Entamoeba histolytica Cell Surface Calreticulin Binds Human C1q and Functions in Amebic Phagocytosis of Host Cells

Vaithilingam, Archana; Teixeira, José E.; Miller, Peter J.; Heron, Bradley T.; Huston, Christopher D.

doi:10.1128/iai.06287-11

Cited by 39 publications

(42 citation statements)

References 54 publications

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“…In contrast, there are no previously characterized assays in which C1q plays a similarly defined role in which function-blocking activity of specific Abs has been assessed. A polyclonal anti-C1q Ab was selected based on wide use in previous studies; specificity for C1q from humans, rats, and mice based on immunoblots; and previous characterization in commercially available human clinical ELISAs and immunoaffinity chromatography (32). In all cases, species-and subtype-matched IgG control Abs were confirmed to lack modifying activity (Table I).…”

Section: Blocking Absmentioning

confidence: 99%

Neutrophils Induce Astroglial Differentiation and Migration of Human Neural Stem Cells via C1q and C3a Synthesis

Hooshmand

Nguyen

Piltti

et al. 2017

The Journal of Immunology

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Inflammatory processes play a key role in pathophysiology of many neurologic diseases/trauma, but the effect of immune cells and factors on neurotransplantation strategies remains unclear. We hypothesized that cellular and humoral components of innate immunity alter fate and migration of human neural stem cells (hNSC). In these experiments, conditioned media collected from polymorphonuclear leukocytes (PMN) selectively increased hNSC astrogliogenesis and promoted cell migration in vitro. PMN were shown to generate C1q and C3a; exposure of hNSC to PMN-synthesized concentrations of these complement proteins promoted astrogliogenesis and cell migration. Furthermore, in vitro, Abs directed against C1q and C3a reversed the fate and migration effects observed. In a proof-of-concept in vivo experiment, blockade of C1q and C3a transiently altered hNSC migration and reversed astroglial fate after spinal cord injury. Collectively, these data suggest that modulation of the innate/humoral inflammatory microenvironment may impact the potential of cell-based therapies for recovery and repair following CNS pathology.

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Section: Blocking Absmentioning

confidence: 99%

Neutrophils Induce Astroglial Differentiation and Migration of Human Neural Stem Cells via C1q and C3a Synthesis

Hooshmand

Nguyen

Piltti

et al. 2017

The Journal of Immunology

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“…Furthermore, opsonins, such as collectin family members (e.g., mannose binding lectin (MBL)) and the structurally related protein C1q bind to Entamoeba histolytica (Eh) C1q receptors (C1qRs) allowing and facilitating the uptake of apoptotic intestinal cells by E. histolytica [73,74]. In the literature, the term trogocytosis tends to be used to refer to the plasma membrane and membrane protein active [75].…”

Section: Perforin/ Granzyme Pathwaymentioning

confidence: 99%

Cell death offers exceptional cellular and molecular windows for pharmacological interventions in protozoan parasites

El‐Ashram¹,

Mehmood²,

Dinçel³

et al. 2017

Integr Mol Med

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The rich repertoire of cell death events is a crucial biological process that deserves extensive review at a formative time for the development of our knowledge concerning the state-of-the-art data on their cellular and molecular mechanisms of action and the ways in which they can be manipulated in and by protozoan parasites. We have attempted to provide a comprehensive overview to reveal intervention points that could be exploited to discover novel therapies, vaccine strategies and prophylactic intervention points for protozoan parasites, and to understand the parasitic disease progression and the infection consequence.

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“…Furthermore, trophozoites recognize human C1q protein, which binds to apoptotic cells, and they more readily phagocytose apoptotic Jurkat T lymphocytes opsonized with C1q (34). E. histolytica calreticulin binds C1q, and cell surface calreticulin functions as a phagocytosis receptor (36). Fluorescently labeled beads coated with C1q are also phagocytosed at a much higher rate than control beads coated with an equal amount of bovine serum albumin (34).…”

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confidence: 99%

Feed-Forward Regulation of Phagocytosis by Entamoeba histolytica

et al. 2012

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The parasitic protozoan Entamoeba histolytica is aptly named for its capacity to destroy host tissue. When E. histolytica trophozoites invade the lamina propria of a host colon, extracellular matrices are degraded while host cells are killed and phagocytosed. The ability of E. histolytica to phagocytose host cells correlates with virulence in vivo. In order to better understand the mechanism of phagocytosis, we used an E. histolytica Affymetrix microarray chip to measure the total gene expression of phagocytic and nonphagocytic subpopulations. Using paramagnetic beads coated with a known host ligand that stimulates phagocytosis, phagocytic and nonphagocytic amoebae from a single culture were purified. Microarray analysis of the subpopulations identified 121 genes with >2-fold higher expression in phagocytic than in nonphagocytic amoebae. Functional annotation identified genes encoding proteins involved in actin binding and cytoskeletal organization as highly enriched gene clusters. Post hoc analyses of selected genes showed that the gene expression profile identified in the microarray experiment did not exist prior to cell sorting but rather was stimulated through phagocytosis. Further, these expression profiles correlated with an increase in phagocytic ability, as E. histolytica cultures exposed to an initial stimulus of phagocytosis showed increased phagocytic ability upon a second stimulus. To our knowledge, this is the first description of such feed-forward regulation of gene expression and phagocytic ability in a phagocyte.

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Entamoeba histolytica Cell Surface Calreticulin Binds Human C1q and Functions in Amebic Phagocytosis of Host Cells

Abstract: ABSTRACTPhagocytosis of host cells is characteristic of tissue invasion by the intestinal amebaEntamoeba histolytica, which causes amebic dysentery and liver abscesses.Entamoeba histolyticainduces host cell apoptosis… Show more

Cited by 39 publications

References 54 publications

Neutrophils Induce Astroglial Differentiation and Migration of Human Neural Stem Cells via C1q and C3a Synthesis

Neutrophils Induce Astroglial Differentiation and Migration of Human Neural Stem Cells via C1q and C3a Synthesis

Cell death offers exceptional cellular and molecular windows for pharmacological interventions in protozoan parasites

Feed-Forward Regulation of Phagocytosis by Entamoeba histolytica

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