scholarly journals Phagosome-lysosome fusion inhibited by algal symbionts of Hydra viridis.

1982 ◽  
Vol 94 (1) ◽  
pp. 56-63 ◽  
Author(s):  
T C Hohman ◽  
P L McNeil ◽  
L Muscatine
Keyword(s):  
Acid Phosphatase ◽  
Host Cells ◽  
Digestive Cells ◽  
Symbiotic Algae ◽  
Algal Symbionts ◽  
Dimethyl Urea ◽  
Photosynthetic Products ◽  
Basal Position ◽  
Hydra Viridis

Certain species of Chlorella live within the digestive cells of the fresh water cnidarian Hydra viridis. When introduced into the hydra gut, these symbiotic algae are phagocytized by digestive cells but avoid host digestion and persist at relatively constant numbers within host cells. In contrast, heat-killed symbionts are rapidly degraded after phagocytosis. Live symbionts appear to persist because host lysosomes fail to fuse with phagosomes containing live symbionts. Neither acid phosphatase nor ferritin was delivered via lysosomes into phagosomes containing live symbionts, whereas these lysosomal markers were found in 50% of the vacuoles containing heat-killed symbionts 1 h after phagocytosis. Treatment of symbiotic algae before phagocytosis with polycationic polypeptides abolishes algal persistence and perturbs the ability of these algae to control the release of photosynthate in vitro. Similarly, inhibition of photosynthesis and hence of the release of photosynthetic products as a result of prolonged darkness and 3-(3,4-dichlorophenyl)-1,1-dimethyl urea (DCMU) treatment also abolishes persistence. Symbiotic algae are not only protected from host digestive attack but are also selectively transported within host cells, moving from the apical site of phagocytosis to a basal position of permanent residence. This process too is disrupted by polycationic polypeptides, DCMU and darkness. Both algal persistence and transport may, therefore, be a function of the release of products from living, photosynthesizing symbionts. Vinblastine treatment of host animals blocked the movement of algae within host cells but did not perturb algal persistence: algal persistence and the transport of algae may be initiated by the same signal, but they are not interdependent processes.

scholarly journals Coxiella burnetiiAcid Phosphatase Inhibits the Release of Reactive Oxygen Intermediates in Polymorphonuclear Leukocytes

2010 ◽  
Vol 79 (1) ◽  
pp. 414-420 ◽  
Author(s):  
J. Hill ◽  
J. E. Samuel
Keyword(s):  
Acid Phosphatase ◽  
Nadph Oxidase ◽  
Polymorphonuclear Leukocytes ◽  
Q Fever ◽  
Reactive Oxygen ◽  
Host Cells ◽  
Reactive Oxygen Intermediates ◽  
Oxygen Intermediates

ABSTRACTCoxiella burnetii, the etiological agent of Q fever, is a small, Gram-negative, obligate intracellular bacterium. Replication ofC. burnetiiduring infection has been shown to be increased by decreasing oxidative stress using p47phox −/−and iNOS−/−micein vivoand by pharmacologic inhibitorsin vitro. Building upon this model, we investigated the role polymorphonuclear leukocytes (PMN) play in the control of infection, since NADPH oxidase-mediated release of reactive oxygen intermediates (ROI) is a primary bactericidal mechanism for these cells that is critical for early innate clearance. Earlier studies suggested thatC. burnetiiactively inhibited release of ROI from PMN through expression of an unidentified acid phosphatase (ACP). Recent genomic annotations identified one open reading frame (CBU0335) which may encode a Sec- and type II-dependent secreted ACP. To test this model, viableC. burnetiipropagated in tissue culture host cells or axenic media,C. burnetiiextracts, or purified recombinant ACP (rACP) was combined with human PMN induced with 4-phorbol 12-myristate 13-acetate (PMA). The release of ROI was inhibited when PMN were challenged with viableC. burnetii,C. burnetiiextracts, or rACP but not when PMN were challenged with electron beam-inactivatedC. burnetii. C. burnetiiextracts and rACP were also able to inhibit PMA-induced formation of NADPH oxidase complex on PMN membranes, suggesting a molecular mechanism responsible for this inhibition. These data support a model in whichC. burnetiieludes the primary ROI killing mechanism of activated PMN by secreting at least one acid phosphatase.

The role of algal antigenic determinants in the recognition of potential algal symbionts by cells of Chlorohydra

1979 ◽  
Vol 35 (1) ◽  
pp. 367-379
Author(s):  
R.R. Pool
Keyword(s):  
Cell Surface ◽  
Algal Cell ◽  
Antigenic Determinants ◽  
Digestive Cells ◽  
Green Hydra ◽  
Algal Symbionts ◽  
Two Systems

Algal cells grown in the green hydra Chlorohydra viridissima were shown to possess characteristic antigenic determinants not found in algae cultured in vitro. These antigenic determinants, including those localized on the algal cell surface, were shown to be responsible for the phagocytic recognition of potential algal symbionts by digestive cells of Chlorohydra. The results of this study indicate the existence of two systems governing phagocytosis in Chlorohydra, one specific for algal cells grown in hydra, another governing the uptake of other particles by the hydra digestive cells.

Laboratory Studies of the Ecological Significance of Host-Algal Nutritional Associations in Solitary and Colonial Radiolaria

1985 ◽  
Vol 65 (1) ◽  
pp. 263-272 ◽  
Author(s):  
O. R. Anderson ◽  
N. R. Swanberg ◽  
P. Bennett
Keyword(s):  
Primary Productivity ◽  
Ecological Significance ◽  
Laboratory Studies ◽  
Symbiotic Algae ◽  
Host Cytoplasm ◽  
Algal Symbionts ◽  
Host Nutrition ◽  
Photosynthetic Products ◽  
Solitary Species

Symbiont-bearing solitary and colonial radiolaria occur abundantly in diverse water masses throughout the major oceans of the world, including oligotrophic surface water (e.g. Strelkov & Reshetnyak, 1971; Casey, 1971, 1977; Anderson, 1983; Swanberg, 1979, 1983). Studies of their nutrition (Anderson, 1978, 1983; Swanberg, 1983) suggest that the algal symbionts may serve a substantial role in sustaining host nutrition. Our studies on the role of symbiotic algae in radiolaria have shown that Amphidinium-type, dinoflagellate symbionts (Anderson, 1983, p. 118) associated with the solitary species, Thalassicolla nucleata, and a colonial form Collosphaera sp. contribute photosynthetically-derived carbon to the host. The amount assimilated by T. nucleata is proportional to the primary productivity of the symbionts (Anderson, Swanberg & Bennett, 1983 b). Little is known, however, about the effects of environmental variables such as light intensity and quality on the primary productivity of the symbionts and the kinds of photosynthetic products accumulated within the host cytoplasm.

Lysosomes and the "toxicity" of Rickettsials. II. Non-cytocidal interactions of egg-grown C. psittaci 6BC and in vitro macrophages

1972 ◽  
Vol 18 (6) ◽  
pp. 869-873 ◽  
Author(s):  
Nonna Kordová ◽  
Linda Poffenroth ◽  
John C. Wilt
Keyword(s):  
Acid Phosphatase ◽  
Cell Damage ◽  
Giant Cells ◽  
Host Cells ◽  
Marked Contrast ◽  
Lysosomal Acid ◽  
Cytoplasmic Vacuoles ◽  
L Cell

During the infection of cultured mouse peritoneal phagocytes with egg-grown C. psittaci 6BC strain, lysosomes retained their integrity and host cells were not damaged. Infected monocytes showed greater ability than uninfected monocytes to spread and transform into giant cells containing enlarged nuclei and masses of cytoplasm with clear cytoplasmic vacuoles. Chlamydial particles were released from the cytoplasm of infected phagocytes by pseudopodia-like extrusions. These events were in marked contrast to the effect of L cell grown C. psittaci 6BC strain which caused early leakage of lysosomal acid phosphatase into the cytoplasm of macrophages and induced a rapidly progressive irreversible cell damage (14).

Regulatory mechanisms maintaining the Hydra-Chlorella symbiosis

1983 ◽  
Vol 219 (1215) ◽  
pp. 193-210 ◽  
Keyword(s):  
Light And Electron Microscopy ◽  
Inorganic Nutrients ◽  
Host Cells ◽  
Regulatory Mechanisms ◽  
Digestive Cell ◽  
Digestive Cells ◽  
Symbiotic Associations ◽  
Symbiotic Algae ◽  
Unicellular Algae

In symbiotic associations between unicellular algae and aquatic invertebrates a relatively constant biomass ratio of algae to host is maintained. The mechanisms that maintain this ratio have not been adequately investigated. This study describes aspects of the mechanisms regulating numbers of algae in Hydra viridis digestive cells. Symbiotic digestive cells that acquire supernumerary algae by phagocytosis restore the number to normal levels by several mechanisms. Light and electron microscopy provide evidence showing that excess algae are expelled intact or digested within the host cells. This finding is significant since, under normal circumstances, symbiotic algae are not expelled and avoid digestion by inhibiting phagosome—lysosome fusion. The role of host cell mitosis in the regulation of the number of algae per cell is also investigated. Quantitative data are presented which show that mitosis alone cannot account for the regulation of supernumerary algae. The hypothesis that the supply of inorganic nutrients may influence the regulation of the number of algae per digestive cell is also tested in this study. Enrichment of the maintenance medium with a combination of nutrients enhances growth of the symbiotic algae, the digestive cells become packed with algae, and eventually the host is overgrown and killed by the algae. Therefore regulatory mechanisms controlling the algal population when exogenous inorganic nutrients are limited, are no longer effective when nutrients are available.

Novel Toxin-antitoxin System Xn-mazEF from Xenorhabdus nematophi-la: Identification, Characterization and Functional Exploration

2020 ◽  
Vol 16 ◽  
Author(s):  
Jogendra Singh Nim ◽  
Mohit Yadav ◽  
Lalit Kumar Gautam ◽  
Chaitali Ghosh ◽  
Shakti Sahi ◽  
...  
Keyword(s):  
Interaction Analysis ◽  
Functional Characterization ◽  
Host Cells ◽  
System Control ◽  
Xenorhabdus Nematophila ◽  
Functional Features ◽  
Dynamics Simulations ◽  
Species Specific ◽  
Rna Interaction

Background: Xenorhabdus nematophila maintains species-specific mutual interaction with nematodes of Steinernema genus. Type II Toxin Antitoxin (TA) systems, the mazEF TA system controls stress and programmed cell death in bacteria. Objective: This study elucidates the functional characterization of Xn-mazEF, a mazEF homolog in X. nematophila by computational and in vitro approaches. Methods: 3 D- structural models for Xn-MazE toxin and Xn-MazF antitoxin were generated, validated and characterized for protein - RNA interaction analysis. Further biological and cellular functions of Xn-MazF toxin were also predicted. Molecular dynamics simulations of 50ns for Xn-MazF toxin complexed with nucleic acid units (DU, RU, RC, and RU) were performed. The MazF toxin and complete MazEF operon were endogenously expressed and monitored for the killing of Escherichia coli host cells under arabinose induced tightly regulated system. Results: Upon induction, E. coli expressing toxin showed rapid killing within four hours and attained up to 65% growth inhibition, while the expression of the entire operon did not show significant killing. The observation suggests that the Xn-mazEF TA system control transcriptional regulation in X. nematophila and helps to manage stress or cause toxicity leading to programmed death of cells. Conclusion: The study provides insights into structural and functional features of novel toxin, XnMazF and provides an initial inference on control of X. nematophila growth regulated by TA systems.

ACIS, A Novel KepTide™, Binds to ACE-2 Receptor and Inhibits the Infection of SARS-CoV2 Virus in vitro in Primate Kidney Cells: Therapeutic Implications for COVID-19 (Preprint)

2020 ◽  
Author(s):  
Avik Sotira Scientific
Keyword(s):  
Social Life ◽  
Plaque Assay ◽  
Host Cells ◽  
Surface Glycoprotein ◽  
Crystallographic Structure ◽  
Therapeutic Implications ◽  
Biochemical Assays ◽  
Targeted Medicine

UNSTRUCTURED Coronavirus disease 2019 (COVID-19) is a severe acute respiratory syndrome (SARS) caused by a virus known as SARS-Coronavirus 2 (SARS-CoV2). Without a targeted-medicine, this disease has been causing a massive humanitarian crisis not only in terms of mortality, but also imposing a lasting damage to social life and economic progress of humankind. Therefore, an immediate therapeutic strategy needs to be intervened to mitigate this global crisis. Here, we report a novel KepTide™ (Knock-End Peptide) therapy that nullifies SARS-CoV2 infection. SARS-CoV2 employs its surface glycoprotein “spike” (S-glycoprotein) to interact with angiotensin converting enzyme-2 (ACE-2) receptor for its infection in host cells. Based on our in-silico-based homology modeling study validated with a recent X-ray crystallographic structure (PDB ID:6M0J), we have identified that a conserved motif of S-glycoprotein that intimately engages multiple hydrogen-bond (H-bond) interactions with ACE-2 enzyme. Accordingly, we designed a peptide, termed as ACIS (ACE-2 Inhibitory motif of Spike), that displayed significant affinity towards ACE-2 enzyme as confirmed by biochemical assays such as BLItz and fluorescence polarization assays. Interestingly, more than one biochemical modifications were adopted in ACIS in order to enhance the inhibitory action of ACIS and hence called as KEpTide™. Consequently, a monolayer invasion assay, plaque assay and dual immunofluorescence analysis further revealed that KEpTide™ efficiently mitigated the infection of SARS-CoV2 in vitro in VERO E6 cells. Finally, evaluating the relative abundance of ACIS in lungs and the potential side-effects in vivo in mice, our current study discovers a novel KepTide™ therapy that is safe, stable, and robust to attenuate the infection of SARS-CoV2 virus if administered intranasally. INTERNATIONAL REGISTERED REPORT RR2-https://doi.org/10.1101/2020.10.13.337584

scholarly journals Bromodomain and Extraterminal Protein Inhibitor, Apabetalone (RVX-208), Reduces ACE2 Expression and Attenuates SARS-Cov-2 Infection In Vitro

Biomedicines ◽  
2021 ◽  
Vol 9 (4) ◽  
pp. 437
Author(s):  
Dean Gilham ◽  
Audrey L. Smith ◽  
Li Fu ◽  
Dalia Y. Moore ◽  
Abenaya Muralidharan ◽  
...  
Keyword(s):  
Antiviral Agents ◽  
Host Cells ◽  
Protein Inhibitor ◽  
Angiotensin Converting Enzyme 2 ◽  
Dipeptidyl Peptidase 4 ◽  
Surface Receptors ◽  
Bet Inhibitor ◽  
Epigenetic Machinery ◽  
Unexplored Area

Effective therapeutics are urgently needed to counter infection and improve outcomes for patients suffering from COVID-19 and to combat this pandemic. Manipulation of epigenetic machinery to influence viral infectivity of host cells is a relatively unexplored area. The bromodomain and extraterminal (BET) family of epigenetic readers have been reported to modulate SARS-CoV-2 infection. Herein, we demonstrate apabetalone, the most clinical advanced BET inhibitor, downregulates expression of cell surface receptors involved in SARS-CoV-2 entry, including angiotensin-converting enzyme 2 (ACE2) and dipeptidyl-peptidase 4 (DPP4 or CD26) in SARS-CoV-2 permissive cells. Moreover, we show that apabetalone inhibits SARS-CoV-2 infection in vitro to levels comparable to those of antiviral agents. Taken together, our study supports further evaluation of apabetalone to treat COVID-19, either alone or in combination with emerging therapeutics.

scholarly journals Effective decellularisation of human saphenous veins for biocompatible arterial tissue engineering applications: Bench optimisation and feasibility in vivo testing

2021 ◽  
Vol 12 ◽  
pp. 204173142098752
Author(s):  
Nadiah S Sulaiman ◽  
Andrew R Bond ◽  
Vito D Bruno ◽  
John Joseph ◽  
Jason L Johnson ◽  
...  
Keyword(s):  
Tissue Engineering ◽  
Mechanical Strength ◽  
Vascular Tissue ◽  
Sodium Dodecyl ◽  
Host Cells ◽  
Replacement Model ◽  
In Vivo Testing ◽  
Vascular Scaffolds

Human saphenous vein (hSV) and synthetic grafts are commonly used conduits in vascular grafting, despite high failure rates. Decellularising hSVs (D-hSVs) to produce vascular scaffolds might be an effective alternative. We assessed the effectiveness of a detergent-based method using 0% to 1% sodium dodecyl sulphate (SDS) to decellularise hSV. Decellularisation effectiveness was measured in vitro by nuclear counting, DNA content, residual cell viability, extracellular matrix integrity and mechanical strength. Cytotoxicity was assessed on human and porcine cells. The most effective SDS concentration was used to prepare D-hSV grafts that underwent preliminary in vivo testing using a porcine carotid artery replacement model. Effective decellularisation was achieved with 0.01% SDS, and D-hSVs were biocompatible after seeding. In vivo xeno-transplantation confirmed excellent mechanical strength and biocompatibility with recruitment of host cells without mechanical failure, and a 50% patency rate at 4-weeks. We have developed a simple biocompatible methodology to effectively decellularise hSVs. This could enhance vascular tissue engineering toward future clinical applications.

scholarly journals Lipoproteins Are Responsible for the Pro-Inflammatory Property of Staphylococcus aureus Extracellular Vesicles

2021 ◽  
Vol 22 (13) ◽  
pp. 7099
Author(s):  
Pradeep Kumar Kopparapu ◽  
Meghshree Deshmukh ◽  
Zhicheng Hu ◽  
Majd Mohammad ◽  
Marco Maugeri ◽  
...  
Keyword(s):  
Extracellular Vesicles ◽  
Inflammatory Responses ◽  
Surface Proteins ◽  
Host Cells ◽  
Immune Stimulation ◽  
Domains Of Life ◽  
Major Surface ◽  
Staphylococcal Aureus

Staphylococcal aureus (S. aureus), a Gram-positive bacteria, is known to cause various infections. Extracellular vesicles (EVs) are a heterogeneous array of membranous structures secreted by cells from all three domains of life, i.e., eukaryotes, bacteria, and archaea. Bacterial EVs are implied to be involved in both bacteria–bacteria and bacteria–host interactions during infections. It is still unclear how S. aureus EVs interact with host cells and induce inflammatory responses. In this study, EVs were isolated from S. aureus and mutant strains deficient in either prelipoprotein lipidation (Δlgt) or major surface proteins (ΔsrtAB). Their immunostimulatory capacities were assessed both in vitro and in vivo. We found that S. aureus EVs induced pro-inflammatory responses both in vitro and in vivo. However, this activity was dependent on lipidated lipoproteins (Lpp), since EVs isolated from the Δlgt showed no stimulation. On the other hand, EVs isolated from the ΔsrtAB mutant showed full immune stimulation, indicating the cell wall anchoring of surface proteins did not play a role in immune stimulation. The immune stimulation of S. aureus EVs was mediated mainly by monocytes/macrophages and was TLR2 dependent. In this study, we demonstrated that not only free Lpp but also EV-imbedded Lpp had high pro-inflammatory activity.

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