Respiration of L cells infected with Chlamydia psittaci

1970 ◽  
Vol 16 (11) ◽  
pp. 1033-1039 ◽  
Author(s):  
Shawn D'arcy Gill ◽  
Robert B. Stewart
Keyword(s):  
Tissue Culture ◽  
Oxidative Phosphorylation ◽  
Host Cell ◽  
Respiratory Quotient ◽  
Culture Medium ◽  
Mouse Fibroblast ◽  
Chlamydia Psittaci ◽  
Concomitant Increase ◽  
L Cells ◽  
Infected Cells

Strain 929 mouse fibroblast L cells demonstrated an increased rate of endogenous and exogenous respiration when infected by the 6BC strain of the psittacosis organism. The respiratory quotient (R.Q.) values for infected cultures were about 1.0. Studies involving the use of 2,4-DNPand reduced phosphate suggested that the accelerated respiration was a result of increased oxidative phosphorylation. Infection was accompanied by a decline in host cell ATP levels with a concomitant increase in the ADP levels. A reduction in tissue culture medium phosphate resulted in a reduced yield of psittacosis organisms from infected cells and lower cellular levels of ATP. These results are discussed in relation to an energy parasite hypothesis.

Glucose requirements of L cells infected with Chlamydia psittaci

1970 ◽  
Vol 16 (10) ◽  
pp. 997-1001 ◽  
Author(s):  
Shawn D'Arcy Gill ◽  
Robert B. Stewart
Keyword(s):  
Tissue Culture ◽  
Lactic Acid ◽  
Acid Production ◽  
Culture Medium ◽  
Lactic Acid Production ◽  
Mouse Fibroblast ◽  
Chlamydia Psittaci ◽  
Tissue Culture Medium ◽  
Normal Amount ◽  
L Cells

Strain 929 mouse fibroblast L cells were found to consume about twice the normal amount of glucose when infected by the 6BC strain of the psittacosis agent. This was accompanied by an increase in lactic acid production. In addition, the yield of psittacosis organisms was related to the availability of glucose in the tissue culture medium when other constituents were held constant. Under conditions of limiting glucose, the addition of NAD or NADP improved the yield of psittacosis organisms. These results were discussed in relation to the energy parasite concept of chlamydial parasitism.

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 A New Model of SARS-CoV-2 Infection Based on (Hydroxy)Chloroquine Activity

2020 ◽  
Author(s):  
Robert J. Sheaff
Keyword(s):  
Oxidative Phosphorylation ◽  
Host Cell ◽  
Disease Progression ◽  
Therapeutic Benefit ◽  
Beta Oxidation ◽  
New Model ◽  
Culture Cells ◽  
Tissue Culture Cells ◽  
Obesity And Diabetes ◽  
Infected Cells

Chloroquine and hydroxychloroquine [(H)CQ] are well known anti-malarial drugs, while their use against COVID-19 is more controversial. (H)CQ activity was examined in tissue culture cells to determine if their anti-viral benefits or adverse effects might be due to altering host cell pathways. Metabolic analysis revealed (H)CQ inhibit oxidative phosphorylation in mitochondria, likely by sequestering protons needed to drive ATP synthase. This activity could cause cardiotoxicity because heart muscle relies on beta oxidation of fatty acids. However, it might also explain their therapeutic benefit against COVID-19. A new model of SARS-CoV-2 infection postulates virus enters host cell mitochondria and uses its protons for genome release. Oxidative phosphorylation is eventually compromised, so glycolysis is upregulated to maintain ATP levels. (H)CQ could prevent viral infection and/or slow its replication by sequestering these protons. In support of this model other potential COVID-19 therapeutics also targeted mitochondria, as did tobacco smoke, which may underlie smokers protection. The mitochondria of young people are naturally more adaptable and resilient, providing a rationale for their resistance to disease progression. Conversely, obesity and diabetes could exacerbate disease severity by providing extra glucose to infected cells dependent on glycolysis. The description of (H)CQ function presented here, together with its implications for understanding SARS-CO-V2 infection, makes testable predictions about disease progression and identifies new approaches for treating COVID-19.

Presence of Trypanosoma cruzi antigen on the surface of both infected and uninfected cells in tissue culture

Parasitology ◽  
1980 ◽  
Vol 80 (1) ◽  
pp. 147-152 ◽  
Author(s):  
I. A. Abrahamsohn ◽  
J. K. Kloetzel
Keyword(s):  
Cell Culture ◽  
Tissue Culture ◽  
Trypanosoma Cruzi ◽  
Culture Medium ◽  
Culture Supernatant ◽  
Uninfected Cell ◽  
Cell Culture Supernatant ◽  
Supernatant Fluid ◽  
Cell Monolayers ◽  
Infected Cells

SummaryLLC-MK2 cell monolayers infected with Trypanosoma cruzi were shown by immunofluorescence to present parasite antigens on the surface of both parasitized and non-parasitized cells after completion of the first intracellular cycle and rupture of infected cells. The cell-culture supernatant fluid at this stage, as well as the supernatant fluid of parasites left overnight in culture medium were concentrated and contained antigen capable of binding to uninfected cell monolayers. The origin of this antigen, as well as its eventual role in the pathogenesis of Chagas' disease, are discussed.

Phosphatase Activity in Homogenates from Normal and Poliovirus Infected Tissue Cultures

1963 ◽  
Vol 18 (11) ◽  
pp. 912-918
Author(s):  
E. Frank Deig ◽  
Louis P. Gebhardt
Keyword(s):  
Tissue Culture ◽  
Nitrogen Content ◽  
Phosphatase Activity ◽  
Total Nitrogen ◽  
Marked Reduction ◽  
Culture Medium ◽  
Sampling Interval ◽  
Tissue Culture Medium ◽  
Normal Cells ◽  
Infected Cells

Concentrated suspensions of equal numbers of normal and poliovirus infected cells at 37°C were sampled periodically. Cell homogenates prepared from these samples were analyzed for total nitrogen content and for total ATP-ase, alkaline phosphatase, and glucose-6-phosphatase activity. The homogenates prepared from equal numbers of virus infected cells showed a logarithmic decrease in nitrogen with respect to time over the period from four to twelve hours after infection. No additional loss in nitrogen occurred during the following twelve hours. Such nitrogen losses were associated with a decrease in the activity of the three enzymes. In the case of ATP-ase this decrease between the four and twelve hour period was linear with respect to time. The activity of this enzyme remained constant during the following twelve hours. The nitrogen content and activity of the three enzymes in homogenates prepared from normal cell suspensions did not increase over the sampling interval. The large amount of bicarbonate required to maintain the pH of the culture under these conditions produced an unfavorable environment for the cells. This was confirmed by the finding that normal cells placed initially in tissue culture medium, at standard pH, containing excessive amounts of bicarbonate showed no metabolic activity. Such cells exhibited a marked reduction in total nitrogen and in the activity of the three enzymes over a sampling interval of twelve hours. When normal cells were placed in the tissue culture medium, at standard pH. containing such excessive concentrations of bicarbonate, and immediately infected with poliovirus, a delay in the synthesis of. and a marked reduction in final titer of the virus resulted from that found under control conditions.

COVID 19 – Eye Issues

2020 ◽  
Vol 5 (Special) ◽  
Keyword(s):  
Host Cell ◽  
Target Cell ◽  
Cell Receptor ◽  
Human Tissues ◽  
Type Ii ◽  
Cell Infection ◽  
Host Cell Receptor ◽  
Infected Cells ◽  
Cellular Entry

The coronavirus illness (COVID-19) is caused by a new recombinant SARS-CoV (SARS-CoV) virus (SARS-CoV-2). Target cell infection by SARS-CoV is mediated by the prickly protein of the coronavirus and host cell receptor, enzyme 2 converting angiotensin (ACE2) [3]. Similarly, a recent study suggests that cellular entry by SARS-CoV-2 is dependent on both ACE2 as well as type II transmembrane axial protease (TMPRSS2) [4]. This means that detection of ACE2 and PRSS2 expression in human tissues can predict potential infected cells and their respective effects in COVID-19 patients [1].

scholarly journals Host Cell Restriction Factors of Bunyaviruses and Viral Countermeasures

Viruses ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 784
Author(s):  
Solène Lerolle ◽  
Natalia Freitas ◽  
François-Loïc Cosset ◽  
Vincent Legros
Keyword(s):  
Host Cell ◽  
Viral Entry ◽  
Current Knowledge ◽  
Restriction Factors ◽  
Antiviral State ◽  
Cellular Factors ◽  
Pathogenic Viruses ◽  
Genome Transcription ◽  
Infected Cells ◽  
Molecular Patterns

The Bunyavirales order comprises more than 500 viruses (generally defined as bunyaviruses) classified into 12 families. Some of these are highly pathogenic viruses infecting different hosts, including humans, mammals, reptiles, arthropods, birds, and/or plants. Host cell sensing of infection activates the innate immune system that aims at inhibiting viral replication and propagation. Upon recognition of pathogen-associated molecular patterns (PAMPs) by cellular pattern recognition receptors (PRRs), numerous signaling cascades are activated, leading to the production of interferons (IFNs). IFNs act in an autocrine and paracrine manner to establish an antiviral state by inducing the expression of hundreds of IFN-stimulated genes (ISGs). Some of these ISGs are known to restrict bunyavirus infection. Along with other constitutively expressed host cellular factors with antiviral activity, these proteins (hereafter referred to as “restriction factors”) target different steps of the viral cycle, including viral entry, genome transcription and replication, and virion egress. In reaction to this, bunyaviruses have developed strategies to circumvent this antiviral response, by avoiding cellular recognition of PAMPs, inhibiting IFN production or interfering with the IFN-mediated response. Herein, we review the current knowledge on host cellular factors that were shown to restrict infections by bunyaviruses. Moreover, we focus on the strategies developed by bunyaviruses in order to escape the antiviral state developed by the infected cells.

scholarly journals Revisiting Ehrlichia ruminantium Replication Cycle Using Proteomics: The Host and the Bacterium Perspectives

2021 ◽  
Vol 9 (6) ◽  
pp. 1144
Author(s):  
Isabel Marcelino ◽  
Philippe Holzmuller ◽  
Ana Coelho ◽  
Gabriel Mazzucchelli ◽  
Bernard Fernandez ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Host Cell ◽  
Cell Metabolism ◽  
Replication Cycle ◽  
Host Cells ◽  
Ehrlichia Ruminantium ◽  
Host Interaction ◽  
Infected Cells ◽  
Related Proteins

The Rickettsiales Ehrlichia ruminantium, the causal agent of the fatal tick-borne disease Heartwater, induces severe damage to the vascular endothelium in ruminants. Nevertheless, E. ruminantium-induced pathobiology remains largely unknown. Our work paves the way for understanding this phenomenon by using quantitative proteomic analyses (2D-DIGE-MS/MS, 1DE-nanoLC-MS/MS and biotin-nanoUPLC-MS/MS) of host bovine aorta endothelial cells (BAE) during the in vitro bacterium intracellular replication cycle. We detect 265 bacterial proteins (including virulence factors), at all time-points of the E. ruminantium replication cycle, highlighting a dynamic bacterium–host interaction. We show that E. ruminantium infection modulates the expression of 433 host proteins: 98 being over-expressed, 161 under-expressed, 140 detected only in infected BAE cells and 34 exclusively detected in non-infected cells. Cystoscape integrated data analysis shows that these proteins lead to major changes in host cell immune responses, host cell metabolism and vesicle trafficking, with a clear involvement of inflammation-related proteins in this process. Our findings led to the first model of E. ruminantium infection in host cells in vitro, and we highlight potential biomarkers of E. ruminantium infection in endothelial cells (such as ROCK1, TMEM16K, Albumin and PTPN1), which may be important to further combat Heartwater, namely by developing non-antibiotic-based strategies.

ON TETHELIN AS A TISSUE CULTURE MEDIUM

1930 ◽  
Vol 1 (9) ◽  
pp. 289-290
Author(s):  
K. C. Richardson ◽  
E. S. Horning
Keyword(s):  
Tissue Culture ◽  
Culture Medium ◽  
Tissue Culture Medium
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