Chlamydia psittaci: inclusion vacuole ultrastructure

1980 ◽  
Vol 26 (3) ◽  
pp. 396-401 ◽  
Author(s):  
Gerald V. Stokes
Keyword(s):  
Cytoplasmic Inclusion ◽  
Chlamydia Psittaci ◽  
Host Cells ◽  
Infected Host ◽  
Electron Microscopic ◽  
Infected Cells ◽  
Microscopic Techniques

The inclusion ultrastructure of fibroblasts infected with Chlamydia psittaci (6BC) was studied. Electron microscopic techniques were used which permitted the observation of whole infected host cells and 1.0-μm sectioned preparations. It was shown that the cytoplasmic inclusion vacuoles of infected cells contained interconnecting structures within which chlamydiae reproduce.

Persistent Infection of Mouse Fibroblasts (L Cells) with Chlamydia psittaci : Evidence for a Cryptic Chlamydial Form

1980 ◽  
Vol 30 (3) ◽  
pp. 874-883
Author(s):  
James W. Moulder ◽  
Nancy J. Levy ◽  
Laura P. Schulman
Keyword(s):  
Host Cell ◽  
Chlamydia Psittaci ◽  
Host Cells ◽  
Developmental Cycle ◽  
Persistently Infected ◽  
Mouse Fibroblasts ◽  
Persistent Infections ◽  
L Cells ◽  
Infected Cells ◽  
Parasite Multiplication

When monolayers of mouse fibroblasts (L cells) were infected with enough Chlamydia psittaci (strain 6BC) to destroy most of the host cells, 1 in every 10 5 to 10 6 originally infected cells gave rise to a colony of L cells persistently infected with strain 6BC. In these populations, the density of L cells and 6BC fluctuated periodically and reciprocally as periods of host cell increase were followed by periods of parasite multiplication. Successive cycles of L-cell and 6BC reproduction were sustained indefinitely by periodic transfer to fresh medium. Isolation of L cells and 6BC from persistent infections provided no evidence that there had been any selection of variants better suited for coexistence. Persistently infected populations consisting mainly of inclusion-free L cells yielded only persistently infected clones, grew more slowly, and cloned less efficiently. They were also almost completely resistant to superinfection with high multiplicities of either 6BC or the lymphogranuloma venereum strain 440L of Chlamydia trachomatis . These properties of persistently infected L cells may be accounted for by assuming that all of the individuals in these populations are cryptically infected with 6BC and that cryptic infection slows the growth of the host cell and makes it immune to infection with exogenous chlamydiae. According to this hypothesis, the fluctuations in host and parasite density occur because some factor periodically sets off the conversion of cryptic chlamydial forms into reticulate bodies that multiply and differentiate into infectious elementary bodies in a conventional chlamydial developmental cycle.

scholarly journals Chlamydia-Infected Cells Continue To Undergo Mitosis and Resist Induction of Apoptosis

2004 ◽  
Vol 72 (1) ◽  
pp. 451-460 ◽  
Author(s):  
Whitney Greene ◽  
Yangming Xiao ◽  
Yanqing Huang ◽  
Grant McClarty ◽  
Guangming Zhong
Keyword(s):  
Dna Synthesis ◽  
Host Cell ◽  
Chlamydial Infection ◽  
Host Cells ◽  
Infected Host ◽  
Apoptosis Induction ◽  
Infected Cells ◽  
Induction Of Apoptosis

ABSTRACT Both anti- and proapoptotic activities have been reported to occur during chlamydial infection. To reconcile the apparent controversy, we compared host cell apoptotic responses to infection with 17 different chlamydial serovars and strains. None of the serovars caused any biologically significant apoptosis in the infected host cells. Host cells in chlamydia-infected cultures can continue to undergo DNA synthesis and mitosis. Chlamydia-infected cells are resistant to apoptosis induction, although the extent of the antiapoptotic ability varied between serovars. These observations have demonstrated that an anti- but not proapoptotic activity is the prevailing event in chlamydia-infected cultures.

scholarly journals Role of Bcl-2 Family Members in Caspase-Independent Apoptosis during Chlamydia Infection

2002 ◽  
Vol 70 (1) ◽  
pp. 55-61 ◽  
Author(s):  
Jean-Luc Perfettini ◽  
John C. Reed ◽  
Nicole Israël ◽  
Jean-Claude Martinou ◽  
Alice Dautry-Varsat ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Chlamydia Psittaci ◽  
Host Cells ◽  
Chlamydia Infection ◽  
Caspase Inhibitor ◽  
Obligate Intracellular Bacterium ◽  
Obligate Intracellular ◽  
Infected Cells ◽  
Induced Apoptosis

ABSTRACT Infection with an obligate intracellular bacterium, the Chlamydia trachomatis lymphogranuloma venereum (LGV/L2) strain or the guinea pig inclusion conjunctivitis serovar of Chlamydia psittaci, leads to apoptosis of host cells. The apoptosis is not affected by a broad-spectrum caspase inhibitor, and caspase-3 is not activated in infected cells, suggesting that apoptosis mediated by these two strains of Chlamydia is independent of known caspases. Overexpression of the proapoptotic Bcl-2 family member, Bax, was previously shown to induce caspase-independent apoptosis, and we find that Bax is activated and translocates from the cytosol to the mitochondria in C. psittaci-infected cells. C. psittaci-induced apoptosis is inhibited in host cells overexpressing Bax inhibitor-1 and is inhibited through overexpression of Bcl-2, which blocks both caspase-dependent and -independent apoptosis. As Bax and mitochondria are ideally located to sense stress-related metabolic changes emanating from the interior of an infected cell, it is likely that Bax-dependent apoptosis may also be observed in cells infected with other intracellular pathogens.

Comparison of microtubules and microfilaments in Tipula iridescent virus-infected and uninfected cells

1985 ◽  
Vol 63 (6) ◽  
pp. 543-552 ◽  
Author(s):  
Robert W. Seagull ◽  
Peter E. Lee ◽  
Monica Frosch
Keyword(s):  
Virus Assembly ◽  
Electron Microscopic ◽  
Iridescent Virus ◽  
Initial Stage ◽  
Large Virus ◽  
Infected Cells ◽  
Specific Association ◽  
Globular Cells ◽  
Cytoskeletal Elements ◽  
Microscopic Techniques

Microfilaments and microtubules were detected in Estigmene acrea virus-infected cells using fluorescent immunochemistry and in sections by electron microscopy. Twelve hours following infection of cells with Tipula iridescent virus, large virus assembly sites developed in the cytoplasm. The majority of infected cells exhibit no detectable changes in the cytoskeleton during the initial stage of infection, when virus assembly sites are forming. Actin was localized either in cytoplasmic spikes or in patches at the cell surface. Microtubules were parallel to the long axis of elongate cells or randomly distributed in globular cells. Intermediate filaments were not detected using either immunofluorscent or electron microscopic techniques. In later stages of infection some cells exhibit a specific association between actin and the virus assembly site. The significance of this observation remains unclear since only a portion of the population exhibits this change. From this study, it does not appear that cytoskeletal elements are of importance in the formation or maintenance of the membrane-free cytoplasmic virus assembly sites.

Effects of an anti-exospore monoclonal antibody on microsporidial development in vitro

Parasitology ◽  
1998 ◽  
Vol 117 (6) ◽  
pp. 515-520 ◽  
Author(s):  
F. J. ENRIQUEZ ◽  
G. WAGNER ◽  
M. FRAGOSO ◽  
O. DITRICH
Keyword(s):  
Monoclonal Antibody ◽  
Host Cells ◽  
Infected Host ◽  
Encephalitozoon Cuniculi ◽  
Isotype Control ◽  
Encephalitozoon Intestinalis ◽  
Infected Cells ◽  
Pre Treatment ◽  
Development In Vitro

In this study we evaluated the effects of the anti-microsporidial exospore monoclonal antibody 3B6, recognizing 3 Encephalitozoon species, Encephalitozoon intestinalis (Syn. Septata intestinalis), Encephalitozoon cuniculi, and Encephalitozoon hellem on microsporidial growth in vitro. Pre-treatment of spores for 24 h with mAb 3B6 resulted in 21–29% fewer infected host cells 4 days after inoculation of the cultures compared to cultures pre-treated with medium or an irrelevant isotype control mAb (P<0·001). Fewer intracellular spores (1·2±0·2) in infected cells were found when mAb 3B6 was present in cultures compared to cultures with medium alone (4·3±0·8) or an irrelevant isotype control mAb (4·2±0·9; P<0·001). This decrease appeared not to be dependent on time of exposure, mAb concentration, or presence of complement. It is concluded that antibodies, particularly those directed to potential neutralizing-sensitive epitopes on spores, may have a role in the control of microsporidial growth in vitro.

Interferon-gamma-induced apoptosis in host cells infected with Neospora caninum

Parasitology ◽  
2001 ◽  
Vol 123 (1) ◽  
pp. 25-31 ◽  
Author(s):  
Y. NISHIKAWA ◽  
M. MISHIMA ◽  
H. NAGASAWA ◽  
I. IGARASHI ◽  
K. FUJISAKI ◽  
...  
Keyword(s):  
Interferon Gamma ◽  
Neospora Caninum ◽  
Flow Cytometric Analysis ◽  
Parasite Infection ◽  
Host Cells ◽  
Infected Host ◽  
Fasl Expression ◽  
Infected Cells ◽  
Ifn Γ

Interferon-gamma (IFN-γ) has a crucial role for host defence against parasite infection. It is not clear, however, how IFN-γ affects the parasite-infected host cells. The effect of IFN-γ on Neospora caninum-infected cells was investigated in murine fibroblasts and canine kidney cells in vitro. In the presence of IFN-γ, the viability of the infected host cell was decreased and apoptotic cell death occurred, as analysed by DNA stainings with propidium iodide and a terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labelling (TUNEL) and DNA fragmentation. The percentage of apoptotic cells depended on the dose of IFN-γ. Flow cytometric analysis indicated a significant increase of FasL expression on the IFN-γ-treated cells following N. caninum infection. Moreover, IFN-γ treatment down-regulated Bcl-2 expression in the cells cultured with N. caninum while parasite infection up-regulated Bcl-2 expression. The present study suggests that the IFN-γ induced increases of FasL expression and down-regulated Bcl-2 expression in N. caninum-infected cells are associated with apoptosis in vitro.

scholarly journals The Occurrence of a Previously Unobserved Polysaccharide in Immature Infected Cells of Root Nodules of Trifolium Ambiguum M. Bieb. And Other Members of the Trifolieae

1957 ◽  
Vol 10 (1) ◽  
pp. 17 ◽  
Author(s):  
FJ Bergersen
Keyword(s):  
Cell Wall ◽  
White Clover ◽  
Small Proportion ◽  
Phase Contrast ◽  
Root Nodules ◽  
Host Cells ◽  
Infected Host ◽  
Trifolium Ambiguum ◽  
Infected Cells

A type of ineffective nodulation is described in which the bacteroids in the nodule cells fail to mature, and in which the infected host cells accumulate watersoluble polysaccharide between protoplast and cell wall. Ineffectiveness of this kind is characteristic of nodules� on Trifolium ambiguum M. Bieb. produced by unadapted strains of bacteria, or produced by adapted strains on a small proportion of plants. It is also found when strains effective with T. ambiguum nodulate subterranean or white clover. The polysaccharide in the peripheries of infected cells is readily seen by phase-contrast observation, provided the sections are not hydrated after removal of wax, but it is not visible by ordinary staining procedures.

Preliminary evidence for the involvement of suberization in infection of Casuarina

1983 ◽  
Vol 61 (11) ◽  
pp. 2910-2918 ◽  
Author(s):  
R. Howard Berg
Keyword(s):  
Chromic Acid ◽  
Hydrolytic Enzymes ◽  
Preliminary Evidence ◽  
Host Cells ◽  
Infected Host ◽  
Tissue Cell ◽  
En Bloc ◽  
Sudan Black B ◽  
Infected Cells ◽  
Mature Nodule

Histochemistry of infected cells in mature nodule lobes of Casuarina showed that walls of infected host cells had a ligninlike component (ultraviolet-stimulated autofluorescence and staining with auramine O, phloroglucinol staining, and resistance to degradation by hydrolytic enzymes). Cytoplasm of infected cells had a pronounced affinity for lipid stains (Sudan black B, Rose Bengal fluorescence), though walls of infected cells were less clearly stained. When nodules were digested several days in cold 50% chromic acid, the walls of infected cells and suberized host tissue (epidermis, endodermis) were not degraded. Endophyte cell wall components were also found to be resistant to chromic acid digestion. The digested tissue retained the capacity to adsorb lipid dyes. These observations suggested that walls of infected host cells had become impregnated with a suberinlike compound. The hydrophobic quality of this wall was evident when its ultrastructure was examined after en bloc staining with the polar stain KMnO4. This stain did not penetrate the walls of mature infected cells, perhaps because of the presence of aliphatic compounds similar to those found in suberin. As is known for suberizing tissue, peroxidase activity (via diaminobenzidine oxidation) was high in nodule cortical tissue cell walls. The peroxidase stain was also localized on endophyte hyphae. This report is the first instance associating a suberizationlike host reaction with infection of an actinorhizal plant.

Further Observations on the Virus of Epizootic Diarrhea of Infant Mice. An Electron Microscopic Study

1967 ◽  
Vol 25 ◽  
pp. 110-111
Author(s):  
W. G. Banfield ◽  
G. Kasnic ◽  
J. H. Blackwell
Keyword(s):  
Electron Microscope ◽  
Infected Cell ◽  
Microscopic Study ◽  
Intestinal Epithelium ◽  
Ultrastructural Study ◽  
Osmium Tetroxide ◽  
Lead Citrate ◽  
Electron Microscopic ◽  
Virus Particles ◽  
Infected Cells

An ultrastructural study of the intestinal epithelium of mice infected with the agent of epizootic diarrhea of infant mice (EDIM virus) was first performed by Adams and Kraft. We have extended their observations and have found developmental forms of the virus and associated structures not reported by them.Three-day-old NLM strain mice were infected with EDIM virus and killed 48 to 168 hours later. Specimens of bowel were fixed in glutaraldehyde, post fixed in osmium tetroxide and embedded in epon. Sections were stained with uranyl magnesium acetate followed by lead citrate and examined in an updated RCA EMU-3F electron microscope.The cells containing virus particles (infected) are at the tips of the villi and occur throughout the intestine from duodenum through colon. All developmental forms of the virus are present from 48 to 168 hours after infection. Figure 1 is of cells without virus particles and figure 2 is of an infected cell. The nucleus and cytoplasm of the infected cells appear clearer than the cells without virus particles.

Polarity Determination in Sphalerite and Wurtzite Structures

1990 ◽  
Vol 48 (2) ◽  
pp. 500-501
Author(s):  
Stuart McKernan ◽  
C. Barry Carter
Keyword(s):  
Opposite Polarity ◽  
Single Domain ◽  
Polar Material ◽  
Electron Microscopic ◽  
Dynamical Interaction ◽  
X Ray ◽  
Polarity Determination ◽  
The Absolute ◽  
Microscopic Techniques

The determination of the absolute polarity of a polar material is often crucial to the understanding of the defects which occur in such materials. Several methods exist by which this determination may be performed. In bulk, single-domain specimens, macroscopic techniques may be used, such as the different etching behavior, using the appropriate etchant, of surfaces with opposite polarity. X-ray measurements under conditions where Friedel’s law (which means that the intensity of reflections from planes of opposite polarity are indistinguishable) breaks down can also be used to determine the absolute polarity of bulk, single-domain specimens. On the microscopic scale, and particularly where antiphase boundaries (APBs), which separate regions of opposite polarity exist, electron microscopic techniques must be employed. Two techniques are commonly practised; the first [1], involves the dynamical interaction of hoLz lines which interfere constructively or destructively with the zero order reflection, depending on the crystal polarity. The crystal polarity can therefore be directly deduced from the relative intensity of these interactions.

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