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.

Cytochemistry of the wall of infected cells in Casuarina actinorhizae

1988 ◽  
Vol 66 (10) ◽  
pp. 2038-2047 ◽  
Author(s):  
R. Howard Berg ◽  
Lorraine McDowell
Keyword(s):  
Infected Cell ◽  
Secondary Wall ◽  
Chromic Acid ◽  
Cortical Cell ◽  
Wall Material ◽  
Primary Cell Wall ◽  
Acid Digestion ◽  
En Bloc ◽  
Lignin Modification ◽  
Infected Cells

Development of the wall of infected cells in Casuarina actinorhizae differs from that of many actinorhizae. After the endophyte penetrates the wall of a cortical cell, that (primary) cell wall becomes lignified, based on histochemical (autofluorescence, phloroglucinol staining) and cytochemical (permanganate staining, enzyme etching) evidence. Subsequently, the remaining walls of the infected cell become lignified. Adjacent noninfected cells somehow are stimulated to deposit a lignified secondary wall only on those walls bordering the infected cell. This remarkable participation of all adjacent noninfected cells in the development of a given infected cell results in an increased thickness and strength of the wall material surrounding infected cells. When they mature, there is a further modification of some of the wall layers surrounding infected cells, manifested in a relative impermeability to en bloc staining with permanganate. Unlike lignified walls, the permanganate-impermeable region is selectively stained by osmium or ferricyanide-reduced osmium and is relatively resistant to concentrated chromic acid digestion. A region that remains permeable to (and stained by) permanganate (part of the secondary wall of bordering noninfected cells) may be developmentally related to phi thickenings. An earlier contention that the permanganate-impermeable region contains suberin is unconfirmed. This region is most likely an unusual lignin modification or results from unidentified material impregnated in its ligninlike matrix.

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.

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.

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.

scholarly journals Entry of Human Parechovirus 1

2001 ◽  
Vol 75 (4) ◽  
pp. 1958-1967 ◽  
Author(s):  
Päivi Joki-Korpela ◽  
Varpu Marjomäki ◽  
Camilla Krogerus ◽  
Jyrki Heino ◽  
Timo Hyypiä
Keyword(s):  
Host Cell ◽  
Preliminary Evidence ◽  
Endocytic Pathway ◽  
Host Cells ◽  
Human Parechovirus ◽  
Double Labeling ◽  
Late Endosomes ◽  
Early Endosomes ◽  
Infected Cells ◽  
Golgi Network

ABSTRACT Human parechovirus 1 (HPEV-1) is a prototype member of parechoviruses, a recently established picornavirus genus. Although there is preliminary evidence that HPEV-1 recognizes αVintegrins as cellular receptors, our understanding of early events during HPEV-1 infection is still very limited. The aim of this study was to clarify the entry mechanisms of HPEV-1, including the attachment of the virus onto the host cell surface and subsequent internalization. In blocking experiments with monoclonal antibodies against different receptor candidates, antibodies against αV and β3 integrin subunits, in particular in combination, appeared to be the most efficient ones in preventing the HPEV-1 infection. To find out whether HPEV-1 uses clathrin-coated vesicles or other routes for the entry into the host cell, we carried out double-labeling experiments of virus-infected cells with anti-HPEV-1 antibodies and antibodies against known markers of the clathrin and the caveolin routes. At the early phase of infection (5 min postinfection [p.i.]) HPEV-1 colocalized with EEA1 (early endosomes), and later, after 30 min p.i., it colocalized with mannose-6-phosphate receptor (late endosomes), whereas no colocalization with caveolin-1 was observed. The data indicate that HPEV-1 utilizes the clathrin-dependent endocytic pathway for entry into the host cells. Interestingly, endocytosed HPEV-1 capsid proteins were observed in the endoplasmic reticulum and cis-Golgi network 30 to 60 min p.i. Depolymerization of microtubules with nocodazole inhibited translocation of the virus to the late endosomes but did not block HPEV-1 replication, suggesting that the RNA genome may be released early during the entry process.

scholarly journals Helicobacter pylori Outer Membrane Vesicles and Extracellular Vesicles from Helicobacter pylori-Infected Cells in Gastric Disease Development

2021 ◽  
Vol 22 (9) ◽  
pp. 4823
Author(s):  
María Fernanda González ◽  
Paula Díaz ◽  
Alejandra Sandoval-Bórquez ◽  
Daniela Herrera ◽  
Andrew F. G. Quest
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Outer Membrane ◽  
Extracellular Vesicles ◽  
Membrane Vesicles ◽  
Outer Membrane Vesicles ◽  
Host Cells ◽  
Gastric Epithelium ◽  
Infected Cells ◽  
H Pylori

Extracellular vesicles (EVs) are cell-derived vesicles important in intercellular communication that play an essential role in host-pathogen interactions, spreading pathogen-derived as well as host-derived molecules during infection. Pathogens can induce changes in the composition of EVs derived from the infected cells and use them to manipulate their microenvironment and, for instance, modulate innate and adaptive inflammatory immune responses, both in a stimulatory or suppressive manner. Gastric cancer is one of the leading causes of cancer-related deaths worldwide and infection with Helicobacter pylori (H. pylori) is considered the main risk factor for developing this disease, which is characterized by a strong inflammatory component. EVs released by host cells infected with H. pylori contribute significantly to inflammation, and in doing so promote the development of disease. Additionally, H. pylori liberates vesicles, called outer membrane vesicles (H. pylori-OMVs), which contribute to atrophia and cell transformation in the gastric epithelium. In this review, the participation of both EVs from cells infected with H. pylori and H. pylori-OMVs associated with the development of gastric cancer will be discussed. By deciphering which functions of these external vesicles during H. pylori infection benefit the host or the pathogen, novel treatment strategies may become available to prevent disease.

scholarly journals “Limiting access to iron decreases infection of Atlantic salmon SHK-1 cells with bacterium Piscirickettsia salmonis”

2021 ◽  
Vol 17 (1) ◽  
Author(s):  
Rodrigo Díaz ◽  
José Troncoso ◽  
Eva Jakob ◽  
Stanko Skugor
Keyword(s):  
Gene Expression ◽  
Iron Deficiency ◽  
Atlantic Salmon ◽  
Bacterial Load ◽  
Host Cells ◽  
Immune Gene ◽  
Immune Signaling ◽  
Immune Effector ◽  
Infected Cells ◽  
Piscirickettsia Salmonis

Abstract Background Vertebrate hosts limit the availability of iron to microbial pathogens in order to nutritionally starve the invaders. The impact of iron deficiency induced by the iron chelator deferoxamine mesylate (DFO) was investigated in Atlantic salmon SHK-1 cells infected with the facultative intracellular bacterium Piscirickettsia salmonis. Results Effects of the DFO treatment and P. salmonis on SHK-1 cells were gaged by assessing cytopathic effects, bacterial load and activity, and gene expression profiles of eight immune biomarkers at 4- and 7-days post infection (dpi) in the control group, groups receiving single treatments (DFO or P. salmonis) and their combination. The chelator appears to be well-tolerated by host cells, while it had a negative impact on the number of bacterial cells and associated cytotoxicity. DFO alone had minor effects on gene expression of SHK-1 cells, including an early activation of IL-1β at 4 dpi. In contrast to few moderate changes induced by single treatments (either infection or chelator), most genes had highest upregulation in the infected groups receiving DFO. The mildest induction of hepcidin-1 (antimicrobial peptide precursor and regulator of iron homeostasis) was observed in cells exposed to DFO alone, followed by P. salmonis infected cells while the addition of DFO to infected cells further increased the mRNA abundance of this gene. Transcripts encoding TNF-α (immune signaling) and iNOS (immune effector) showed sustained increase at both time points in this group while cathelicidin-1 (immune effector) and IL-8 (immune signaling) were upregulated at 7 dpi. The stimulation of protective gene responses seen in infected cultures supplemented with DFO coincided with the reduction of bacterial load and activity (judged by the expression of P. salmonis 16S rRNA), and damage to cultured host cells. Conclusion The absence of immune gene activation under normal iron conditions suggests modulation of host responses by P. salmonis. The negative effect of iron deficiency on bacteria likely allowed host cells to respond in a more protective manner to the infection, further decreasing its progression. Presented findings encourage in vivo exploration of iron chelators as a promising strategy against piscirickettsiosis.

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