamydia pneumoniae and Chlamydia pecorum, formerly known as strains of C. psittaci, were designated as distinct species in and , respectively. More recently, a new taxonomy was proposed that increases the number of species in the family Chlamydiaceae to nine and groups these species into two genera (31). Abstract. Chlamydia trachomatis and Chlamydia pneumoniae appear to share a common immunobiology with about 80% of their protein coding genes being orthologs. Progress in DNA vaccine development for C. trachomatis suggests that such a subunit approach may prove useful for C. recent finding that it is possible to select for chlamydiae with targeted mutations in .
The first experiments showing the antimicrobial potential of IFN-γ-induced tryptophan degradation were performed with the obligate intracellular parasite Toxoplasma gondii and the intracellular bacterium Chlamydia psittaci. Later, we and others demonstrated that this effector mechanism is also able to inhibit the growth of extracellular bacteria. Type 1 CD4 +-T-cell-mediated immunity is crucial for the resolution of chlamydial infection of the murine female genital us studies demonstrating a correlation between CD4 +-T-cell-mediated inhibition of chlamydial growth and gamma interferon (IFN-γ)-mediated induction of nitric oxide synthase suggested a potential role for the nitric oxide (NO) effector pathway in the .
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The type III secretion system (T3SS) is a needle-like molecular syringe that enables the direct injection of bacterial effector molecules across host membranes Chlamydia spp. use the T3SS at various stages of infection, including during initial host cell contact with the plasma membrane and during the intracellular phase, in which effectors are injected into the cytosol of the host cell Cited by: Gamma interferon-mediated cytotoxicity related to murine Chlamydia trachomatis infection.
Infect Immun. Aug; 56 (8)– [PMC free article] Byrne GI, Lehmann LK, Landry GJ. Induction of tryptophan catabolism is the mechanism for gamma-interferon-mediated inhibition of intracellular Chlamydia psittaci replication in T24 by: Chlamydia psittaci serotype 1 is an obligate intracellular bacterium which can colonize very different types of placenta (ruminant, porcine, human, and murine), causing abortion during the last third of the gestation period.
The disease is especially important in small ruminants, the natural hosts of the bacterium, because of the economic losses it by: IFN-γ-mediated effector mechanisms in the control of Chlamydia The indoleamine 2,3-dioxygenase (IDO) pathway, which converts L-tryptophan to N -formylkynurenine (thereby limiting tryptophan availability), is implicated in IFN-γ-mediated inhibition of chlamydial replication and in persistence in human cells .Cited by: Neta Brender-Gotlieb, Merav Lidar, in Infection and Autoimmunity (Second Edition), Chlamydia.
Chlamydia pneumoniae, a gram-negative, obligate, intracellular bacterium, has been associated with several autoimmune diseases such as sarcoidosis and multiple sclerosis. 30 Given the predilection of C. pneumoniae to colonize human endothelial and epithelial tissue, it was postulated to.
Chlamydia pneumoniae is a highly specialized gram-negative intracellular bacterium with a biphasic life cycle, in which the spore-like elementary bodies facilitate transit between cells and the metabolically active reticulate bodies are responsible for intracellular replication (30, 59).
pneumoniae infection is by far the most common human chlamydial infection, with seropositivity in at. The anti-chlamydial and anti-proliferative activities of recombinant murine interferon-gamma are not dependent on tryptophan concentrations.
J Immunol. Dec; (6)– Hatch TP. Competition between Chlamydia psittaci and L cells for host isoleucine pools: a limiting factor in chlamydial multiplication. Weidner, J. et al. Interferon-induced cell membrane proteins, IFITM3 and tetherin, inhibit vesicular stomatitis virus infection via distinct mechanisms.
Virol. 84, – (). The intonation “The king is dead, long live the king” aptly describes the state of Chlamydia research.
Genetic-based approaches are rapidly replacing correlative strategies to provide new insights. We describe how current transformation technologies are enhancing progress in understanding Chlamydia infection biology and present key opportunities for further development.
Byrne G.I., Lehmann L.K., Landry ion of tryptophan catabolism is the mechanism for gamma interferon-mediated inhibition of intracellular Chlamydia psittaci multiplication in T24 cells Infection and Immunity, 53 (), pp. Lymphokine-mediated microbistatic mechanisms restrict Chlamydia psittaci growth in macrophages.
J Immunol. Jan; (1)– [Google Scholar] Byrne GI, Lehmann LK, Landry GJ. Induction of tryptophan catabolism is the mechanism for gamma-interferon-mediated inhibition of intracellular Chlamydia psittaci replication in T24 cells.
rabbits also showed that C. pneumoniae infection leads to in-ﬂammatory changes in the aorta (11, 32, 41). More recently, Bachmaier et al. (2) reported that a peptide from the murine heart muscle-speciﬁc a myosin heavy chain that has sequence homology to the kDa cysteine-rich outer membrane pro-teins of C.
pneumoniae, Chlamydia psittaci. The immune mechanisms in response to Chlamydophila abortus (Chlamydia psittaci serotype 1) infection were studied in C57BL/6 and CBA mice. The infection was monitored and the following aspects of the immune response were evaluated: the nature of the leucocyte infiltrate in the liver, the percentages of polymorphonuclear neutrophils (PMNs), macrophages and lymphocytes in.
This chapter discusses the possible role of gamma interferon (IFN-γ) and heat shock proteins (Hsps) in the pathogenesis of chlamydial disease. It reviews preliminary evidence from trachoma and pelvic inflammatory disease (PID) suggesting that human genotype exerts a substantial influence.
It discusses some of the evidence behind current concepts of chlamydial disease mechanisms, and focuses. IFNs, especially IFNγ, are the major cytokines involved in anti-microbial defense against Chlamydia (Rottenberg et al., ) but the individual cell-autonomous effector mechanisms activated by.
ABSTRACT Interferon-γ (IFN-γ) previously has been shown to inhibit the replication of Chlamydia psittaci in epithelial cells by inducing indoleamine 2,3-dioxygenase, the enzyme that decyclizes tryp. murine Chlamydia psittaci infection. J Immunol – (Ctrq3) has been shown to influence tolerance to Chlamydia psittaci infection, The book will open the way for including.
Interferon-γ (IFN-γ) previously has been shown to inhibit the replication of Chlamydia psittaci in epithelial cells by inducing indoleamine 2,3-dioxygenase, the enzyme that decyclizes tryptophan to role of indoleamine 2,3-dioxygenase in IFN-mediated inhibition of C.
psittaci in human macrophages has now been examined. Peripheral blood monocytes from. mation to murine Chlamydia psittaci infection. J Immunol – cell-autonomous host defense mechanisms could provide insight into mechanisms Role for an Interferon-Induced Host.
Request PDF | Pathogenic mechanisms of chronic Chlamydia infections | Chlamydiae are obligate intracellular bacteria. The genus Chlamydia consists of the species C. trachomatis, C. psittaci. Abstract.
IFN-γ and/or LPS induced nitrite production and inhibition of Chlamydia trachomatis (CT) replication in the murine macrophage cell line, RAW Linear regression analysis demonstrated a strong correlation between nitrite production and inhibition of CT replication (correlation coefficients: −, P.For example, TNFa activation of the NF-jb pathway immediately prior to the infection is known to enable HEp-2 cells to resist infection by Chlamydia.
1 Chlamydia has many mechanisms to subvert.Tryptophan depletion resulting from indoleamine 2,3-dioxygenase (IDO) activity within the kynurenine pathway is one of the most prominent gamma interferon (IFN-γ)-inducible antimicrobial effector mechanisms in human cells.
On the other hand, nitric oxide (NO) produced by the inducible isoform of NO synthase (iNOS) serves a more immunoregulatory role in human cells and thereby interacts with.