Inhibition of TRIG Agents by Virus-Induced Interferon.

Hanna, Lavelle; Merigan, Thomas C.; Jawetz, Ernest

doi:10.3181/00379727-122-31150

Cited by 93 publications

(58 citation statements)

References 3 publications

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“…The production of bactericidal nitric oxide free radicals is not a plausible mechanism because mice genetically deficient in inducible nitric oxide synthase resolve both primary and secondary chlamydial infections with kinetics similar to those of wild-type mice (Table 1) (37,74,80). Conversely, the depletion of intracellular tryptophan pools by indoleamine 2,3-dioxygenase is inhibitory to chlamydial growth due to the parasite's tryptophan auxotrophy (1,6,7,14,30,48,60,90). The MoPn and human strains of C. trachomatis exhibit differences in susceptibility to the growth-inhibiting effects of IFN-␥.…”

Section: Effector Mechanisms Of the Adaptive Immune Response Cd4mentioning

confidence: 99%

Immunity to Murine Chlamydial Genital Infection

2002

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Section: Effector Mechanisms Of the Adaptive Immune Response Cd4mentioning

confidence: 99%

Immunity to Murine Chlamydial Genital Infection

2002

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“…4B). Furthermore, interferon enhanced the antibody-absorbing capacity of L 1210 cells even when (1), inhibition of replication of other intracellular parasites (4,(6)(7)(8), inhibition of cell division (3,9,11,19), decreased tumorigenicity and decreased colony-forming capacity of L 1210 cells in agarose (10), enhanced phagocytosis by macrophages (12), and cytotoxicity by sensitized lymphocytes (15), enhanced production of specific proteins, such as interferon (2,13) or aryl hydrocarbon hydroxylase (17), and enhanced cellular sensitivity to the toxic effects of vaccinia virus (5,14) and double-stranded polynucleotides (16). It may be that a common mechanism of action underlies these different effects and that modification of the cell surface plays an important part in the expression of these effects.…”

Section: Antibodymentioning

confidence: 99%

“…In addition to the well-known antiviral action (1), interferon preparations also exert various biologic effects on cells (2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17). The nature of some of these effects suggested the possibility that interferon treatment might be associated with modifications of the cell surface.…”

mentioning

confidence: 99%

Enhancement by Interferon of the Expression of Surface Antigens on Murine Leukemia L 1210 Cells

Lindahl

Leary

Gresser

1973

Proc. Natl. Acad. Sci. U.S.A.

181

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Preparations of mouse interferon enhanced the expression of surface antigens of murine leukemia L 1210 cells, as determined by their alloantibodyabsorbing capacity. The factor responsible for the enhancement of surface antigen expression could not be dissociated from the antiviral activity of interferon by standard physicochemical means. Likewise, interferon did not increase the antibody-absorbing capacity of an interferonresistant subline of L 1210 cells. We conclude that interferon treatment of L 1210 cells is accompanied by modifications of the cell surface.In addition to the well-known antiviral action (1), interferon preparations also exert various biologic effects on cells (2-17). The nature of some of these effects suggested the possibility that interferon treatment might be associated with modifications of the cell surface. To test this hypothesis we have determined the effect of interferon on the surface antigen expression of mouse leukemia L 1210 cells by measuring their alloantibody-absorbing capacity. We report herein the results of these experiments. MATERIALS AND METHODSCell Culture. Murine leukemia L 1210 cells (18) and an interferon-resistant subline, L 1210-R (19), were cultivated in nonagitated suspension cultures in nutrient medium RPMI 1640 (Gibco), supplemented with 20% heat-inactivated horse serum and 1% i-glutamine (10 mmol/ml). EL4 cells (provided by Dr. K. T. Brunner) were cultivated in suspension cultures in the same nutrient medium, supplemented with 10% heat-inactivated calf serum, glutamine, asparagine (36 mg/liter) folic acid (6 mg/liter), and 5% trypticase soy broth.Interferon and Control Preparations. Preparations of mouse interferon were obtained from the nutrient medium of monolayer cultures of MSV-Ia (20), or C-243 cells (21) (provided through the courtesy of Dr. S. Baron) inoculated with Newcastle disease virus (NDV), and from brains of C57BI/6 mice inoculated intracerebrally with West Nile virus (22). Preparations of rabbit interferon were obtained from the nutrient medium of monolayer cultures of RK 13 cells, inoculated with NDV. Control preparations consisted of the medium of uninoculated cell cultures or tissues of uninoculated animals. Preparation and semipurification of murine interferon have been described (15 (L 1210 and EL4 cells were maintained by serial passage in ascitic form in DBA/2 and C57B1/6 mice, respectively). The mice were bled 1 week after the last injection. The sera were decomplemented and stored at -20°. Isoantisera prepared by intraperitoneal injection of C57B1/6 mice with Balb/c splenic lymphocytes or intraperitoneal injection of Balb/c mice with C57B1/6 splenic lymphocytes were generously provided by Dr. J. P. Levy.Labeling of Target Cells. For labeling with radioactive chromium (56Cr), 1 ml of a cell suspension (5 X 106 viable cells per ml) was incubated for 30 min at 370 with 0.1 ml of Na2CrO4 (2 mCi/ml, specific activity 400 Ci/mg of chromium, Centre d'Energie Atomique, France) (24).Cytotoxic Assay. 1 ml of 5"Cr-labeled target cells (2 X 1...

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“…Morphologically aberrant RBs have been observed in clinical specimens (3). This abnormal developmental cycle can be recapitulated in a laboratory setting by exposing C. trachomatis to various stressors such as host cytokines (4)(5)(6), excess amino acids (7), iron deficiency (8,9), virus coinfections (10), and antibiotics (11,12) (reviewed in reference 13). Under these conditions, normal C. trachomatis RBs can transition into persistent forms that do not divide, are enlarged, and have aberrant morphology (13).…”

mentioning

confidence: 99%

Beyond Tryptophan Synthase: Identification of Genes That Contribute to Chlamydia trachomatis Survival during Gamma Interferon-Induced Persistence and Reactivation

et al. 2016

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cChlamydia trachomatis can enter a viable but nonculturable state in vitro termed persistence. A common feature of C. trachomatis persistence models is that reticulate bodies fail to divide and make few infectious progeny until the persistence-inducing stressor is removed. One model of persistence that has relevance to human disease involves tryptophan limitation mediated by the host enzyme indoleamine 2,3-dioxygenase, which converts L-tryptophan to N-formylkynurenine. Genital C. trachomatis strains can counter tryptophan limitation because they encode a tryptophan-synthesizing enzyme. Tryptophan synthase is the only enzyme that has been confirmed to play a role in interferon gamma (IFN-␥)-induced persistence, although profound changes in chlamydial physiology and gene expression occur in the presence of persistence-inducing stressors. Thus, we screened a population of mutagenized C. trachomatis strains for mutants that failed to reactivate from IFN-␥-induced persistence. Six mutants were identified, and the mutations linked to the persistence phenotype in three of these were successfully mapped. One mutant had a missense mutation in tryptophan synthase; however, this mutant behaved differently from previously described synthase null mutants. Two hypothetical genes of unknown function, ctl0225 and ctl0694, were also identified and may be involved in amino acid transport and DNA damage repair, respectively. Our results indicate that C. trachomatis utilizes functionally diverse genes to mediate survival during and reactivation from persistence in HeLa cells. Chlamydia trachomatis has a characteristic biphasic developmental cycle in cell culture (1). The two dominant chlamydial forms are elementary bodies (EBs) and reticulate bodies (RBs) (1). EBs represent the infectious, nonreplicative form capable of invading host cells (1). Following entry, EBs differentiate into RBs that replicate inside parasitophorous vacuoles termed inclusions (1). Maturing RBs then redifferentiate back to EBs and exit the host cell via lysis or extrusion (2). Morphologically aberrant RBs have been observed in clinical specimens (3). This abnormal developmental cycle can be recapitulated in a laboratory setting by exposing C. trachomatis to various stressors such as host cytokines (4-6), excess amino acids (7), iron deficiency (8, 9), virus coinfections (10), and antibiotics (11, 12) (reviewed in reference 13). Under these conditions, normal C. trachomatis RBs can transition into persistent forms that do not divide, are enlarged, and have aberrant morphology (13). Upon removal of the persistence-inducing stressor, RBs transition back into normal RBs and continue normal development (13). Aberrant RB morphology is a shared feature of multiple C. trachomatis persistence models and may reflect activation of a common stress response program (13). Thus, characterizing how C. trachomatis enters, survives, and reactivates from persistence could reveal new insights into chlamydial pathogenesis.The Th1 cytokine interferon gamma (IFN-␥) can induce dif...

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Inhibition of TRIG Agents by Virus-Induced Interferon.

Cited by 93 publications

References 3 publications

Immunity to Murine Chlamydial Genital Infection

Immunity to Murine Chlamydial Genital Infection

Enhancement by Interferon of the Expression of Surface Antigens on Murine Leukemia L 1210 Cells

Beyond Tryptophan Synthase: Identification of Genes That Contribute to Chlamydia trachomatis Survival during Gamma Interferon-Induced Persistence and Reactivation

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