scholarly journals Lipid rafts and pathogens: the art of deception and exploitation

2019 ◽  
Vol 61 (5) ◽  
pp. 601-610 ◽  
Author(s):  
Michael I. Bukrinsky ◽  
Nigora Mukhamedova ◽  
Dmitri Sviridov
Keyword(s):  
Immune Response ◽  
Plasma Membrane ◽  
Host Cell ◽  
Lipid Rafts ◽  
Therapeutic Approach ◽  
Host Cells ◽  
Infectious Agents ◽  
Systematic Overview ◽  
Intracellular Parasites ◽  
A Cell

Lipid rafts, solid regions of the plasma membrane enriched in cholesterol and glycosphingolipids, are essential parts of a cell. Functionally, lipid rafts present a platform that facilitates interaction of cells with the outside world. However, the unique properties of lipid rafts required to fulfill this function at the same time make them susceptible to exploitation by pathogens. Many steps of pathogen interaction with host cells, and sometimes all steps within the entire lifecycle of various pathogens, rely on host lipid rafts. Such steps as binding of pathogens to the host cells, invasion of intracellular parasites into the cell, the intracellular dwelling of parasites, microbial assembly and exit from the host cell, and microbe transfer from one cell to another all involve lipid rafts. Interaction also includes modification of lipid rafts in host cells, inflicted by pathogens from both inside and outside the cell, through contact or remotely, to advance pathogen replication, to utilize cellular resources, and/or to mitigate immune response. Here, we provide a systematic overview of how and why pathogens interact with and exploit host lipid rafts, as well as the consequences of this interaction for the host, locally and systemically, and for the microbe. We also raise the possibility of modulation of lipid rafts as a therapeutic approach against a variety of infectious agents.

Ultrastructure of compatible and incompatible reactions of sunflower to Plasmopara halstedii

1979 ◽  
Vol 57 (4) ◽  
pp. 315-323 ◽  
Author(s):  
Glenn Wehtje ◽  
Larry J. Littlefield ◽  
David E. Zimmer
Keyword(s):  
Cell Wall ◽  
Plasma Membrane ◽  
Host Cell ◽  
Epidermal Cell ◽  
Cortical Cell ◽  
Hypersensitive Reaction ◽  
Host Cells ◽  
Plasmopara Halstedii ◽  
Host Cell Wall ◽  
Host Plasma Membrane

Penetration of sunflower, Heliantluis animus, root epidermal cells by zoospores of Plasmopara halstedii is preceded by formation of a papilla on the inner surface of the host cell wall that invaginates the host plasma membrane. Localized degradation and penetration of the host cell wall by the pathogen follow. The invading fungus forms an allantoid primary infection vesicle in the penetrated epidermal cell. The host plasma membrane invaginates around the infection vesicle but its continuity is difficult to follow. Upon exit from the epidermal cell the fungus may grow intercellularly, producing terminal haustorial branches which extend into adjacent host cells. The fungus may grow through one or two cortical cell is after growing from the epidermal cell before it becomes intercellular. Host plasma membrane is not penetrated by haustoria. Intercellular hyphae grow toward the apex of the plant and ramify the seedling tissue. Resistance in an immune cultivar is hypersensitive and is triggered upon contact of the host cell with the encysting zoospore before the host cell wall is penetrated. Degeneration of zoospore cytoplasm accompanies the hypersensitive reaction of the host. Zoospores were often parasitized by bacteria and did not germinate unless penicillin and streptomycin were added to the inoculum suspension.

Regulation of ecto-5′-nucleotidase activity via Ca2+-dependent, annexin 2-mediated membrane rearrangement?

2006 ◽  
Vol 34 (3) ◽  
pp. 374-376 ◽  
Author(s):  
E.B. Babiychuk ◽  
A. Draeger
Keyword(s):  
Signal Transduction ◽  
Plasma Membrane ◽  
Lipid Rafts ◽  
Binding Proteins ◽  
Extracellular Atp ◽  
Membrane Rafts ◽  
Nucleotidase Activity ◽  
Annexin 2 ◽  
Associated Proteins ◽  
A Cell

The spatial segregation of the plasma membrane plays a prominent role in distinguishing and sorting a large number of signals a cell receives simultaneously. The plasma membrane comprises regions known as lipid rafts, which serve as signal-transduction hubs and platforms for sorting membrane-associated proteins. Ca2+-binding proteins of the annexin family have been ascribed a role in the regulation of raft dynamics. Glycosylphosphatidylinositol-anchored 5′-nucleotidase is an extracellular, raft-associated enzyme responsible for conversion of extracellular ATP into adenosine. Our results point to a regulation of ecto-5′-nucleotidase activity by Ca2+-dependent, annexin-mediated stabilization of membrane rafts.

The cell as an extreme environment

1979 ◽  
Vol 204 (1155) ◽  
pp. 199-210 ◽  
Keyword(s):  
Host Cell ◽  
Extreme Environments ◽  
Extreme Environment ◽  
Host Cells ◽  
Limiting Factors ◽  
Limiting Factor ◽  
Free Access ◽  
Fitness Traits ◽  
Intracellular Parasites ◽  
The Face

Living cells and their intracellular parasites show many of the characteristics ascribed to extreme environments and their dominant species. The diversity of species colonizing intracellular habitats is low, and successful inhabitants exhibit special fitness traits that often render them obligately dependent on residence within a host cell. However, the diversity-limiting factor in the extreme environment of the host cell interior is not abiotic, as it is in conventional extreme environments. It is biotic: the living cell itself and its many activities. Host cells bar the entrance to most would-be parasites, they destroy most of those that do manage to get inside, and they deny parasites free access to many components of their soluble metabolite pools. Successful intracellular parasites have evolved fitness traits that give them the capacity to survive in the face of diversity-limiting factors or to modify the intracellular habitat so that those factors no longer operate. Looking on the cell as an extreme habitat emphasizes its simultaneous roles as environment, antagonist, and competitor.

scholarly journals Invasion by Toxoplasma gondii Establishes a Moving Junction That Selectively Excludes Host Cell Plasma Membrane Proteins on the Basis of Their Membrane Anchoring

1999 ◽  
Vol 190 (12) ◽  
pp. 1783-1792 ◽  
Author(s):  
Dana G. Mordue ◽  
Naishadh Desai ◽  
Michael Dustin ◽  
L. David Sibley
Keyword(s):  
Plasma Membrane ◽  
Toxoplasma Gondii ◽  
Host Cell ◽  
Transmembrane Domain ◽  
Membrane Lipids ◽  
Transmembrane Proteins ◽  
Host Cells ◽  
Cell Plasma Membrane ◽  
Cell Plasma ◽  
Membrane Anchoring

The protozoan parasite Toxoplasma gondii actively penetrates its host cell by squeezing through a moving junction that forms between the host cell plasma membrane and the parasite. During invasion, this junction selectively controls internalization of host cell plasma membrane components into the parasite-containing vacuole. Membrane lipids flowed past the junction, as shown by the presence of the glycosphingolipid GM1 and the cationic lipid label 1.1′-dihexadecyl-3-3′-3-3′-tetramethylindocarbocyanine (DiIC16). Glycosylphosphatidylinositol (GPI)-anchored surface proteins, such as Sca-1 and CD55, were also readily incorporated into the parasitophorous vacuole (PV). In contrast, host cell transmembrane proteins, including CD44, Na+/K+ ATPase, and β1-integrin, were excluded from the vacuole. To eliminate potential differences in sorting due to the extracellular domains, parasite invasion was examined in host cells transfected with recombinant forms of intercellular adhesion molecule 1 (ICAM-1, CD54) that differed in their mechanism of membrane anchoring. Wild-type ICAM-1, which contains a transmembrane domain, was excluded from the PV, whereas both GPI-anchored ICAM-1 and a mutant of ICAM-1 missing the cytoplasmic tail (ICAM-1–Cyt−) were readily incorporated into the PV membrane. Our results demonstrate that during host cell invasion, Toxoplasma selectively excludes host cell transmembrane proteins at the moving junction by a mechanism that depends on their anchoring in the membrane, thereby creating a nonfusigenic compartment.

scholarly journals Molecular cloning and characterization ofNcROP2Fam-1, a member of the ROP2 family of rhoptry proteins inNeospora caninumthat is targeted by antibodies neutralizing host cell invasionin vitro

Parasitology ◽  
2013 ◽  
Vol 140 (8) ◽  
pp. 1033-1050 ◽  
Author(s):  
FERIAL ALAEDDINE ◽  
ANDREW HEMPHILL ◽  
KARIM DEBACHE ◽  
CHRISTOPHE GUIONAUD
Keyword(s):  
Host Cell ◽  
Family Member ◽  
Vaccine Candidate ◽  
Neospora Caninum ◽  
Parasitophorous Vacuole ◽  
Host Cells ◽  
General Belief ◽  
Intracellular Parasites ◽  
Promising Vaccine Candidate

SUMMARYRecent publications demonstrated that a fragment of aNeospora caninumROP2 family member antigen represents a promising vaccine candidate. We here report on the cloning of the cDNA encoding this protein,N. caninumROP2 family member 1 (NcROP2Fam-1), its molecular characterization and localization. The protein possesses the hallmarks of ROP2 family members and is apparently devoid of catalytic activity. NcROP2Fam-1 is synthesized as a pre-pro-protein that is matured to 2 proteins of 49 and 55 kDa that localize to rhoptry bulbs. Upon invasion the protein is associated with the nascent parasitophorous vacuole membrane (PVM), evacuoles surrounding the host cell nucleus and, in some instances, the surface of intracellular parasites. Staining was also observed within the cyst wall of ‘cysts’ producedin vitro. Interestingly, NcROP2Fam-1 was also detected on the surface of extracellular parasites entering the host cells and antibodies directed against NcROP2Fam-1-specific peptides partially neutralized invasionin vitro. We conclude that, in spite of the general belief that ROP2 family proteins are intracellular antigens, NcROP2Fam-1 can also be considered as an extracellular antigen, a property that should be taken into account in further experiments employing ROP2 family proteins as vaccines.

Trypanosoma cruzi does not induce apoptosis in murine fibroblasts

Parasitology ◽  
1999 ◽  
Vol 118 (2) ◽  
pp. 167-175 ◽  
Author(s):  
R. K. CLARK ◽  
R. E. KUHN
Keyword(s):  
Trypanosoma Cruzi ◽  
Host Cell ◽  
Cell Apoptosis ◽  
Membrane Integrity ◽  
Host Cells ◽  
Mammalian Host ◽  
Host Cell Apoptosis ◽  
Intracellular Parasites ◽  
Murine Fibroblasts ◽  
Infected Cells

The intracellular cycle of Trypanosoma cruzi in mammalian host cells involves the differentiation of dividing amastigote forms into flagellated trypomastigote forms. The mechanism(s) regulating the growth and differentiation of the intracellular parasites is (are) not known. The number of parasites in infected cells can be several hundred and may be enough to induce apoptosis, a suicide-like death programme, generating products (e.g. nuclear proteins) that could function as signals to initiate the differentiation of amastigotes into trypomastigotes. Murine fibroblasts infected with T. cruzi were examined during a 5-day course of infection for evidence of apoptosis. However, characteristics of apoptosis, including degeneration of nuclear structure, condensation of chromatin, loss of plasma membrane integrity, or the cleavage of DNA into nucleosomal fragments, were not observed. Therefore, it is unlikely that products resulting from host cell apoptosis function to induce parasite differentiation. The possibility that T. cruzi might inhibit host cell apoptosis by increasing intracellular levels of Bcl-2, an endogenous inhibitor of apoptosis, was then investigated. Analysis of infected cells by flow cytometry did not demonstrate a significant amount of intracellular Bcl-2. This suggests that if the parasite is inhibiting host cell apoptosis, it is by a method that does not involve increasing levels of Bcl-2.

scholarly journals The Nascent Parasitophorous Vacuole Membrane of Encephalitozoon cuniculi Is Formed by Host Cell Lipids and Contains Pores Which Allow Nutrient Uptake

2008 ◽  
Vol 7 (6) ◽  
pp. 1001-1008 ◽  
Author(s):  
Karin Rönnebäumer ◽  
Uwe Gross ◽  
Wolfgang Bohne
Keyword(s):  
Plasma Membrane ◽  
Host Cell ◽  
Fluorescent Dyes ◽  
Parasitophorous Vacuole ◽  
Time Lapse ◽  
Host Cells ◽  
Encephalitozoon Cuniculi ◽  
Invasion Mechanism ◽  
Cell Plasma ◽  
Metabolite Exchange

ABSTRACT Microsporidia are obligate intracellular pathogens which enter host cells by the discharge of a hollow tube through which the sporoplasma is extruded into the host cell. Since this invasion mechanism is very different from common entry strategies, the formation of the parasitophorous vacuole (PV) in Encephalitozoon species is likely to be distinct from known principles. We investigated the origin of the nascent Encephalitozoon cuniculi PV membrane with the aid of fluorescent lipid probes. When Bodipy 500/510-C12-HPC-labeled spores were used for infection, the emerging PV membrane was unlabeled, suggesting that sporoplasma-derived lipids do not significantly contribute to the formation of the PV membrane. In contrast, when raft and nonraft microdomains of the host cell plasma membrane were selectively labeled with DiIC16 and Speedy DiO, both tracers were detectable in the nascent PV membrane shortly after infection, indicating that the bulk lipids of the PV membrane are host cell derived. Time-lapse fluorescence microscopy revealed that the formation of the PV membrane is a fast event (<1.3 s), which occurred simultaneously with the extrusion of the sporoplasma. The portion of the discharged tube which is in contact with the host cell was found to be coated with labeled host cell lipids, which might be an indication for a plasma membrane invagination at the contact site. To investigate the presence of pores in the E. cuniculi PV membrane, we microinjected fluorescent dyes of different sizes into infected host cells. A 0.5-kDa dextran as well as 0.8- to 1.1-kDa peptides could rapidly enter the PV, while a 10-kDa dextran was stably excluded from the PV lumen, indicating that the PV membrane possesses pores with an exclusion size of <10 kDa, which should allow metabolite exchange.

scholarly journals From infection to cancer: how DNA tumour viruses alter host cell central carbon and lipid metabolism

Open Biology ◽  
2021 ◽  
Vol 11 (3) ◽  
Author(s):  
Kamini L. Magon ◽  
Joanna L. Parish
Keyword(s):  
Host Cell ◽  
Cell Metabolism ◽  
Life Cycles ◽  
Host Cells ◽  
Barr Virus ◽  
Cell Functions ◽  
Intracellular Parasites ◽  
B Virus ◽  
Central Carbon ◽  
Epstein Barr

Infections cause 13% of all cancers globally, and DNA tumour viruses account for almost 60% of these cancers. All viruses are obligate intracellular parasites and hijack host cell functions to replicate and complete their life cycles to produce progeny virions. While many aspects of viral manipulation of host cells have been studied, how DNA tumour viruses manipulate host cell metabolism and whether metabolic alterations in the virus life cycle contribute to carcinogenesis are not well understood. In this review, we compare the differences in central carbon and fatty acid metabolism in host cells following infection, oncogenic transformation, and virus-driven cancer of DNA tumour viruses including: Epstein–Barr virus, hepatitis B virus, human papillomavirus, Kaposi's sarcoma-associated herpesvirus and Merkel cell polyomavirus.

scholarly journals Relevance of host cell surface glycan structure for cell specificity of influenza A virus

2017 ◽  
Author(s):  
Markus Kastner ◽  
Andreas Karner ◽  
Rong Zhu ◽  
Qiang Huang ◽  
Dandan Zhang ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Host Cell ◽  
Influenza A ◽  
Host Cells ◽  
Cell Contact ◽  
Glycan Structure ◽  
Cell Binding ◽  
Receptor Specificity ◽  
Cell Specificity ◽  
Binding Preference

AbstractInfluenza A viruses (IAV) initiate infection via binding of the viral hemagglutinin (HA) to sialylated glycan receptors on host cells. HAs receptor specificity towards sialic acid (SA) is well studied and clearly critical for virus infection, but the contribution of the highly complex cellular plasma membrane to the cellular specificity remains elusive. In addition, some studies indicated that other host cell factors such as the epidermal growth factor receptor might contribute to the initial virus-cell contact and further downstream signaling1.Here we use two complementary methods, glycan arrays and single-virus force spectroscopy (SVFS) to compare influenza virus receptor specificity with actual host cell binding. Unexpectedly, our study reveals that HAs receptor binding preference does not necessarily reflect virus-cell specificity. We propose SVFS as a tool to elucidate the cell binding preference of IAV thereby including the complex environment of sialylated receptors within the plasma membrane of living cells.

scholarly journals The autophagic machinery ensures nonlytic transmission of mycobacteria

2015 ◽  
Vol 112 (7) ◽  
pp. E687-E692 ◽  
Author(s):  
Lilli Gerstenmaier ◽  
Rachel Pilla ◽  
Lydia Herrmann ◽  
Hendrik Herrmann ◽  
Monica Prado ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Host Cell ◽  
Bacterial Pathogens ◽  
Host Cells ◽  
Phagocytic Cells ◽  
Ejection Process ◽  
Cell Transmission ◽  
Host Plasma Membrane

In contrast to mechanisms mediating uptake of intracellular bacterial pathogens, bacterial egress and cell-to-cell transmission are poorly understood. Previously, we showed that the transmission of pathogenic mycobacteria between phagocytic cells also depends on nonlytic ejection through an F-actin based structure, called the ejectosome. How the host cell maintains integrity of its plasma membrane during the ejection process was unknown. Here, we reveal an unexpected function for the autophagic machinery in nonlytic spreading of bacteria. We show that ejecting mycobacteria are escorted by a distinct polar autophagocytic vacuole. If autophagy is impaired, cell-to-cell transmission is inhibited, the host plasma membrane becomes compromised and the host cells die. These findings highlight a previously unidentified, highly ordered interaction between bacteria and the autophagic pathway and might represent the ancient way to ensure nonlytic egress of bacteria.

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