Journal articles on the topic 'Intracellular spread'
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Minton, Kirsty. "Intracellular tunnels spread disease." Nature Reviews Molecular Cell Biology 17, no. 10 (September 1, 2016): 609. http://dx.doi.org/10.1038/nrm.2016.124.
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Pieper, Rembert, C. R. Fisher, Moo-Jin Suh, S. T. Huang, P. Parmar, and S. M. Payne. "Analysis of the Proteome of Intracellular Shigella flexneri Reveals Pathways Important for Intracellular Growth." Infection and Immunity 81, no. 12 (October 7, 2013): 4635–48. http://dx.doi.org/10.1128/iai.00975-13.
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ABSTRACTGlobal proteomic analysis was performed withShigella flexneristrain 2457T in association with three distinct growth environments:S. flexnerigrowing in broth (in vitro),S. flexnerigrowing within epithelial cell cytoplasm (intracellular), andS. flexnerithat were cultured with, but did not invade, Henle cells (extracellular). Compared toin vitroand extracellular bacteria, intracellular bacteria had increased levels of proteins required for invasion and cell-to-cell spread, including Ipa, Mxi, and Ics proteins. Changes in metabolic pathways in response to the intracellular environment also were evident. There was an increase in glycogen biosynthesis enzymes, altered expression of sugar transporters, and a reduced amount of the carbon storage regulator CsrA. Mixed acid fermentation enzymes were highly expressed intracellularly, while tricarboxylic acid (TCA) cycle oxidoreductive enzymes and most electron transport chain proteins, except CydAB, were markedly decreased. This suggested that fermentation and the CydAB system primarily sustain energy generation intracellularly. Elevated levels of PntAB, which is responsible for NADPH regeneration, suggested a shortage of reducing factors for ATP synthesis. These metabolic changes likely reflect changes in available carbon sources, oxygen levels, and iron availability. Intracellular bacteria showed strong evidence of iron starvation. Iron acquisition systems (Iut, Sit, FhuA, and Feo) and the iron starvation, stress-associated Fe-S cluster assembly (Suf) protein were markedly increased in abundance. Mutational analysis confirmed that the mixed-acid fermentation pathway was required for wild-type intracellular growth and spread ofS. flexneri. Thus, iron stress and changes in carbon metabolism may be key factors in theS. flexneritransition from the extra- to the intracellular milieu.
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Keegan, Richard M., Lillian R. Talbot, Yung-Heng Chang, Michael J. Metzger, and Josh Dubnau. "Intercellular viral spread and intracellular transposition of Drosophila gypsy." PLOS Genetics 17, no. 4 (April 22, 2021): e1009535. http://dx.doi.org/10.1371/journal.pgen.1009535.
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It has become increasingly clear that retrotransposons (RTEs) are more widely expressed in somatic tissues than previously appreciated. RTE expression has been implicated in a myriad of biological processes ranging from normal development and aging, to age related diseases such as cancer and neurodegeneration. Long Terminal Repeat (LTR)-RTEs are evolutionary ancestors to, and share many features with, exogenous retroviruses. In fact, many organisms contain endogenous retroviruses (ERVs) derived from exogenous retroviruses that integrated into the germ line. These ERVs are inherited in Mendelian fashion like RTEs, and some retain the ability to transmit between cells like viruses, while others develop the ability to act as RTEs. The process of evolutionary transition between LTR-RTE and retroviruses is thought to involve multiple steps by which the element loses or gains the ability to transmit copies between cells versus the ability to replicate intracellularly. But, typically, these two modes of transmission are incompatible because they require assembly in different sub-cellular compartments. Like murine IAP/IAP-E elements, the gypsy family of retroelements in arthropods appear to sit along this evolutionary transition. Indeed, there is some evidence that gypsy may exhibit retroviral properties. Given that gypsy elements have been found to actively mobilize in neurons and glial cells during normal aging and in models of neurodegeneration, this raises the question of whether gypsy replication in somatic cells occurs via intracellular retrotransposition, intercellular viral spread, or some combination of the two. These modes of replication in somatic tissues would have quite different biological implications. Here, we demonstrate that Drosophila gypsy is capable of both cell-associated and cell-free viral transmission between cultured S2 cells of somatic origin. Further, we demonstrate that the ability of gypsy to move between cells is dependent upon a functional copy of its viral envelope protein. This argues that the gypsy element has transitioned from an RTE into a functional endogenous retrovirus with the acquisition of its envelope gene. On the other hand, we also find that intracellular retrotransposition of the same genomic copy of gypsy can occur in the absence of the Env protein. Thus, gypsy exhibits both intracellular retrotransposition and intercellular viral transmission as modes of replicating its genome.
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Weddle, Erin, and Hervé Agaisse. "Principles of intracellular bacterial pathogen spread from cell to cell." PLOS Pathogens 14, no. 12 (December 13, 2018): e1007380. http://dx.doi.org/10.1371/journal.ppat.1007380.
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Ireton, Keith. "Molecular mechanisms of cell–cell spread of intracellular bacterial pathogens." Open Biology 3, no. 7 (July 2013): 130079. http://dx.doi.org/10.1098/rsob.130079.
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Several bacterial pathogens, including Listeria monocytogenes , Shigella flexneri and Rickettsia spp., have evolved mechanisms to actively spread within human tissues. Spreading is initiated by the pathogen-induced recruitment of host filamentous (F)-actin. F-actin forms a tail behind the microbe, propelling it through the cytoplasm. The motile pathogen then encounters the host plasma membrane, forming a bacterium-containing protrusion that is engulfed by an adjacent cell. Over the past two decades, much progress has been made in elucidating mechanisms of F-actin tail formation. Listeria and Shigella produce tails of branched actin filaments by subverting the host Arp2/3 complex. By contrast, Rickettsia forms tails with linear actin filaments through a bacterial mimic of eukaryotic formins. Compared with F-actin tail formation, mechanisms controlling bacterial protrusions are less well understood. However, recent findings have highlighted the importance of pathogen manipulation of host cell–cell junctions in spread. Listeria produces a soluble protein that enhances bacterial protrusions by perturbing tight junctions. Shigella protrusions are engulfed through a clathrin-mediated pathway at ‘tricellular junctions’—specialized membrane regions at the intersection of three epithelial cells. This review summarizes key past findings in pathogen spread, and focuses on recent developments in actin-based motility and the formation and internalization of bacterial protrusions.
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Roos, Tomas T., Megg G. Garcia, Isak Martinsson, Rana Mabrouk, Bodil Israelsson, Tomas Deierborg, Asgeir Kobro-Flatmoen, Heikki Tanila, and Gunnar K. Gouras. "Neuronal spreading and plaque induction of intracellular Aβ and its disruption of Aβ homeostasis." Acta Neuropathologica 142, no. 4 (July 16, 2021): 669–87. http://dx.doi.org/10.1007/s00401-021-02345-9.
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AbstractThe amyloid-beta peptide (Aβ) is thought to have prion-like properties promoting its spread throughout the brain in Alzheimer’s disease (AD). However, the cellular mechanism(s) of this spread remains unclear. Here, we show an important role of intracellular Aβ in its prion-like spread. We demonstrate that an intracellular source of Aβ can induce amyloid plaques in vivo via hippocampal injection. We show that hippocampal injection of mouse AD brain homogenate not only induces plaques, but also damages interneurons and affects intracellular Aβ levels in synaptically connected brain areas, paralleling cellular changes seen in AD. Furthermore, in a primary neuron AD model, exposure of picomolar amounts of brain-derived Aβ leads to an apparent redistribution of Aβ from soma to processes and dystrophic neurites. We also observe that such neuritic dystrophies associate with plaque formation in AD-transgenic mice. Finally, using cellular models, we propose a mechanism for how intracellular accumulation of Aβ disturbs homeostatic control of Aβ levels and can contribute to the up to 10,000-fold increase of Aβ in the AD brain. Our data indicate an essential role for intracellular prion-like Aβ and its synaptic spread in the pathogenesis of AD.
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Meyer, Diane Hutchins, John E. Rose, Joan E. Lippmann, and Paula M. Fives-Taylor. "Microtubules Are Associated with Intracellular Movement and Spread of the Periodontopathogen Actinobacillus actinomycetemcomitans." Infection and Immunity 67, no. 12 (December 1, 1999): 6518–25. http://dx.doi.org/10.1128/iai.67.12.6518-6525.1999.
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ABSTRACT Actinobacillus actinomycetemcomitans SUNY 465, the invasion prototype strain, enters epithelial cells by an actin-dependent mechanism, escapes from the host cell vacuole, and spreads intracellularly and to adjacent epithelial cells via intercellular protrusions. Internalized organisms also egress from host cells into the assay medium via protrusions that are associated with just a single epithelial cell. Here we demonstrate that agents which inhibit microtubule polymerization (e.g., colchicine) and those which stabilize polymerized microtubules (e.g., taxol) both increase markedly the number of intracellular A. actinomycetemcomitansorganisms. Furthermore, both colchicine and taxol prevented the egression of A. actinomycetemcomitans from host cells into the assay medium. Immunofluorescence microscopy revealed that protrusions that mediate the bacterial spread contain microtubules.A. actinomycetemcomitans SUNY 465 and 652, strains that are both invasive and egressive, interacted specifically with the plus ends (growing ends) of the filaments of microtubule asters in a KB cell extract. By contrast, neither A. actinomycetemcomitans 523, a strain that is invasive but not egressive, nor Haemophilus aphrophilus, a noninvasive oral bacterium with characteristics similar to those of A. actinomycetemcomitans, bound to microtubules. Together these data suggest that microtubules function in the spread and movement of A. actinomycetemcomitans and provide the first evidence that host cell dispersion of an invasive bacterium may involve the usurption of host cell microtubules.
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Reeves, Stephanie A., Alfredo G. Torres, and Shelley M. Payne. "TonB Is Required for Intracellular Growth and Virulence of Shigella dysenteriae." Infection and Immunity 68, no. 11 (November 1, 2000): 6329–36. http://dx.doi.org/10.1128/iai.68.11.6329-6336.2000.
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ABSTRACT To assess the importance of TonB-dependent iron transport systems to growth of Shigella in vivo, a tonB mutant ofShigella dysenteriae was isolated and tested in cultured cells. The tonB mutant invaded epithelial cells, but did not form plaques in confluent monolayers of Henle cells, indicating an inability of this mutant to spread from cell to cell. The rate of intracellular multiplication of the tonB mutant was reduced significantly compared to that of the wild type. The loss of virulence in the tonB mutant was not due to loss of either Shu or Ent, the TonB-dependent systems which allow for transport of heme and ferrienterobactin, respectively. A shuA mutant lacking the outer membrane receptor for heme, an entB mutant defective in enterobactin synthesis, and a shuA entB double mutant each were able to invade cultured cells, multiply intracellularly, and form wild-type plaques. The ability of S. dysenteriae to access iron during intracellular growth was assessed by flow cytometric analysis of an iron- and Fur-regulated shuA-gfp reporter construct. Low levels of green fluorescent protein expression in the intracellular environment were observed in all strains, indicating that iron is available to intracellular bacteria, even in the absence of TonB-dependent iron transport. The failure of the tonBmutant to grow well in an iron-replete intracellular environment suggests that TonB plays a role in addition to heme- and siderophore-mediated iron acquisition in vivo, and this function is required for the intracellular growth and intercellular spread ofS. dysenteriae.
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Drevets, Douglas A., Todd A. Jelinek, and Nancy E. Freitag. "Listeria monocytogenes-Infected Phagocytes Can Initiate Central Nervous System Infection in Mice." Infection and Immunity 69, no. 3 (March 1, 2001): 1344–50. http://dx.doi.org/10.1128/iai.69.3.1344-1350.2001.
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ABSTRACT Listeria monocytogenes-infected phagocytes are present in the bloodstream of experimentally infected mice, but whether they play a role in central nervous system (CNS) invasion is unclear. To test whether bacteria within infected leukocytes could establish CNS infection, experimentally infected mice were treated with gentamicin delivered by surgically implanted osmotic pumps. Bacterial inhibitory titers in serum and plasma ranged from 1:16 to 1:256, and essentially all viable bacteria in the bloodstream of treated mice were leukocyte associated. Nevertheless, CNS infection developed in gentamicin-treated animals infected intraperitoneally or by gastric lavage, suggesting that intracellular bacteria could be responsible for neuroinvasion. This was supported by data showing that 43.5% of bacteria found with blood leukocytes were intracellular and some colocalized with F-actin, indicating productive intracellular parasitism. Experiments using an L. monocytogenes strain containing a chromosomal actA-gfpuv-plcB transcriptional fusion showed that blood leukocytes were associated with intracellular and extracellularly bound green fluorescent protein-expressing (GFP+) bacteria. Treatment with gentamicin decreased the numbers of extracellularly bound GFP+ bacteria significantly but did not affect the numbers of intracellular GFP+ bacteria, suggesting that the latter were the result of intercellular spread of GFP+ bacteria to leukocytes. These data demonstrate that infected leukocytes and the intracellularL. monocytogenes harbored within them play key roles in neuroinvasion. Moreover, they suggest that phagocytes recruited to infected organs such as the liver or spleen are themselves parasitized by intercellular spread of L. monocytogenes and then reenter the bloodstream and contribute to the systemic dissemination of bacteria.
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Zeldovich, Varvara B., Jennifer R. Robbins, Mirhan Kapidzic, Peter Lauer, and Anna I. Bakardjiev. "Invasive Extravillous Trophoblasts Restrict Intracellular Growth and Spread of Listeria monocytogenes." PLoS Pathogens 7, no. 3 (March 3, 2011): e1002005. http://dx.doi.org/10.1371/journal.ppat.1002005.
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Wang, Jiahui, Jane E. King, Marie Goldrick, Martin Lowe, Frank B. Gertler, and Ian S. Roberts. "Lamellipodin Is Important for Cell-to-Cell Spread and Actin-Based Motility in Listeria monocytogenes." Infection and Immunity 83, no. 9 (July 13, 2015): 3740–48. http://dx.doi.org/10.1128/iai.00193-15.
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Listeria monocytogenesis a foodborne pathogen capable of invading a broad range of cell types and replicating within the host cell cytoplasm. This paper describes the colocalization of host cell lamellipodin (Lpd) with intracellularL. monocytogenesdetectable 6 h postinfection of epithelial cells. The association was mediated via interactions between both the peckstrin homology (PH) domain in Lpd and phosphatidylinositol (3,4)-bisphosphate [PI(3,4)P2] on the bacterial surface and by interactions between the C-terminal EVH1 (Ena/VASP [vasodilator-stimulated phosphoprotein] homology domain 1) binding domains of Lpd and the host VASP (vasodilator-stimulated phosphoprotein) recruited to the bacterial cell surface by the listerial ActA protein. Depletion of Lpd by short interfering RNA (siRNA) resulted in reduced plaque size and number, indicating a role for Lpd in cell-to-cell spread. In contrast, overexpression of Lpd resulted in an increase in the number ofL. monocytogenes-containing protrusions (listeriopods). Manipulation of the levels of Lpd within the cell also affected the intracellular velocity ofL. monocytogenes, with a reduction in Lpd corresponding to an increase in intracellular velocity. These data, together with the observation that Lpd accumulated at the interface between the bacteria and the developing actin tail at the initiation of actin-based movement, indicate a possible role for Lpd in the actin-based movement and the cell-to-cell spread ofL. monocytogenes.
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Polymenidou, Magdalini, and Don W. Cleveland. "Prion-like spread of protein aggregates in neurodegeneration." Journal of Experimental Medicine 209, no. 5 (May 7, 2012): 889–93. http://dx.doi.org/10.1084/jem.20120741.
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Protein misfolding is common to most neurodegenerative diseases, including Alzheimer’s and Parkinson’s diseases. Recent work using animal models with intracellular α-synuclein and tau inclusions adds decisively to a growing body of evidence that misfolded protein aggregates can induce a self-perpetuating process that leads to amplification and spreading of pathological protein assemblies. When coupled with the progressive nature of neurodegeneration, recognition of such cell-to-cell aggregate spread suggests a unifying mechanism underlying the pathogenesis of these disorders.
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Burt, J. M. "Block of intercellular communication: interaction of intracellular H+ and Ca2+." American Journal of Physiology-Cell Physiology 253, no. 4 (October 1, 1987): C607—C612. http://dx.doi.org/10.1152/ajpcell.1987.253.4.c607.
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The influence of elevated intracellular levels of H+ and Ca2+ on intercellular communication between cultured neonatal rat myocardial cells was examined by quantifying the percent of primary neighboring cells to which intracellularly injected Lucifer yellow had spread within 10 s of injection. Partial acidosis was induced by incubation in and then removal of NH4Cl. Intracellular Ca2+ was raised through the use of treatments that are standard in studies of heart muscle: reduction of the Na+ gradient, addition of caffeine, and combinations of these interventions. Under control conditions and during application of NH4Cl, cells exhibited spontaneous electrical and contractile activity and were well coupled (dye detectable in 100% of primary neighbors). Sustained intracellular acidosis without simultaneous elevation of intracellular Ca2+ (NH4Cl exposure followed by zero Na+, zero Ca2+) reduced the incidence of dye transfer to 90%. Elevation of intracellular Ca2+ (exposure to zero Na+, Ca2+-containing solution, with or without 10 mM caffeine) had no effect on coupling. These same interventions, when employed together, reduced the incidence of dye coupling to 18%. The results are consistent with a synergism of action of Ca2+ and H+ in the regulation of junctional permeability.
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Mastroeni, Pietro, Andrew Grant, Olivier Restif, and Duncan Maskell. "A dynamic view of the spread and intracellular distribution of Salmonella enterica." Nature Reviews Microbiology 7, no. 1 (January 2009): 73–80. http://dx.doi.org/10.1038/nrmicro2034.
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Jia, Zhiheng, Harold Bien, Yohannes Shiferaw, and Emilia Entcheva. "Cardiac Cellular Coupling and the Spread of Early Instabilities in Intracellular Ca2+." Biophysical Journal 102, no. 6 (March 2012): 1294–302. http://dx.doi.org/10.1016/j.bpj.2012.02.034.
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Law, Mansun, Ruth Hollinshead, and Geoffrey L. Smith. "Antibody-sensitive and antibody-resistant cell-to-cell spread by vaccinia virus: role of the A33R protein in antibody-resistant spread." Journal of General Virology 83, no. 1 (January 1, 2002): 209–22. http://dx.doi.org/10.1099/0022-1317-83-1-209.
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The roles of vaccinia virus (VV) intracellular mature virus (IMV), intracellular enveloped virus (IEV), cell-associated enveloped virus (CEV) and extracellular enveloped virus (EEV) and their associated proteins in virus spread were investigated. The plaques made by VV mutants lacking individual IEV- or EEV-specific proteins (vΔA33R, vΔA34R, vΔA36R, vΔA56R, vΔB5R, vΔF12L and vΔF13L) were compared in the presence of IMV- or EEV-neutralizing antibodies (Ab). Data presented show that for long-range spread, the comet-shaped plaques of VV were caused by the unidirectional spread of EEV probably by convection currents, and for cell-to-cell spread, VV uses a combination of Ab-resistant and Ab-sensitive pathways. Actin tails play a major role in the Ab-resistant pathway, but mutants such as vΔA34R and vΔA36R that do not make actin tails still spread from cell to cell in the presence of Ab. Most strikingly, the Ab-resistant pathway was abolished when the A33R gene was deleted. This effect was not due to alterations in the efficiency of neutralization of EEV made by this mutant, nor due to a deficiency in IMV wrapping to form IEV, which was indispensable for EEV formation by vΔA33R and vΔA34R. We suggest a role for A33R in promoting Ab-resistant cell-to-cell spread of virus. The roles of the different virus forms in the VV life-cycle are discussed.
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Mogull, Scott A., Laura J. Runyen-Janecky, Mei Hong, and Shelley M. Payne. "dksA Is Required for Intercellular Spread of Shigella flexneri via an RpoS-Independent Mechanism." Infection and Immunity 69, no. 9 (September 1, 2001): 5742–51. http://dx.doi.org/10.1128/iai.69.9.5742-5751.2001.
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ABSTRACT Pathogenesis of Shigella flexneri is dependent on the ability of the bacterium to invade and spread within epithelial cells. In this study, we identified dksA as a gene necessary for intercellular spread in, but not invasion of, cultured cells. The S. flexneri dksA mutant exhibited sensitivity to acid and oxidative stress, in part due to an effect of DksA on production of RpoS. However, an S. flexneri rpoS mutant formed plaques on tissue culture monolayers, thus excluding DksA regulation of RpoS as the mechanism responsible for the inability of the dksA mutant to spread intercellularly. Intracellular analysis of the dksA mutant indicates that it survived and divided within the Henle cell cytoplasm, but thedksA mutant cells were elongated, and some exhibited filamentation in the intracellular environment. Some of the S. flexneri dksA mutant cells showed aberrant localization of virulence protein IcsA, which may inhibit spread between epithelial cells.
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Waligora, E. A., C. R. Fisher, N. J. Hanovice, A. Rodou, E. E. Wyckoff, and S. M. Payne. "Role of Intracellular Carbon Metabolism Pathways in Shigella flexneri Virulence." Infection and Immunity 82, no. 7 (April 14, 2014): 2746–55. http://dx.doi.org/10.1128/iai.01575-13.
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ABSTRACTShigella flexneri, which replicates in the cytoplasm of intestinal epithelial cells, can use the Embden-Meyerhof-Parnas, Entner-Doudoroff, or pentose phosphate pathway for glycolytic carbon metabolism. To determine which of these pathways is used by intracellularS. flexneri, mutants were constructed and tested in a plaque assay for the ability to invade, replicate intracellularly, and spread to adjacent epithelial cells. Mutants blocked in the Embden-Meyerhof-Parnas pathway (pfkABandpykAFmutants) invaded the cells but formed very small plaques. Loss of the Entner-Doudoroff pathway geneedaresulted in small plaques, but the doubleeda eddmutant formed normal-size plaques. This suggested that the plaque defect of theedamutant was due to buildup of the toxic intermediate 2-keto-3-deoxy-6-phosphogluconic acid rather than a specific requirement for this pathway. Loss of the pentose phosphate pathway had no effect on plaque formation, indicating that it is not critical for intracellularS. flexneri. Supplementation of the epithelial cell culture medium with pyruvate allowed the glycolysis mutants to form larger plaques than those observed with unsupplemented medium, consistent with data from phenotypic microarrays (Biolog) indicating that pyruvate metabolism was not disrupted in these mutants. Interestingly, the wild-typeS. flexnerialso formed larger plaques in the presence of supplemental pyruvate or glucose, with pyruvate yielding the largest plaques. Analysis of the metabolites in the cultured cells showed increased intracellular levels of the added compound. Pyruvate increased the growth rate ofS. flexneriin vitro, suggesting that it may be a preferred carbon source inside host cells.
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Wolf, S. G., S. Levin-Zaidman, D. Frenkiel-Krispin, E. Shimoni, I. Sabanay, and A. Minsky. "Ordered Intracellular Reca-Dna Assemblies." Microscopy and Microanalysis 6, S2 (August 2000): 860–61. http://dx.doi.org/10.1017/s1431927600036795.
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The inducible SOS response increases the ability of bacteria to cope with DNA damage through various DNA repair processes in which the RecA protein plays a central role. We find that induction of the SOS system in wild-type E. coli bacteria results in fast and massive intracellular coaggregation of RecA and DNA into lateral assemblies, which comprise substantial portions of both the cellular RecA and the DNA complement. The structural features of the coaggregates and their relation to in-vitro RecA-DNA are consistent with the possibility that the intracellular assemblies represent a functional entity in which RecA-mediated DNA repair and protection activities occur.Bacterial chromatin is demarcated in electron micrographs of metabolically active cells as amorphous ribosome-free spaces that are irregularly spread over the cytoplasm (Fig. A). Wild-type E. coli cells exposed to DNA-damaging agents that induce the SOS response reveal a strikingly different morphology (Fig. B).
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Collins, Wendy J., and David C. Johnson. "Herpes Simplex Virus gE/gI Expressed in Epithelial Cells Interferes with Cell-to-Cell Spread." Journal of Virology 77, no. 4 (February 15, 2003): 2686–95. http://dx.doi.org/10.1128/jvi.77.4.2686-2695.2003.
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ABSTRACT The herpes simplex virus (HSV) glycoprotein heterodimer gE/gI plays an important role in virus cell-to-cell spread in epithelial and neuronal tissues. In an analogous fashion, gE/gI promotes virus spread between certain cell types in culture, e.g., keratinocytes and epithelial cells, cells that are polarized or that form extensive cell junctions. One mechanism by which gE/gI facilitates cell-to-cell spread involves selective sorting of nascent virions to cell junctions, a process that requires the cytoplasmic domain of gE. However, the large extracellular domains of gE/gI also appear to be involved in cell-to-cell spread. Here, we show that coexpression of a truncated form of gE and gI in a human keratinocyte line, HaCaT cells, decreased the spread of HSV between cells. This truncated gE/gI was found extensively at cell junctions. Expression of wild-type gE/gI that accumulates at intracellular sites, in the trans-Golgi network, did not reduce cell-to-cell spread. There was no obvious reduction in production of infectious HSV in cells expressing gE/gI, and virus particles accumulated at cell junctions, not at intracellular sites. Expression of HSV gD, which is known to bind virus receptors, also blocked cell-to-cell spread. Therefore, like gD, gE/gI appears to be able to interact with cellular components of cell junctions, gE/gI receptors which can promote HSV cell-to-cell spread.
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Mounier, J., V. Laurent, A. Hall, P. Fort, M. F. Carlier, P. J. Sansonetti, and C. Egile. "Rho family GTPases control entry of Shigella flexneri into epithelial cells but not intracellular motility." Journal of Cell Science 112, no. 13 (July 1, 1999): 2069–80. http://dx.doi.org/10.1242/jcs.112.13.2069.
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Shigella flexneri, an invasive bacterial pathogen, promotes formation of two cytoskeletal structures: the entry focus that mediates bacterial uptake into epithelial cells and the actin-comet tail that enables the bacteria to spread intracellularly. During the entry step, secretion of bacterial invasins causes a massive burst of subcortical actin polymerization leading the formation of localised membrane projections. Fusion of these membrane ruffles leads to bacterial internalization. Inside the cytoplasm, polar expression of the IcsA protein on the bacterial surface allows polymerization of actin filaments and their organization into an actin-comet tail leading to bacterial spread. The Rho family of small GTPases plays an essential role in the organization and regulation of cellular cytoskeletal structures (i.e. filopodia, lamellipodia, adherence plaques and intercellular junctions). We show here that induction of Shigella entry foci is controlled by the Cdc42, Rac and Rho GTPases, but not by RhoG. In contrast, actin-driven intracellular motility of Shigella does not require Rho GTPases. Therefore, Shigella appears to manipulate the epithelial cell cytoskeleton both by Rho GTPase-dependent and -independent processes.
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Gedde, Margaret M., Darren E. Higgins, Lewis G. Tilney, and Daniel A. Portnoy. "Role of Listeriolysin O in Cell-to-Cell Spread ofListeria monocytogenes." Infection and Immunity 68, no. 2 (February 1, 2000): 999–1003. http://dx.doi.org/10.1128/iai.68.2.999-1003.2000.
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ABSTRACT Listeria monocytogenes is a facultative intracellular bacterial pathogen that escapes from a host vacuolar compartment and grows rapidly in the cytosol. Listeriolysin O (LLO) is a secreted pore-forming protein essential for the escape of L. monocytogenes from the vacuole formed upon initial internalization. However, its role in intracellular growth and cell-to-cell spread events has not been testable by a genetic approach. In this study, purified six-His-tagged LLO (HisLLO) was noncovalently coupled to the surface of nickel-treated LLO-negative mutants. Bound LLO mediated vacuolar escape in approximately 2% of the mutants. After 5.5 h of growth, cytosolic bacteria were indistinguishable from wild-type bacteria with regard to formation of pseudopod-like extensions, here termed listeriopods, and spread to adjacent cells. However, bacteria in adjacent cells failed to multiply and were found in double-membrane vacuoles. Addition of bound LLO to mutants lacking LLO and two distinct phospholipases C (PLCs) also resulted in spread to adjacent cells, but these triple mutants became trapped in multiple-membrane vacuoles that are reminiscent of autophagocytic vacuoles. These studies show that neither LLO nor the PLCs are necessary for listeriopod formation and uptake of bacteria into neighboring cells but that LLO is required for the escape ofL. monocytogenes from the double-membrane vacuole that forms upon cell-to-cell spread.
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Rudin, D. E., P. X. Gao, C. X. Cao, H. C. Neu, and S. C. Silverstein. "Gemfibrozil enhances the listeriacidal effects of fluoroquinolone antibiotics in J774 macrophages." Journal of Experimental Medicine 176, no. 5 (November 1, 1992): 1439–47. http://dx.doi.org/10.1084/jem.176.5.1439.
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J774 macrophage-like cells express organic anion transporters that promote the efflux of fluoroquinolone antibiotics such as norfloxacin (NFX) from these cells. Gemfibrozil (GFZ) blocks organic anion transport in J774 cells, thereby facilitating the intracellular accumulation of NFX (Cao, C., H.C. Neu, and S.C. Silverstein. 1991. J. Cell Biol. 115:467a [Abstr.]). To determine whether GFZ enhances the efficacy of fluoroquinolone antibiotics against intracellular bacterial pathogens, J774 cells were infected with Listeria monocytogenes and incubated in medium containing a fluoroquinolone antibiotic in the presence or absence of GFZ. Intracellular growth of L. monocytogenes was evaluated by lysing J774 cells and assaying for colony-forming units of Listeria. GFZ intensified the bacteriostatic effect of 4 micrograms/ml NFX and rendered 8 micrograms/ml bactericidal for L. monocytogenes. GFZ had a similar potentiating effect when used in combination with 2 micrograms/ml ciprofloxacin (CFX). CFX plus GFZ was bactericidal for intracellular L. monocytogenes. Treatment of J774 cells with NFX plus GFZ markedly reduced the cytotoxic effect of the bacteria on these cells. Over 55% of cells treated with 8 micrograms/ml NFX alone were dead 16 h after infection, whereas only 5% of cells treated with 8 micrograms/ml NFX plus GFZ were dead at 16 h. Similarly, GFZ potentiated the ability of 2 micrograms/ml to protect J774 cells against the cytocidal effect of Listeria. NFX in combination with GFZ limited cell-to-cell spread of L. monocytogenes. In antibiotic-free medium, > 99% of J774 cells contained intracellular L. monocytogenes at 14 h after infection. NFX alone in the medium did not change this outcome. However, 4 micrograms/ml NFX plus GFZ decreased bacterial spread by approximately 40% at 24 h postinfection, and 8 micrograms/ml NFX plus GFZ prevented all spread beyond the initially infected cell population. These results suggest that GFZ could be used clinically to enhance the efficacy of fluoroquinolone and of other anionic antibiotics against bacteria that grow and/or reside within macrophages and/or other cells.
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Pilgrim, Sabine, Annette Kolb-Mäurer, Ivaylo Gentschev, Werner Goebel, and Michael Kuhn. "Deletion of the Gene Encoding p60 in Listeria monocytogenes Leads to Abnormal Cell Division and Loss of Actin-Based Motility." Infection and Immunity 71, no. 6 (June 2003): 3473–84. http://dx.doi.org/10.1128/iai.71.6.3473-3484.2003.
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ABSTRACT Protein p60 encoded by the iap gene is regarded as an essential gene product of Listeria monocytogenes. Here we report, however, the successful construction of a viable iap deletion mutant of L. monocytogenes EGD. The mutant, which produces no p60, shows abnormal septum formation and tends to form short filaments and hooked forms during logarithmic growth. These abnormal bacterial cells break into almost normal sized single bacteria in the late-stationary-growth phase. The iap mutant is strongly attenuated in a mouse model after intravenous injection, demonstrating the importance of p60 during infection, and the invasiveness of the Δiap mutant for 3T6 fibroblasts and Caco-2 epithelial cells is slightly reduced. Upon uptake by epithelial cells and macrophages, the iap mutant escapes from the phagosome into the cytosol with the same efficiency as the wild-type strain, and the mutant bacteria also grow intracellularly at a rate similar to that of the wild-type strain. Intracellular movement and cell-to-cell spread are drastically reduced in various cell lines, since the iap-negative bacteria fail to induce the formation of actin tails. However, the bacteria are covered with actin filaments. Most intracellular bacteria show a nonpolar and uneven distribution of ActA around the cell, in contrast to that for the wild-type strain, where ActA is concentrated at the old pole. In an iap+ revertant strain that produces wild-type levels of p60, intracellular movement, cell-to-cell spread, and polar distribution of ActA are fully restored. In vitro analysis of ActA distribution on the filaments of the Δiap strain shows that the loss of bacterial septum formation leads to ActA accumulation at the presumed division sites. In the light of data presented here and elswhere, we propose to rename iap (invasion-associated protein) cwhA (cell wall hydrolase A).
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Tilney, L. G., and D. A. Portnoy. "Actin filaments and the growth, movement, and spread of the intracellular bacterial parasite, Listeria monocytogenes." Journal of Cell Biology 109, no. 4 (October 1, 1989): 1597–608. http://dx.doi.org/10.1083/jcb.109.4.1597.
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Listeria monocytogenes was used as a model intracellular parasite to study stages in the entry, growth, movement, and spread of bacteria in a macrophage cell line. The first step in infection is phagocytosis of the Listeria, followed by the dissolution of the membrane surrounding the phagosome presumably mediated by hemolysin secreted by Listeria as nonhemolytic mutants remain in intact vacuoles. Within 2 h after infection, each now cytoplasmic Listeria becomes encapsulated by actin filaments, identified as such by decoration of the actin filaments with subfragment 1 of myosin. These filaments are very short. The Listeria grow and divide and the actin filaments rearrange to form a long tail (often 5 microns in length) extending from only one end of the bacterium, a "comet's tail," in which the actin filaments appear randomly oriented. The Listeria "comet" moves to the cell surface with its tail oriented towards the cell center and becomes incorporated into a cell extension with the Listeria at the tip of the process and its tail trailing into the cytoplasm behind it. This extension contacts a neighboring macrophage that phagocytoses the extension of the first macrophage. Thus, within the cytoplasm of the second macrophage is a Listeria with its actin tail surrounded by a membrane that in turn is surrounded by the phagosome membrane of the new host. Both these membranes are then solubilized by the Listeria and the cycle is repeated. Thus, once inside a host cell, the infecting Listeria and their progeny can spread from cell to cell by remaining intracellular and thus bypass the humoral immune system of the organism. To establish if actin filaments are essential for the spread of Listeria from cell to cell, we treated infected macrophages with cytochalasin D. The Listeria not only failed to spread, but most were found deep within the cytoplasm, rather than near the periphery of the cell. Thin sections revealed that the net of actin filaments is not formed nor is a "comet" tail produced.
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Bajgar, Adam, Ivan Saloň, Gabriela Krejčová, Tomáš Doležal, Marek Jindra, and František Štěpánek. "Yeast glucan particles enable intracellular protein delivery in Drosophila without compromising the immune system." Biomaterials Science 7, no. 11 (2019): 4708–19. http://dx.doi.org/10.1039/c9bm00539k.
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Glucan particles spread through the whole organism quickly, accumulate in sites of macrophage occurrence and can deliver cargo into the macrophages with a negligible effect on immune response activation.
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Marquis, Hélène, Howard Goldfine, and Daniel A. Portnoy. "Proteolytic Pathways of Activation and Degradation of a Bacterial Phospholipase C during Intracellular Infection by Listeria monocytogenes." Journal of Cell Biology 137, no. 6 (June 16, 1997): 1381–92. http://dx.doi.org/10.1083/jcb.137.6.1381.
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Listeria monocytogenes is a facultative intracellular bacterial pathogen that spreads cell to cell without exposure to the extracellular environment. Bacterial cell-to-cell spread is mediated in part by two secreted bacterial phospholipases C (PLC), a broad spectrum PLC (PC-PLC) and a phosphatidylinositolspecific PLC (PI-PLC). PI-PLC is secreted in an active state, whereas PC-PLC is secreted as an inactive proenzyme (proPC-PLC) whose activation is mediated in vitro by an L. monocytogenes metalloprotease (Mpl). Analysis of PI-PLC, PC-PLC, and Mpl single and double mutants revealed that Mpl also plays a role in the spread of an infection, but suggested that proPC-PLC has an Mpl-independent activation pathway. Using biochemical and microscopic approaches, we describe three intracellular proteolytic pathways regulating PCPLC activity. Initially, proPC-PLC secreted in the cytosol of infected cells was rapidly degraded in a proteasome-dependent manner. Later during infection, PCPLC colocalized with bacteria in lysosome-associated membrane protein 1–positive vacuoles. Activation of proPC-PLC in vacuoles was mediated by Mpl and an Mpl-independent pathway, the latter being sensitive to inhibitors of cysteine proteases. Lastly, proPC-PLC activation by either pathway was sensitive to bafilomycin A1, a specific inhibitor of vacuolar ATPase, suggesting that activation was dependent on acidification of the vacuolar compartment. These results are consistent with a model in which proPC-PLC activation is compartment specific and controlled by a combination of bacterial and host factors.
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Dancz, Christina E., Andrea Haraga, Daniel A. Portnoy, and Darren E. Higgins. "Inducible Control of Virulence Gene Expression in Listeria monocytogenes: Temporal Requirement of Listeriolysin O during Intracellular Infection." Journal of Bacteriology 184, no. 21 (November 1, 2002): 5935–45. http://dx.doi.org/10.1128/jb.184.21.5935-5945.2002.
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ABSTRACT We have constructed a lac repressor/operator-based system to tightly regulate expression of bacterial genes during intracellular infection by Listeria monocytogenes. An L. monocytogenes strain was constructed in which expression of listeriolysin O was placed under the inducible control of an isopropyl-β-d-thiogalactopyranoside (IPTG)-dependent promoter. Listeriolysin O (LLO) is a pore-forming cytolysin that mediates lysis of L. monocytogenes-containing phagosomes. Using hemolytic-activity assays and Western blot analysis, we demonstrated dose-dependent IPTG induction of LLO during growth in broth culture. Moreover, intracellular growth of the inducible-LLO (iLLO) strain in the macrophage-like cell line J774 was strictly dependent upon IPTG. We have further shown that iLLO bacteria trapped within primary phagocytic vacuoles can be induced to escape into the cytosol following addition of IPTG to the cell culture medium, thus yielding the ability to control bacterial escape from the phagosome and the initiation of intracellular growth. Using the iLLO strain in plaque-forming assays, we demonstrated an additional requirement for LLO in facilitating cell-to-cell spread in L2 fibroblasts, a nonprofessional phagocytic cell line. Furthermore, the efficiency of cell-to-cell spread of iLLO bacteria in L2 cells was IPTG dose dependent. The potential use of this system for determining the temporal requirements of additional virulence determinants of intracellular pathogenesis is discussed.
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Stelzner, Kathrin, Ann-Cathrin Winkler, Chunguang Liang, Aziza Boyny, Carsten P. Ade, Thomas Dandekar, Martin J. Fraunholz, and Thomas Rudel. "Intracellular Staphylococcus aureus Perturbs the Host Cell Ca2+ Homeostasis To Promote Cell Death." mBio 11, no. 6 (December 15, 2020): e02250-20. http://dx.doi.org/10.1128/mbio.02250-20.
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ABSTRACTThe opportunistic human pathogen Staphylococcus aureus causes serious infectious diseases that range from superficial skin and soft tissue infections to necrotizing pneumonia and sepsis. While classically regarded as an extracellular pathogen, S. aureus is able to invade and survive within human cells. Host cell exit is associated with cell death, tissue destruction, and the spread of infection. The exact molecular mechanism employed by S. aureus to escape the host cell is still unclear. In this study, we performed a genome-wide small hairpin RNA (shRNA) screen and identified the calcium signaling pathway as being involved in intracellular infection. S. aureus induced a massive cytosolic Ca2+ increase in epithelial host cells after invasion and intracellular replication of the pathogen. This was paralleled by a decrease in endoplasmic reticulum Ca2+ concentration. Additionally, calcium ions from the extracellular space contributed to the cytosolic Ca2+ increase. As a consequence, we observed that the cytoplasmic Ca2+ rise led to an increase in mitochondrial Ca2+ concentration, the activation of calpains and caspases, and eventually to cell lysis of S. aureus-infected cells. Our study therefore suggests that intracellular S. aureus disturbs the host cell Ca2+ homeostasis and induces cytoplasmic Ca2+ overload, which results in both apoptotic and necrotic cell death in parallel or succession.IMPORTANCE Despite being regarded as an extracellular bacterium, the pathogen Staphylococcus aureus can invade and survive within human cells. The intracellular niche is considered a hideout from the host immune system and antibiotic treatment and allows bacterial proliferation. Subsequently, the intracellular bacterium induces host cell death, which may facilitate the spread of infection and tissue destruction. So far, host cell factors exploited by intracellular S. aureus to promote cell death are only poorly characterized. We performed a genome-wide screen and found the calcium signaling pathway to play a role in S. aureus invasion and cytotoxicity. The intracellular bacterium induces a cytoplasmic and mitochondrial Ca2+ overload, which results in host cell death. Thus, this study first showed how an intracellular bacterium perturbs the host cell Ca2+ homeostasis.
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Eklund, Daniel, Amanda Welin, Thomas Schön, Olle Stendahl, Kris Huygen, and Maria Lerm. "Validation of a Medium-Throughput Method for Evaluation of Intracellular Growth of Mycobacterium tuberculosis." Clinical and Vaccine Immunology 17, no. 4 (January 27, 2010): 513–17. http://dx.doi.org/10.1128/cvi.00446-09.
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ABSTRACT Intracellular pathogens such as Mycobacterium tuberculosis have adapted to a life inside host cells, in which they utilize host nutrients to replicate and spread. Ineffective methods for the evaluation of growth of intracellular pathogens in their true environment pose an obstacle for basic research and drug screening. Here we present the validation of a luminometry-based method for the analysis of intramacrophage growth of M. tuberculosis. The method, which is performed in a medium-throughput format, can easily be adapted for studies of other intracellular pathogens and cell types. The use of host cells in drug-screening assays dedicated to find antimicrobials effective against intracellular pathogens permits the discovery of not only novel antibiotics but also compounds with immunomodulatory and virulence-impairing activities, which may be future alternatives or complements to antibiotics.
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Widden, Paul. "The morphology of vesicular – arbuscular mycorrhizae in Clintonia borealis and Medeola virginiana." Canadian Journal of Botany 74, no. 5 (May 1, 1996): 679–85. http://dx.doi.org/10.1139/b96-086.
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During a survey of the vesicular–arbuscular mycorrhizal (VAM) associations of forest herbs in a deciduous forest in the southern Laurentian mountains in Quebec, two liliaceous species, Clintonia borealis and Medeola virginiana, revealed very distinctive morphology. In both species, once the epidermis was penetrated, the fungus spread towards the centre of the root via intracellular hyphae until the innermost layer of the cortex was reached, at which point the fungus spread laterally and tangentially through the cortical cells adjacent to the endodermis via a series of banana-shaped projections (bobbits). These eventually differentiated into the arbuscules and the VAM might spread from this inner cortical layer back into the outer cortical layers. In C. borealis, the hyphae coiled in the cortex, and vesicles were formed in the upper cortical cells. In M. virginiana, no coiling took place, but extensive diverticulae were produced by the intracellular hyphae in the cortical cells, close to their point of exit, and vesicles were produced in the inner cortex as swellings from the bobbits. These two mycorrhizae have some similarities to one in Colchicum autumnale described by I. Gallaud (1905. Rev. Gen. Bot. 17). Keywords: vesicular–arbuscular mycorrhizae, Clintonia borealis, Medeola virginiana, Liliaceae, morphology.
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Pál, T., J. W. Newland, B. D. Tall, S. B. Formal, and T. L. Hale. "Intracellular spread of Shigella flexneri associated with the kcpA locus and a 140-kilodalton protein." Infection and Immunity 57, no. 2 (1989): 477–86. http://dx.doi.org/10.1128/iai.57.2.477-486.1989.
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Zayas, Janet P., and João I. Mamede. "HIV Infection and Spread between Th17 Cells." Viruses 14, no. 2 (February 16, 2022): 404. http://dx.doi.org/10.3390/v14020404.
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HIV mainly targets CD4+ T cells, from which Th17 cells represent a major cell type, permissive, and are capable of supporting intracellular replication at mucosal sites. Th17 cells possess well-described dual roles, while being central to maintaining gut integrity, these may induce inflammation and contribute to autoimmune disorders; however, Th17 cells’ antiviral function in HIV infection is not completely understood. Th17 cells are star players to HIV-1 pathogenesis and a potential target to prevent or decrease HIV transmission. HIV-1 can be spread among permissive cells via direct cell-to-cell and/or cell-free infection. The debate on which mode of transmission is more efficient is still ongoing without a concrete conclusion yet. Most assessments of virus transmission analyzing either cell-to-cell or cell-free modes use in vitro systems; however, the actual interactions and conditions in vivo are not fully understood. The fact that infected breast milk, semen, and vaginal secretions contain a mix of both cell-free viral particles and infected cells presents an argument for the probability of HIV taking advantage of both modes of transmission to spread. Here, we review important insights and recent findings about the role of Th17 cells during HIV pathogenesis in mucosal surfaces, and the mechanisms of HIV-1 infection spread among T cells in tissues.
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JOHNSON, DIANNA A., STEPHEN L. MILLS, MICHAEL F. HABERECHT, and STEPHEN C. MASSEY. "Dye coupling in horizontal cells of developing rabbit retina." Visual Neuroscience 17, no. 2 (March 2000): 255–62. http://dx.doi.org/10.1017/s0952523800172074.
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In the mature rabbit retina, two classes of horizontal cells, A type and B type, provide lateral inhibition in the outer plexiform layer (OPL) and spatially modify the activation of bipolar cells by photoreceptors. Gap junctions connecting homologous horizontal cells determine the extent to which this inhibitory activity spreads laterally across the OPL. Little is currently known about the expression of gap junctions in horizontal cells during postnatal development or how cell–cell coupling might contribute to subsequent maturational events. We have examined the morphological attributes and coupling properties of developing A and B type horizontal cells in neonatal rabbit retina using intracellular injections of Lucifer Yellow and Neurobiotin. Prelabeling with DAPI permitted the targeting of horizontal cell bodies for intracellular injection in perfused preparations of isolated retina. A and B type horizontal cells were identifiable at birth although their dendritic field sizes had not reached adult proportions and their synaptic contacts in the OPL were minimal. Both cell types exhibited homologous dye coupling at birth. Similar to that seen in the adult, no heterologous coupling was observed, and homologous coupling among A type cells was stronger than that observed among B type cells. The spread of tracer compounds through gap junctions of morphologically immature horizontal cells suggests that ions and other small, bioactive compounds may likewise spread through coupled, horizontal networks to coordinate the subsequent maturational of emerging outer plexiform layer pathways.
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Tamai, Atsushi, and Tetsuo Meshi. "Cell-to-Cell Movement of Potato virus X: The Role of p12 and p8 Encoded by the Second and Third Open Reading Frames of the Triple Gene Block." Molecular Plant-Microbe Interactions® 14, no. 10 (October 2001): 1158–67. http://dx.doi.org/10.1094/mpmi.2001.14.10.1158.
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Potato virus X (PVX) requires three proteins, p25, p12, and p8, encoded by the triple gene block plus the coat protein (CP) for cell-to-cell movement. When each of these proteins was co-expressed with a cytosolic green fluorescent protein (GFP) in the epidermal cells of Nicotiana benthamiana by the microprojectile bombardment-mediated gene delivery method, only p12 enhanced diffusion of co-expressed GFP, indicating an ability to alter plasmodesmal permeability. p25, p12, and CP, expressed transiently in the initially infected cells, transcomplemented the corresponding movement-defective mutants to spread through two or more cell boundaries. Thus, these proteins probably move from cell to cell with the genomic RNA. In contrast, p8 only functioned intracellularly and was not absolutely required for cell-to-cell movement. Since overexpression of p12 overcame the p8 deficiency, p8 appears to facilitate the functioning of p12, presumably by mediating its intracellular trafficking. Considering the likelihood that p12 and p8 are membrane proteins, it is suggested that intercellular as well as intracellular movement of PVX involves a membrane-mediated process.
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Goldberg, Marcia B. "Actin-Based Motility of Intracellular Microbial Pathogens." Microbiology and Molecular Biology Reviews 65, no. 4 (December 1, 2001): 595–626. http://dx.doi.org/10.1128/mmbr.65.4.595-626.2001.
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SUMMARY A diverse group of intracellular microorganisms, including Listeria monocytogenes, Shigella spp., Rickettsia spp., and vaccinia virus, utilize actin-based motility to move within and spread between mammalian host cells. These organisms have in common a pathogenic life cycle that involves a stage within the cytoplasm of mammalian host cells. Within the cytoplasm of host cells, these organisms activate components of the cellular actin assembly machinery to induce the formation of actin tails on the microbial surface. The assembly of these actin tails provides force that propels the organisms through the cell cytoplasm to the cell periphery or into adjacent cells. Each of these organisms utilizes preexisting mammalian pathways of actin rearrangement to induce its own actin-based motility. Particularly remarkable is that while all of these microbes use the same or overlapping pathways, each intercepts the pathway at a different step. In addition, the microbial molecules involved are each distinctly different from the others. Taken together, these observations suggest that each of these microbes separately and convergently evolved a mechanism to utilize the cellular actin assembly machinery. The current understanding of the molecular mechanisms of microbial actin-based motility is the subject of this review.
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Segal, S. S., and J. L. Beny. "Intracellular recording and dye transfer in arterioles during blood flow control." American Journal of Physiology-Heart and Circulatory Physiology 263, no. 1 (July 1, 1992): H1—H7. http://dx.doi.org/10.1152/ajpheart.1992.263.1.h1.
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We tested for dye coupling between arteriolar smooth muscle cells (SMC) and endothelial cells (EC) and investigated the correspondence of vasomotor activity with changes in the membrane potential (Vm) of EC and SMC during blood flow control. Female golden hamsters (n = 8, 90-170 g) were anesthetized (pentobarbital sodium, 60 mg/kg ip). A cheek pouch was spread over an optical pedestal, transilluminated, and irrigated with physiological saline solution (37 degrees C, pH 7.4). Glass microelectrodes were filled with 3 M KCl or with Lucifer yellow dye (LY, mol wt 470; 106 mM). SMC or EC of arterioles (ID, 20-50 microns) containing blood flow were impaled under a stereomicroscope. Vm was similar [-48 +/- 3 and -52 +/- 4 mV (means +/- SE)] with KCl (n = 6) or LY (n = 13) microelectrodes, respectively. Acetylcholine (5 x 10(-6) M) increased Vm from -47 +/- 3 to -67 +/- 4 mV (n = 5; P less than 0.01) concomitant with vasodilation. Spontaneous slow waves in Vm (2/min, 15-30 mV) were observed in arterioles with vasomotion. In cells identified with LY microinjection, resting Vm was -52 +/- 8 and -44 +/- 2 mV for EC (n = 3) and SMC (n = 3), respectively. SMC injected with LY did not show evidence of dye transfer to other SMC or to EC. When an EC was injected, the dye spread to many contiguous EC but not to SMC.(ABSTRACT TRUNCATED AT 250 WORDS)
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Wallace, Nathan, Erica Rinehart, and Yvonne Sun. "Stimulating Respiratory Activity Primes Anaerobically Grown Listeria monocytogenes for Subsequent Intracellular Infections." Pathogens 7, no. 4 (December 8, 2018): 96. http://dx.doi.org/10.3390/pathogens7040096.
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Listeria monocytogenes (L. monocytogenes) is a Gram-positive, enteric pathogen and the causative agent of listeriosis. During transition through the gastrointestinal tract, L. monocytogenes routinely encounters suboxic conditions. However, how the exposure to the low oxygen environment affects subsequent pathogenesis is not completely understood. Our lab previously reported that anaerobically grown L. monocytogenes exhibited an intracellular growth defect in macrophages even though the infection took place under aerobic conditions. This phenotype suggests that prior growth conditions have a prolonged effect on the outcome of subsequent intracellular infection. In this study, to further investigate the mechanisms that contribute to the compromised intracellular growth after anaerobic exposure, we hypothesized that the lack of respiratory activity under anaerobic conditions prevented anaerobically grown L. monocytogenes to establish subsequent intracellular growth under aerobic conditions. To test this hypothesis, respiratory activity in anaerobically grown L. monocytogenes was stimulated by exogenous fumarate and subsequent intracellular pathogenesis was assessed. The results showed that fumarate supplementation significantly increased the respiratory activity of anaerobically grown L. monocytogenes and rescued the subsequent intracellular growth defect, likely through promoting the production of listeriolysin O, phagosomal escape, and cell-cell spread. This study highlights the importance of respiratory activity in L. monocytogenes in modulating the outcome of subsequent intracellular infections.
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Albowitz, B., P. König, and U. Kuhnt. "Spatiotemporal Distribution of Intracellular Calcium Transients During Epileptiform Activity in Guinea Pig Hippocampal Slices." Journal of Neurophysiology 77, no. 1 (January 1, 1997): 491–501. http://dx.doi.org/10.1152/jn.1997.77.1.491.
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Albowitz, B., P. König, and U. Kuhnt. Spatiotemporal distribution of intracellular calcium transients during epileptiform activity in guinea pig hippocampal slices. J. Neurophysiol. 77: 491–501, 1997. Calcium ions are known to play an important role in epileptogenesis. Although there is clear evidence for increased neuronal calcium influx during epileptiform potentials, direct measurements of the corresponding intracellular calcium transients are rare and the origin of calcium influx is not known. Therefore the spatial and temporal distribution of intracellular calcium transients during epileptiform activity in guinea pig hippocampal slices was monitored with the use of the indicator Calcium-Green and a fast optical recording method. Two models of epilepsy (bicuculline and low Mg2+) were compared. In both models, single epileptiform events were evoked by electrical stimulation of the Schaffer collaterals in CA1 or of stratum pyramidale in area CA3. Intracellular calcium transients during epileptiform activity were ∼5 times larger than during control stimulation. Calcium transients during epileptiform activity were present across at least the entire CA1 area, whereas presynaptic calcium transients from stimulated fibers were only seen at a distance up to 1 mm from the stimulation site. dl-2-amino-5-phosphonovaleric acid (APV), a specific antagonist of the N-methyl-d-aspartate (NMDA) receptor, abolished low-Mg2+ epileptiform activity and reduced bicuculline-induced epileptiform activity; it reduced calcium transients following stimulation of CA1 by only 29% (bicuculline) and 38% (low Mg2+). For comparison, calcium transients during control stimulation were 78% (bicuculline) and 69% (low Mg2+) smaller than epileptiform calcium transients. At a distance from the stimulation site, calcium transients and their NMDA-receptor-dependent components were largest in stratum pyramidale in the bicuculline model and in stratum oriens in the low-Mg2+ model. In both models, minimal onset latencies of calcium influx shifted with increasing distance to the stimulation electrode from stratum radiatum to stratum oriens. APV reduced the extent of spread of calcium transients in the low-Mg2+ model. In the bicuculline model, the spatial extent of spread of epileptiform calcium transients was not affected by application of APV; however, the mean velocity of spread was reduced from 0.20 to 0.12 m/s. In conclusion, the large size of calcium transients and of their NMDA-receptor-dependent components in stratum pyramidale or stratum oriens as well as shortest onset latencies of calcium transients at these sites suggest an important role of cell somata, basal dendrites, and possibly local circuit excitatory interactions for the generation and spread of epileptiform activity.
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Hernández, Sara B., Sónia Castanheira, M. Graciela Pucciarelli, Juan J. Cestero, Gadea Rico-Pérez, Alberto Paradela, Juan A. Ayala, et al. "Peptidoglycan editing in non-proliferating intracellular Salmonella as source of interference with immune signaling." PLOS Pathogens 18, no. 1 (January 25, 2022): e1010241. http://dx.doi.org/10.1371/journal.ppat.1010241.
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Salmonella enterica causes intracellular infections that can be limited to the intestine or spread to deeper tissues. In most cases, intracellular bacteria show moderate growth. How these bacteria face host defenses that recognize peptidoglycan, is poorly understood. Here, we report a high-resolution structural analysis of the minute amounts of peptidoglycan purified from S. enterica serovar Typhimurium (S. Typhimurium) infecting fibroblasts, a cell type in which this pathogen undergoes moderate growth and persists for days intracellularly. The peptidoglycan of these non-proliferating bacteria contains atypical crosslinked muropeptides with stem peptides trimmed at the L-alanine-D-glutamic acid-(γ) or D-glutamic acid-(γ)-meso-diaminopimelic acid motifs, both sensed by intracellular immune receptors. This peptidoglycan has a reduced glycan chain average length and ~30% increase in the L,D-crosslink, a type of bridge shared by all the atypical crosslinked muropeptides identified. The L,D-transpeptidases LdtD (YcbB) and LdtE (YnhG) are responsible for the formation of these L,D-bridges in the peptidoglycan of intracellular bacteria. We also identified in a fraction of muropeptides an unprecedented modification in the peptidoglycan of intracellular S. Typhimurium consisting of the amino alcohol alaninol replacing the terminal (fourth) D-alanine. Alaninol was still detectable in the peptidoglycan of a double mutant lacking LdtD and LdtE, thereby ruling out the contribution of these enzymes to this chemical modification. Remarkably, all multiple mutants tested lacking candidate enzymes that either trim stem peptides or form the L,D-bridges retain the capacity to modify the terminal D-alanine to alaninol and all attenuate NF-κB nuclear translocation. These data inferred a potential role of alaninol-containing muropeptides in attenuating pro-inflammatory signaling, which was confirmed with a synthetic tetrapeptide bearing such amino alcohol. We suggest that the modification of D-alanine to alaninol in the peptidoglycan of non-proliferating intracellular S. Typhimurium is an editing process exploited by this pathogen to evade immune recognition inside host cells.
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Yang, Jun, Hanliang Du, Zhenhao Chai, Lei Zhang, Ben Q. Li, Jianlei Cui, and Xuesong Mei. "Optimization of Spot Efficiency of Double-Helix Point Spread Function and Its Application in Intracellular Imaging." Applied Sciences 12, no. 4 (February 9, 2022): 1778. http://dx.doi.org/10.3390/app12041778.
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The nano-scale spatial positioning of nanoparticles in tumor cells can be achieved through the double-helix point spread functions (DH-PSF). Nevertheless, certain issues such as low light intensity concentration of the main lobes, the influence of the side lobes, and the aberrations of the imaging system result in poor image quality and reduce the positioning accuracy of the fluorescent nanoparticles. In this paper, an iterative optimization algorithm that combines Laguerre–Gaussian modes and Zernike polynomials is proposed. The double-helix point spread function, constructed by the linear superposition of the Laguerre–Gaussian mode and Zernike polynomials, is used to express aberrations in the imaging system. The simulation results indicated that the light intensity concentration of the main lobes is increased by 45.51% upon the use of the optimization process. Based on the simulation results, the phase modulation plate was designed and processed while a 4f positioning imaging system was built. Human osteosarcoma cells, labeled by CdTe/CdS/ZnS quantum dots, were used as samples, and the position imaging experiment was carried out. The image information entropy was used as the clarity evaluation index. The experimental results showed that the image information entropy of the DH-PSF position imaging was reduced from 4.22 before optimization to 2.65 after optimization, and the image clarity was significantly improved. This result verified the effectiveness of the optimization method that was proposed in this work.
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Sun, A. N., A. Camilli, and D. A. Portnoy. "Isolation of Listeria monocytogenes small-plaque mutants defective for intracellular growth and cell-to-cell spread." Infection and Immunity 58, no. 11 (1990): 3770–78. http://dx.doi.org/10.1128/iai.58.11.3770-3778.1990.
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Kawano, Tomonori, and François Bouteau. "Crosstalk between intracellular and extracellular salicylic acid signaling events leading to long-distance spread of signals." Plant Cell Reports 32, no. 7 (May 21, 2013): 1125–38. http://dx.doi.org/10.1007/s00299-013-1451-0.
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Hong, Bangxing, Upasana Sahu, Matthew P. Mullarkey, and Balveen Kaur. "Replication and Spread of Oncolytic Herpes Simplex Virus in Solid Tumors." Viruses 14, no. 1 (January 10, 2022): 118. http://dx.doi.org/10.3390/v14010118.
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Oncolytic herpes simplex virus (oHSV) is a highly promising treatment for solid tumors. Intense research and development efforts have led to first-in-class approval for an oHSV for melanoma, but barriers to this promising therapy still exist that limit efficacy. The process of infection, replication and transmission of oHSV in solid tumors is key to obtaining a good lytic destruction of infected cancer cells to kill tumor cells and release tumor antigens that can prime anti-tumor efficacy. Intracellular tumor cell signaling and tumor stromal cells present multiple barriers that resist oHSV activity. Here, we provide a review focused on oncolytic HSV and the essential viral genes that allow for virus replication and spread in order to gain insight into how manipulation of these pathways can be exploited to potentiate oHSV infection and replication among tumor cells.
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Ribot, Wilson J., and Ricky L. Ulrich. "The Animal Pathogen-Like Type III Secretion System Is Required for the Intracellular Survival of Burkholderia mallei within J774.2 Macrophages." Infection and Immunity 74, no. 7 (July 2006): 4349–53. http://dx.doi.org/10.1128/iai.01939-05.
Full textAbstract:
ABSTRACT Burkholderia mallei is a highly infectious gram-negative pathogen and is the causative agent of human and animal glanders. By generating polar mutations (disruption of bsaQ and bsaZ) in the B. mallei ATCC 23344 animal pathogen-like type III secretion system (TTS), we demonstrate that this bacterial protein delivery system is required for intracellular growth of B. mallei in J774.2 cells, formation of macrophage membrane protrusions, actin polymerization, and phagosomal escape. These findings suggest that TTS plays a role in the intracellular trafficking of B. mallei and may facilitate cell-to-cell spread via actin-based motility.
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Nathanson, M. H., and A. D. Burgstahler. "Coordination of hormone-induced calcium signals in isolated rat hepatocyte couplets: demonstration with confocal microscopy." Molecular Biology of the Cell 3, no. 1 (January 1992): 113–21. http://dx.doi.org/10.1091/mbc.3.1.113.
Full textAbstract:
Excitable cells often display rapid coordination of hormone-induced intracellular calcium signals. Calcium elevations that begin in a single epithelial cell also may spread to adjacent cells, but coordination of hormone-induced signals among epithelial cells has not been described. We report the use of confocal microscopy to determine the inter- and intracellular distribution of cytosolic calcium in isolated rat hepatocyte couplets, an isolated epithelial cell system in which functional polarity is maintained. Both vasopressin and phenylephrine evoked sequential coordinated calcium signals in the couplets, even during cytosolic calcium oscillations. The coupling was abolished by closure of intercellular gap junction channels by treatment with octanol. These observations demonstrate that hormone-induced intracellular calcium signals are coordinated among hepatocytes and suggest that gap junction channels mediate this intercellular integration of tissue responsiveness.
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Hanani, M., and N. Lasser-Ross. "Activity-dependent changes in intracellular calcium in myenteric neurons." American Journal of Physiology-Gastrointestinal and Liver Physiology 273, no. 6 (December 1, 1997): G1359—G1363. http://dx.doi.org/10.1152/ajpgi.1997.273.6.g1359.
Full textAbstract:
The spatial distribution and changes in intracellular calcium concentration ([Ca2+]i) in myenteric neurons were measured using fura 2 in the longitudinal muscle-myenteric plexus preparation from the guinea pig duodenum. These measurements were made simultaneously with intracellular voltage recordings. The generation of action potentials in the cell bodies of both S- and AH-type neurons increased [Ca2+]iin the processes and cell bodies. There was no measurable delay between the [Ca2+]ichanges in the somata and the processes, indicating that these changes were caused by the spread of electrical signals and not by diffusion. The rate of Ca2+ removal was faster in the processes than in the somata, apparently due to the large surface-to-volume ratio in the former. In AH neurons, the [Ca2+]itransient was shorter than the duration of the after-spike hyperpolarization. It is concluded that the two main types of myenteric neurons possess voltage-gated Ca2+channels in both somata and processes.
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Genovés, Ainhoa, Jose Antonio Navarro, and Vicente Pallás. "The Intra- and Intercellular Movement of Melon necrotic spot virus (MNSV) Depends on an Active Secretory Pathway." Molecular Plant-Microbe Interactions® 23, no. 3 (March 2010): 263–72. http://dx.doi.org/10.1094/mpmi-23-3-0263.
Full textAbstract:
Plant viruses hijack endogenous host transport machinery to aid their intracellular spread. Here, we study the localization of the p7B, the membrane-associated viral movement protein (MP) of the Melon necrotic spot virus (MNSV), and also the potential involvement of the secretory pathway on the p7B targeting and intra- and intercellular virus movements. p7B fused to fluorescent proteins was located throughout the endoplasmic reticulum (ER) at motile Golgi apparatus (GA) stacks that actively tracked the actin microfilaments, and at the plasmodesmata (PD). Hence, the secretory pathway inhibitor, Brefeldin A (BFA), and the overexpression of the GTPase-defective mutant of Sar1p, Sar1[H74L], fully retained the p7B within the ER, revealing that the protein is delivered to PD in a BFA-sensitive and COPII-dependent manner. Disruption of the actin cytoskeleton with latrunculin B led to the accumulation of p7B in the ER, which strongly suggests that p7B is also targeted to the cell periphery in an actin-dependent manner. Remarkably, the local spread of the viral infection was significantly restricted either with the presence of BFA or under the overexpression of Sar1[H74L], thus revealing the involvement of an active secretory pathway in the intracellular movement of MNSV. Overall, these findings support a novel route for the intracellular transport of a plant virus led by the GA.
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Fratazzi, C., R. D. Arbeit, C. Carini, and H. G. Remold. "Programmed cell death of Mycobacterium avium serovar 4-infected human macrophages prevents the mycobacteria from spreading and induces mycobacterial growth inhibition by freshly added, uninfected macrophages." Journal of Immunology 158, no. 9 (May 1, 1997): 4320–27. http://dx.doi.org/10.4049/jimmunol.158.9.4320.
Full textAbstract:
Abstract Mycobacterium avium, an opportunistic pathogen in AIDS patients, replicates in human macrophages (Mphi) and induces programmed cell death (PCD). In this study we examine the effect of freshly added, uninfected Mphi on M. avium growth in apoptotic Mphi cultures. Incubation of uninfected autologous Mphi with apoptotic Mphi infected with M. avium for 6 h results in 90% inhibition of bacterial growth. The uninfected Mphi adhere to M. avium-infected apoptotic, but not to nonapoptotic M. avium-infected Mphi, suggesting a specific interaction between apoptotic and nonapoptotic Mphi. PCD of the host Mphi also prevents the release of intracellular components and the spread of the mycobacterial infection. Once the apoptotic infected Mphi reach the necrotic stage, mycobacteria and other intracellular material are released; the latter suffice to support extracellular mycobacterial replication. Necrosis of M. avium-infected Mphi is significantly augmented by the transglutaminase inhibitors dansyl-cadaverine and cystamine, indicating that apoptosis of Mphi is dependent on the extent of cross-linking of cell proteins by transglutaminases. Consequently, transglutaminase inhibitors accelerate the release of mycobacteria and intracellular components from the infected Mphi into the medium. These findings indicate that PCD of M. avium-infected Mphi is an important defense mechanism, preventing the spread of infection by sequestering the mycobacteria and by contributing to their demise by activation of newly recruited uninfected Mphi.
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Dupont, Maeva, and Quentin James Sattentau. "Macrophage Cell-Cell Interactions Promoting HIV-1 Infection." Viruses 12, no. 5 (April 28, 2020): 492. http://dx.doi.org/10.3390/v12050492.
Full textAbstract:
Many pathogens infect macrophages as part of their intracellular life cycle. This is particularly true for viruses, of which HIV-1 is one of the best studied. HIV-1 infection of macrophages has important consequences for viral persistence and pathogenesis, but the mechanisms of macrophage infection remain to be fully elucidated. Despite expressing viral entry receptors, macrophages are inefficiently infected by cell-free HIV-1 virions, whereas direct cell-cell spread is more efficient. Different modes of cell-cell spread have been described, including the uptake by macrophages of infected T cells and the fusion of infected T cells with macrophages, both leading to macrophage infection. Cell-cell spread can also transmit HIV-1 between macrophages and from macrophages to T cells. Here, we describe the current state of the field concerning the cell-cell spread of HIV-1 to and from macrophages, discuss mechanisms, and highlight potential in vivo relevance.