Involvement of secretory and cytosolic phospholipases A2 during infection of THP1 human monocytic cells with Toxoplasma gondii . Effect of interferon γ

2002 ◽  
Vol 88 (3) ◽  
pp. 208-216 ◽  
Author(s):  
Jorge Gomez-Marín ◽  
Hassan El'Btaouri ◽  
Annie Bonhomme ◽  
Frank Antonicelli ◽  
Nathalie Pezzella ◽  
...  
Keyword(s):  
Toxoplasma Gondii ◽  
Interferon Γ ◽  
Monocytic Cells ◽  
Phospholipases A2 ◽  
Cytosolic Phospholipases A2

scholarly journals Autophagy gene-dependent intracellular immunity triggered by interferon-γ

2021 ◽  
Author(s):  
Michael R McAllaster ◽  
Jaya Bhushan ◽  
Dale R Balce ◽  
Anthony Orvedahl ◽  
Arnold Park ◽  
...  
Keyword(s):  
Toxoplasma Gondii ◽  
Interferon Γ ◽  
Degradation Pathway ◽  
Lysosomal Degradation ◽  
Cellular Processes ◽  
Binding Domains ◽  
New Genes ◽  
Autophagy Gene ◽  
Atg Genes ◽  
Dependent Processes

Genes required for the lysosomal degradation pathway of autophagy play key roles in topologically distinct cellular processes with significant physiologic importance. One of the first-described of these ATG gene-dependent processes is the requirement for a subset of ATG genes in interferon-γ (IFNγ)-induced inhibition of Norovirus and Toxoplasma gondii replication. Herein we identified new genes that are required for or that negatively regulate this immune mechanism. Enzymes involved in the conjugation of UFM1 to target proteins including UFC1 and UBA5, negatively regulated IFNγ-induced inhibition of norovirus replication via effects of Ern1. IFNγ-induced inhibition of norovirus replication required Wipi2b and Atg9a, but not Becn1 (encoding Beclin1), Atg14, or Sqstm1. The phosphatidylinositol-3-phosphate and ATG16L1 binding domains of WIPI2B were required for IFNγ-induced inhibition of norovirus replication. Both WIPI2 and SQSTM1 were required for IFN?-induced inhibition of Toxoplasma gondii replication in HeLa cells. These studies further delineate the mechanisms of a programmable form of cytokine-induced intracellular immunity that relies on an expanding cassette of essential ATG genes to restrict the growth of phylogenetically diverse pathogens.

scholarly journals Innate, adaptive, and cell-autonomous immunity against Toxoplasma gondii infection

2019 ◽  
Vol 51 (12) ◽  
pp. 1-10 ◽  
Author(s):  
Miwa Sasai ◽  
Masahiro Yamamoto
Keyword(s):  
Immune Response ◽  
Toxoplasma Gondii ◽  
Immune Responses ◽  
Parasitophorous Vacuole ◽  
Interferon Γ ◽  
Protective Role ◽  
Ifn Γ ◽  
Acquired Immune Responses ◽  
Toxoplasma Gondii Infection ◽  
Antimicrobial Immunity

AbstractHosts have been fighting pathogens throughout the evolution of all infectious diseases. Toxoplasma gondii is one of the most common infectious agents in humans but causes only opportunistic infection in healthy individuals. Similar to antimicrobial immunity against other organisms, the immune response against T. gondii activates innate immunity and in turn induces acquired immune responses. After activation of acquired immunity, host immune cells robustly produce the proinflammatory cytokine interferon-γ (IFN-γ), which activates a set of IFN-γ-inducible proteins, including GTPases. IFN-inducible GTPases are essential for cell-autonomous immunity and are specialized for effective clearance and growth inhibition of T. gondii by accumulating in parasitophorous vacuole membranes. Recent studies suggest that the cell-autonomous immune response plays a protective role in host defense against not only T. gondii but also various intracellular bacteria. Moreover, the negative regulatory mechanisms of such strong immune responses are also important for host survival after infection. In this review, we will discuss in detail recent advances in the understanding of host defenses against T. gondii and the roles played by cell-autonomous immune responses.

Enhanced B7-2 Gene Expression by Interferon-γ in Human Monocytic Cells Is Controlled Through Transcriptional and Posttranscriptional Mechanisms

Blood ◽  
1999 ◽  
Vol 94 (5) ◽  
pp. 1782-1789 ◽  
Author(s):  
R.E. Curiel ◽  
C.S. Garcia ◽  
S. Rottschafer ◽  
M.C. Bosco ◽  
I. Espinoza-Delgado
Keyword(s):  
T Cell Activation ◽  
Cell Activation ◽  
Molecular Mechanisms ◽  
De Novo ◽  
Costimulatory Molecule ◽  
Interferon Γ ◽  
Monocytic Cell ◽  
Monocytic Cells ◽  
Enhanced Expression ◽  
Ifn Γ

B7-2 is a costimulatory molecule expressed on professional antigen-presenting cells that provides T cells with a critical signal resulting in T-cell activation. Interferon-γ (IFN-γ) enhances B7-2 protein expression in monocytic cells. However, the molecular mechanisms controlling the enhanced expression of B7-2 are poorly understood. Northern blot and flow cytometry analysis revealed that human monocytes and the human monocytic cell line MonoMac6 (MM6) constitutively expressed B7-2 mRNA and protein and IFN-γ treatment further enhanced the expression of both molecules. The ability of IFN-γ to enhance B7-2 mRNA was evident at the dose of 31 U/mL and reached plateau levels at 500 U/mL. The effects of IFN-γ on B7-2 mRNA expression were time dependent and occurred within 3 hours of treatment and increased through 24 hours. In vitro transcription assays and mRNA stability experiments showed that IFN-γ increases both transcriptional activity and the stability of B7-2 mRNA. Treatment of MM6 cells with cycloheximide showed that de novo protein synthesis was not required for the IFN-γ–enhanced expression of B7-2 mRNA. Overall, these studies show for the first time that IFN-γ–enhanced expression of B7-2 protein in human monocytic cells is controlled at the gene level through a dual mechanism involving transcriptional and posttranscriptional mechanisms.

Mechanism for uptake of silica particles by monocytic U937 cells

2000 ◽  
Vol 19 (7) ◽  
pp. 412-419 ◽  
Author(s):  
G Hetland ◽  
E Namork ◽  
P E Schwarze ◽  
A Aase
Keyword(s):  
Pulmonary Inflammation ◽  
Interferon Γ ◽  
Silica Particles ◽  
U937 Cells ◽  
Fcγ Receptors ◽  
Monocytic Cells ◽  
Carbon Particles ◽  
Alternative Complement ◽  
Heparin Plasma

We examined the mechanism for uptake by monocytic cells of particles found in the atmosphere of some industrial work places. As a model system, irregular crystalline silica particles (SPs), sphere-like cryptocrystalline microsilica particles (MPs) and carbon particles (CPs) were exposed to pro-monocytic U937 cells. Plasma-treated SP and MP, but not CP, activated the alternative complement pathway, but bound little C3b. However, all particles adsorbed serum IgG, IgA and IgM unspecifically. Phenotyping of U937 cells for complement receptors (CRs) and Fcγ receptors (FcγRs) showed that interferon γ (INFγ) increased expression of FcγRI, CR3 (CD11b/CD18) and CR4 (CD11c/CD18) and that phorbol-12-myristate-13-acetate (PMA) increased expression of CR4. Scanning electron microscopy (SEM) demonstrated higher phagocytosis of plasma-treated SP than native SP by both PMA and INFγ-stimulated, but not unstimulated, cells. MP and CP could not be distinguished from cellular structures. Inhibition experiments in SEM revealed uptake of heparin-plasma-treated SP via Fc'yRI on INFγ-stimulated U937 cells, but could not exclude possible participation of CR3. The results indicate that plasma-treated SPs bind Ig and are internalized by differentiated monocytic cells via FcγR1, which is known to trigger cellular production of toxic oxygen species that may induce pulmonary inflammation in vivo.

scholarly journals Gamma Radiation-Attenuated Toxoplasma gondii Provokes Apoptosis in Ehrlich Ascites Carcinoma-Bearing Mice Generating Long-Lasting Immunity

2020 ◽  
Vol 19 ◽  
pp. 153303382092659
Author(s):  
Eman N. Hafez ◽  
Fatma S. M. Moawed ◽  
Gehan R. Abdel-Hamid ◽  
Nermeen M. Elbakary
Keyword(s):  
Growth Factor ◽  
Toxoplasma Gondii ◽  
Gamma Radiation ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Ehrlich Ascites Carcinoma ◽  
Interferon Γ ◽  
Ehrlich Ascites ◽  
Matrix Metallopeptidase ◽  
Factor Α

Purpose: Pathological angiogenesis and apoptosis evasions are common hallmarks of cancer. A different approach to the antitumor effect of parasitic diseases caused by certain protozoans and helminthes had been adopted in recent years as they can affect many cancer characteristics. The present work is an attempt to assess the effect of gamma radiation-attenuated Toxoplasma gondii ME49 as an antiapoptotic and angiogenic regulator modifier on tumor growth aimed at improving cancer protective protocols. Methods: Attenuated Toxoplasma gondii ME49 was administered orally to mice 2 weeks before inoculation with Ehrlich ascites carcinoma to allow stimulation of the immune response. Hepatic histopathology and immune responses were determined for each group. Results: Marked suppression of the tumor proliferation with induction of long-lasting immunity by stimulating interferon γ and downregulating transforming growth factor β. The level of tumor promoting inflammatory markers (STAT-3 and tumor necrosis factor α), the angiogenic factors (vascular endothelial growth factor A, integrin, and matrix metallopeptidase 2 and matrix metallopeptidase 9), as well as nitric oxide concentration were significantly decreased. This was collimated with an improvement in apoptotic regulators (cytochrome-c, Bax, Bak, and caspase 3) in liver tissues of vaccinated mice group compared to Ehrlich ascites carcinoma-bearing one. Moreover, the histopathological investigations confirmed this improvement. Conclusion: Hence, there is an evidence of potency of radiation attenuated Toxoplasma vaccine in immune activation and targeting tumor cell that can be used as a prophylactic or an adjuvant in combination with chemotherapeutic drugs.

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