Characterization of the parasite-host cell interactions involved inTheileria parvasporozoite invasion of bovine lymphocytes

Parasitology ◽  
1996 ◽  
Vol 113 (3) ◽  
pp. 267-277 ◽  
Author(s):  
M. K. Shaw
Keyword(s):  
Host Cell ◽  
De Novo ◽  
Experimental Conditions ◽  
Surface Molecules ◽  
Lymphocyte Surface ◽  
Host Cell Interactions ◽  
Host Cell Surface ◽  
Ph Dependent ◽  
Bovine Lymphocytes

SUMMARYSporozoite invasion of bovine lymphocytes byTheileria parvais a pH-dependent process that occurs without the need forde novoprotein synthesis. The process was inhibited by RGD(S) peptides, fibronectin and, in the presence of serum, by antibodies reactive with fibronectin. Invasion was also blocked by a range of sulphated glycoconjugates, but treatment of lymphocytes with heparitinase did not inhibit entry. Enzymic modifications of the lymphocyte surface demonstrated that trypsin-insensitive glycoproteins containingO- andN-linked carbohydrates as well as phospholipase-sensitive molecules on the host cell surface were critical to sporozoite entry. Modification of the lymphocyte surface with NEM and DTT had only marginal effects on sporozoite binding but blocked parasite internalization. Invasion was also blocked by several antibodies which cross-reacted with sporozoite surface molecules. While only a few experimental conditions specifically blocked sporozoite binding, a wider range of reagents and treatments inhibited parasite entry. The reasons for this are discussed in terms of the nature of the zippering process that facilitates sporozoite internalization.

Characterization of the pathway for transport of the cytoadherence-mediating protein, PfEMP1, to the host cell surface in malaria parasite-infected erythrocytes

2003 ◽  
Vol 50 (4) ◽  
pp. 1215-1227 ◽  
Author(s):  
Neline Kriek ◽  
Leann Tilley ◽  
Paul Horrocks ◽  
Robert Pinches ◽  
Barry C. Elford ◽  
...  
Keyword(s):  
Cell Surface ◽  
Host Cell ◽  
Malaria Parasite ◽  
Host Cell Surface

scholarly journals Evidence for Antibiosis and Induced Host Defense Reactions in the Interaction Between Verticillium lecanii and Penicillium digitatum, the Causal Agent of Green Mold

2000 ◽  
Vol 90 (9) ◽  
pp. 932-943 ◽  
Author(s):  
Nicole Benhamou ◽  
Jacques Brodeur
Keyword(s):  
Plasma Membrane ◽  
Host Cell ◽  
De Novo ◽  
Penicillium Digitatum ◽  
Verticillium Lecanii ◽  
Intercellular Interaction ◽  
Green Mold ◽  
Transmission Electron ◽  
Host Cell Wall ◽  
Host Cell Surface

Chronological events of the intercellular interaction between Verticillium lecanii and the postharvest pathogen Penicillium digitatum were investigated by transmission electron microscopy and gold cytochemistry. Growth inhibition of P. oligandrum as a response to V. lecanii attack correlated with striking host changes including retraction of the plasma membrane and cytoplasm disorganization. Such changes were associated with the deposition on the inner host cell surface of a chitin- and cellulose-enriched material which appeared to be laid down as a structural defense reaction. The accumulation of chitin in the newly formed material correlated with a decrease in the amount of wallbound chitin. However, the deposition of cellulose appeared to correspond to a de novo synthesis, as evidenced by the occurrence of cellulose-containing vesicles which released their content in the space between the invaginated plasma membrane and the host cell wall. Results of the present study provide the first ultrastructural and cytochemical evidence that antagonism, triggered by V. lecanii, is a multifaceted process in which antibiosis, with alteration of the host hyphae prior to contact with the antagonist, appears to be the key process in the antagonism against P. digitatum.

scholarly journals Division and adaptation to host nutritional environment of apicomplexan parasites depend on apicoplast lipid metabolic plasticity and host organelles remodelling

2019 ◽  
Author(s):  
Souad Amiar ◽  
Nicholas J. Katris ◽  
Laurence Berry ◽  
Sheena Dass ◽  
Melanie J. Shears ◽  
...  
Keyword(s):  
Host Cell ◽  
De Novo ◽  
Acid Synthesis ◽  
Apicomplexan Parasites ◽  
Metabolic Plasticity ◽  
Lipid Source ◽  
Nutritional Conditions ◽  
Membrane Bound ◽  
Nutritional Environment

AbstractApicomplexan parasites are unicellular eukaryotes responsible for major human diseases including malaria and toxoplasmosis. Apicomplexan parasites must obtain and combine lipids both from host cell scavenging andde novosynthesis to maintain parasite propagation and survival within their human host. Major questions on the actual role for each lipid source or how these are regulated upon fluctuating host nutritional conditions remain unanswered. Characterization of an apicoplast acyltransferase TgATS2, shows that the apicoplast provides local (lyso)phosphatidic acid balance, which is required for the recruitment of a novel dynamin (TgDrpC) critical during parasite cytokinesis. Disruption of TgATS2 led parasites to shift metabolic lipid acquisition fromde novosynthesis towards host scavenging. Importantly, both lipid scavenging andde novosynthesis pathways exhibit major metabolic and cellular plasticity upon sensing host lipid-deprived environments through concomitant (i) up-regulation ofde novofatty acid synthesis capacities in the apicoplast, and (ii) parasite-driven host cell remodelling to generate multi-membrane-bound structures from host organelles that are imported towards the parasite.

scholarly journals Phospholipid Composition of PurifiedChlamydia trachomatis Mimics That of the Eucaryotic Host Cell

1998 ◽  
Vol 66 (8) ◽  
pp. 3727-3735 ◽  
Author(s):  
Grant M. Hatch ◽  
Grant McClarty
Keyword(s):  
Host Cell ◽  
Phospholipid Composition ◽  
Brefeldin A ◽  
Host Cells ◽  
Cho Cell ◽  
Experimental Conditions ◽  
Obligate Intracellular ◽  
Wide Range ◽  
Host Cell Surface ◽  
Cellular Phospholipid

ABSTRACT Chlamydia trachomatis is an obligate intracellular eubacterial parasite capable of infecting a wide range of eucaryotic host cells. Purified chlamydiae contain several lipids typically found in eucaryotes, and it has been established that eucaryotic lipids are transported from the host cell to the parasite. In this report, we examine the phospholipid composition of C. trachomatispurified from host cells grown under a variety of conditions in which the cellular phospholipid composition was altered. A mutant CHO cell line, with a thermolabile CDP-choline synthetase, was used to show that decreased host cell phosphatidylcholine levels had no significant effect on C. trachomatis growth. However, less phosphatidylcholine was transported to the parasite and purified elementary bodies contained decreased levels of phosphatidylcholine. Brefeldin A, fumonisin B1, and exogenous sphingomyelinase were used to alter levels of host cell sphingomyelin. None of the agents had a significant effect on C. trachomatisreplication. Treatment with fumonisin B1 and exogenous sphingomyelinase resulted in decreased levels of host cell sphingomyelin. This had no effect on glycerophospholipid trafficking to chlamydiae; however, sphingomyelin trafficking was reduced and elementary bodies purified from treated cells had reduced sphingomyelin content. Exposure to brefeldin A, which had no adverse effect on chlamydia growth, resulted in an increase in cellular levels of sphingomyelin and a concomitant increase in the amount of sphingomyelin in purified chlamydiae. Under the experimental conditions used, brefeldin A treatment had only a small effect on sphingomyelin trafficking to the host cell surface or to C. trachomatis. Thus, the final phospholipid composition of purified C. trachomatis mimics that of the host cell in which it is grown.

scholarly journals Infectious Keratitis: Secreted Bacterial Proteins That Mediate Corneal Damage

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Mary E. Marquart ◽  
Richard J. O'Callaghan
Keyword(s):  
Host Cell ◽  
Bacterial Infections ◽  
Cell Surface Molecules ◽  
Bacterial Proteins ◽  
Surface Molecules ◽  
Host Cell Death ◽  
Common Causes ◽  
Host Cell Surface ◽  
Stromal Collagen ◽  
Corneal Damage

Ocular bacterial infections are universally treated with antibiotics, which can eliminate the organism but cannot reverse the damage caused by bacterial products already present. The three very common causes of bacterial keratitis—Pseudomonas aeruginosa,Staphylococcus aureus, andStreptococcus pneumoniae—all produce proteins that directly or indirectly cause damage to the cornea that can result in reduced vision despite antibiotic treatment. Most, but not all, of these proteins are secreted toxins and enzymes that mediate host cell death, degradation of stromal collagen, cleavage of host cell surface molecules, or induction of a damaging inflammatory response. Studies of these bacterial pathogens have determined the proteins of interest that could be targets for future therapeutic options for decreasing corneal damage.

scholarly journals Entry, infection, replication, and egress of human polyomaviruses: an update

2017 ◽  
Vol 63 (3) ◽  
pp. 193-211 ◽  
Author(s):  
Soumen Bhattacharjee ◽  
Sutanuka Chattaraj
Keyword(s):  
Viral Infection ◽  
Host Cell ◽  
Decisive Role ◽  
Host Protein ◽  
Host Animal ◽  
Dna Viruses ◽  
The Family ◽  
Host Cell Surface ◽  
Membrane Bound

Polyomaviruses (PyVs), belonging to the family Polyomaviridae, are a group of small, nonenveloped, double-stranded, circular DNA viruses widely distributed in the vertebrates. PyVs cause no apparent disease in adult laboratory mice but cause a wide variety of tumors when artificially inoculated into neonates or semipermissive animals. A few human PyVs, such as BK, JC, and Merkel cell PyVs, have been unequivocally linked to pathogenesis under conditions of immunosuppression. Infection is thought to occur early in life and persists for the lifespan of the host. Over evolutionary time scales, it appears that PyVs have slowly co-evolved with specific host animal lineages. Host cell surface glycoproteins and glycolipids seem to play a decisive role in the entry stage of viral infection and in channeling the virions to specific intracellular membrane-bound compartments and ultimately to the nucleus, where the genomes are replicated and packaged for release. Therefore the transport of the infecting virion or viral genome to this site of multiplication is an essential process in productive viral infection as well as in latent infection and transformation. This review summarizes the major findings related to the characterization of the nature of the interactions between PyV and host protein and their impact in host cell invasion.

scholarly journals Transcriptional Studies on Trypanosoma cruzi – Host Cell Interactions: A Complex Puzzle of Variables

2021 ◽  
Vol 11 ◽  
Author(s):  
María Gabriela Libisch ◽  
Natalia Rego ◽  
Carlos Robello
Keyword(s):  
Trypanosoma Cruzi ◽  
Host Cell ◽  
Protozoan Parasite ◽  
Cell Interactions ◽  
Host Cells ◽  
Molecular Signaling ◽  
Cell Type ◽  
Experimental Conditions ◽  
Functional Studies ◽  
Host Cell Interactions

Chagas Disease, caused by the protozoan parasite Trypanosoma cruzi, affects nearly eight million people in the world. T. cruzi is a complex taxon represented by different strains with particular characteristics, and it has the ability to infect and interact with almost any nucleated cell. The T. cruzi-host cell interactions will trigger molecular signaling cascades in the host cell that will depend on the particular cell type and T. cruzi strain, and also on many different experimental variables. In this review we collect data from multiple transcriptomic and functional studies performed in different infection models, in order to highlight key differences between works that in our opinion should be addressed when comparing and discussing results. In particular, we focus on changes in the respiratory chain and oxidative phosphorylation of host cells in response to infection, which depends on the experimental model of T. cruzi infection. Finally, we also discuss host cell responses which reiterate independently of the strain, cell type and experimental conditions.

Burkholderia pseudomallei-induced cell fusion in U937 macrophages can be inhibited by monoclonal antibodies against host cell surface molecules

2011 ◽  
Vol 13 (12-13) ◽  
pp. 1006-1011 ◽  
Author(s):  
Supaporn Suparak ◽  
Veerachat Muangsombut ◽  
Donporn Riyapa ◽  
Joanne M. Stevens ◽  
Mark P. Stevens ◽  
...  
Keyword(s):  
Monoclonal Antibodies ◽  
Cell Surface ◽  
Host Cell ◽  
Cell Fusion ◽  
Burkholderia Pseudomallei ◽  
Cell Surface Molecules ◽  
Surface Molecules ◽  
Host Cell Surface
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