Macrophage-Mediated Inhibitory Effect ofZingiber officinaleRosc, A Traditional Oriental Herbal Medicine, on the Growth of Influenza A/Aichi/2/68 Virus

2006 ◽  
Vol 34 (01) ◽  
pp. 157-169 ◽  
Author(s):  
Nobuko Imanishi ◽  
Tsugunobu Andoh ◽  
Naoki Mantani ◽  
Shinya Sakai ◽  
Katsutoshi Terasawa ◽  
...  
Keyword(s):  
Herbal Medicine ◽  
Influenza A ◽  
Mdck Cells ◽  
Zingiber Officinale ◽  
Inhibitory Effect ◽  
Aichi Virus ◽  
Tnf Α ◽  
Infected Cells ◽  
Necrosis Factor ◽  
Darby Canine Kidney

The inhibitory effect of Zingiber officinale Rosc (ZOR), an Oriental traditional herbal medicine, on the growth of influenza A/Aichi/2/68 (Aichi) virus was investigated in Madin-Darby canine kidney (MDCK) cells. Direct addition of ZOR (0.1 ~ 100 μ g/ml ) to the infected cells did not have any inhibitory effect. However, the ZOR-induced conditioned medium (ZOR-CM) of RAW cells, a murine macrophage (Mφ) cell line, exhibited an apparent inhibitory effect on MDCK cells without cytotoxicity. In accordance with the time-dependent inhibitory effect of ZOR-CM, it has been demonstrated that tumor necrosis factor (TNF)-α was gradually accumulated in ZOR-CM by the induction of TNF-α mRNA expression in ZOR-stimulated RAW cells. Conversely, the inhibitory effect of ZOR-CM was reduced significantly by the removal of TNF-α after the formation of an immune complex with anti-TNF-α monoclonal antibody. These data suggested that ZOR itself has no inhibitory effect on the growth of influenza virus, but could exert its effect via macrophage activation leading to production of TNF-α.

Inhibitory Effect of TNF-α Produced by Macrophages Stimulated withGrifola frondosaExtract (ME) on the Growth of Influenza A/Aichi/2/68 Virus in MDCK Cells

2008 ◽  
Vol 36 (06) ◽  
pp. 1171-1183 ◽  
Author(s):  
Nobuko Obi ◽  
Katsumi Hayashi ◽  
Tatsurou Miyahara ◽  
Yutaka Shimada ◽  
Katsutoshi Terasawa ◽  
...  
Keyword(s):  
Influenza A ◽  
Mdck Cells ◽  
Inhibitory Effect ◽  
Fixed Dose ◽  
Madin Darby Canine Kidney ◽  
Tnf Α ◽  
Ultra Filtration ◽  
Infected Cells ◽  
Darby Canine Kidney

We investigated the inhibitory effect of the conditioned medium (CM) from P338D1 (D1) cells, a murine macrophage cell line, stimulated for 10 hours with a fixed dose (100 μg/ml) of the extracts from the fruit bodies of Grifola frondosa (ME) or its ultra filtration-based fractions (MFs), on the growth of influenza A/Aichi/2/68 virus in Madin-Darby canine kidney cells. Direct addition of ME and 3 kinds of MFs (MF1, MF2 and MF3) to the infected cells had no obvious inhibitory effect. However, virus yields were reduced in the presence of CMs. Notably, the inhibitory effect of the CM prepared by using MF2 (molecular weight of 30 Kd to 100 Kd) was the strongest (28% reduction compared to the control). RT-PCR and ELISA assays showed that the CMs could induce the expression of TNF-α mRNA in D1 cells leading to production of TNF-α, known as an antiviral cytokine. These findings suggest that ME and MFs (especially MF-2) might induce the production of certain factors, including TNF-α, which are responsible for the inhibition of viral growth in vitro.

scholarly journals Additional Inhibitory Effect of Tea Extract on the Growth of Influenza A and B Viruses in MDCK Cells

2002 ◽  
Vol 46 (7) ◽  
pp. 491-494 ◽  
Author(s):  
Nobuko Imanishi ◽  
Yumiko Tuji ◽  
Yuko Katada ◽  
Miyuki Maruhashi ◽  
Satoko Konosu ◽  
...  
Keyword(s):  
Influenza A ◽  
Mdck Cells ◽  
Inhibitory Effect ◽  
Tea Extract

scholarly journals Aging-induced IL27Ra signaling impairs hematopoietic stem cells

Blood ◽  
2020 ◽  
Vol 136 (2) ◽  
pp. 183-198 ◽  
Author(s):  
Hanqing He ◽  
Panglian Xu ◽  
Xiaofei Zhang ◽  
Min Liao ◽  
Qiongye Dong ◽  
...  
Keyword(s):  
Functional Decline ◽  
Inhibitory Effect ◽  
Myeloid Differentiation ◽  
Myeloproliferative Disease ◽  
Hematopoietic Stem ◽  
Tnf Α ◽  
Increasing Risk ◽  
Factor Α ◽  
Inflammatory Insult ◽  
Necrosis Factor

Abstract Hematopoietic stem cell (HSC) aging correlates with an increasing risk of myeloproliferative disease and immunosenescence. In this study, we show that aging-related inflammation promotes HSC aging through tumor necrosis factor-α (TNF-α)→ERK→ETS1→interleukin27Ra (IL27Ra) pathway. TNF-α, a well-known biomarker of inflammation, increases during aging and induces the expression of IL27Ra on HSCs via ERK-ETS1 signaling. Deletion of IL27Ra rescues the functional decline and myeloid bias of HSCs and also reverses the inhibitory effect of TNF-α on HSCs. Aged IL27Ra−/− mice had a reduced proportion of myeloid-biased HSCs and did not display the biased myeloid differentiation that occurs in aged wild-type mice. IL27Ra+ HSCs exhibit impaired reconstitution capacity and myeloid-bias compared with IL27Ra− HSCs and serve as a myeloid-recovery pool upon inflammatory insult. Inflammation-related genes were enriched in IL27Ra+ HSCs and this enrichment increases with aging. Our study demonstrates that age-induced IL27Ra signaling impairs HSCs and raises the possibility that interfering with IL27Ra signaling can counter the physiologically deleterious effect of aging on hematopoietic capacity.

Inhibition of endotoxin-induced lung inflammation by interleukin-10 gene transfer in mice

2000 ◽  
Vol 279 (5) ◽  
pp. L872-L877 ◽  
Author(s):  
Sujatha Dokka ◽  
Carl J. Malanga ◽  
Xianglin Shi ◽  
Fei Chen ◽  
Vincent Castranova ◽  
...  
Keyword(s):  
Gene Transfer ◽  
Lung Inflammation ◽  
Transgene Expression ◽  
Tumor Necrosis ◽  
Interleukin 10 ◽  
Inhibitory Effect ◽  
Biologically Active ◽  
Tnf Α ◽  
Anti Inflammatory Cytokine ◽  
Necrosis Factor

Interleukin (IL)-10 is an anti-inflammatory cytokine that has great potential for use in the treatment of inflammatory and immune illnesses. In this study, gene transfer was used to induce IL-10 transgene expression in murine lungs for treatment of endotoxin-induced lung inflammation. Gene transfer was performed with a cytomegalovirus (CMV)-IL-10 plasmid with the aid of the liposomal agents LipofectAMINE and N-[1-(2,3-dioleoyl)propyl]- N, N, N-trimethylammonium methylsulfate (DOTAP). Administration of the endotoxin caused a marked increase in lung inflammation as indicated by increased tumor necrosis factor (TNF)-α release and neutrophil count. Pretreatment of the mice with IL-10 plasmid with and without LipofectAMINE had no inhibitory effect on lung inflammation and IL-10 transgene expression. LipofectAMINE by itself induced lung inflammation, an effect that was not observed with DOTAP. IL-10 plasmid when codelivered with DOTAP expressed biologically active IL-10 protein and caused a reduction in endotoxin-induced inflammation. Transgene expression was observed as early as 3 h after administration, peaked at 12 h, and declined thereafter. We conclude that IL-10 gene transfer is a feasible approach for the treatment of lung inflammation.

scholarly journals Defective presentation to class I-restricted cytotoxic T lymphocytes in vaccinia-infected cells is overcome by enhanced degradation of antigen.

1988 ◽  
Vol 168 (4) ◽  
pp. 1211-1224 ◽  
Author(s):  
A Townsend ◽  
J Bastin ◽  
K Gould ◽  
G Brownlee ◽  
M Andrew ◽  
...  
Keyword(s):  
Influenza A ◽  
Signal Sequence ◽  
Late Phase ◽  
Inhibitory Effect ◽  
Class I ◽  
Detectable Effect ◽  
Protein Fragments ◽  
Infected Target Cell ◽  
Infected Cells ◽  
The Relationship

Vaccinia infection interferes with the presentation of influenza Haemagglutinin (HA) and Nucleoprotein (NP) to class I-restricted CTL. The inhibitory effect is selective for certain epitopes, and is more profound during the late phase of infection. For influenza A/NT/60/68 NP, the block is present during both early and late phases of infection, and is selective for the COOH-terminal epitope defined by peptide 366-379, having no detectable effect on the presentation of the NH2-terminal epitope 50-63. The presentation of HA is inhibited only during the late phase of vaccinia infection. For both proteins, presentation is partially (NP) or completely (HA) restored by expression of rapidly degraded protein fragments in the vaccinia infected target cell. For HA, deletion of the NH2-terminal signal sequence completely overcomes the block. For NP, either a large NH2-terminal deletion or the construction of a rapidly degraded ubiquitin-NP fusion protein partially restores presentation. These results illustrate the relationship between degradation of viral proteins in the cytoplasm of an infected cell and recognition of epitopes at the cell surface by class I-restricted T cells.

scholarly journals Mechanisms of liver disease: cross-talk between the NF-κB and JNK pathways

2009 ◽  
Vol 390 (10) ◽  
Author(s):  
Salvatore Papa ◽  
Concetta Bubici ◽  
Francesca Zazzeroni ◽  
Guido Franzoso
Keyword(s):  
Cell Death ◽  
Liver Disease ◽  
Liver Injury ◽  
Cellular Response ◽  
Protective Role ◽  
Activation Of Transcription ◽  
Tnf Α ◽  
Infected Cells ◽  
Hepatocyte Death ◽  
Necrosis Factor

Abstract The liver plays a central role in the transformation and degradation of endogenous and exogenous chemicals, and in the removal of unwanted cells such as damaged, genetically mutated and virus-infected cells. Because of this function, the liver is susceptible to toxicity caused by the products generated during these natural occurrences. Hepatocyte death is the major feature of liver injury. In response to liver injury, specific intracellular processes are initiated to maintain liver integrity. Inflammatory cytokines including tumor necrosis factor (TNF)α and interleukin-6 (IL-6) are key mediators of these processes and activate different cellular response such as proliferation, survival and death. TNFα induces specific signaling pathways in hepatocytes that lead to activation of either pro-survival mediators or effectors of cell death. Whereas activation of transcription factor NF-κB promotes survival, c-Jun N-terminal kinases (JNKs) and caspases are strategic effectors of cell death in the TNFα-mediated signaling pathway. This review summarizes recent advances in the mechanisms of TNFα-induced hepatotoxicity and suggests that NF-κB plays a protective role against JNK-induced hepatocyte death. Identification of the mechanisms regulating interplay between the NF-κB and JNK pathways is required in the search for novel targets for the treatment of liver disease, including hepatitis and hepatocellular carcinoma.

scholarly journals Protective Role of Combined Polyphenols and Micronutrients against Influenza A Virus and SARS-CoV-2 Infection In Vitro

Biomedicines ◽  
2021 ◽  
Vol 9 (11) ◽  
pp. 1721
Author(s):  
Marta De Angelis ◽  
David Della-Morte ◽  
Gabriele Buttinelli ◽  
Angela Di Martino ◽  
Francesca Pacifici ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Influenza A ◽  
Viral Proteins ◽  
Antiviral Effect ◽  
Inhibitory Effect ◽  
Protective Role ◽  
Virus Infections ◽  
Infected Cells ◽  
Respiratory Virus Infections

Polyphenols have been widely studied for their antiviral effect against respiratory virus infections. Among these, resveratrol (RV) has been demonstrated to inhibit influenza virus replication and more recently, it has been tested together with pterostilbene against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. In the present work, we evaluated the antiviral activity of polydatin, an RV precursor, and a mixture of polyphenols and other micronutrients, named A5+, against influenza virus and SARS-CoV-2 infections. To this end, we infected Vero E6 cells and analyzed the replication of both respiratory viruses in terms of viral proteins synthesis and viral titration. We demonstrated that A5+ showed a higher efficacy in inhibiting both influenza virus and SARS-CoV-2 infections compared to polydatin treatment alone. Indeed, post infection treatment significantly decreased viral proteins expression and viral release, probably by interfering with any step of virus replicative cycle. Intriguingly, A5+ treatment strongly reduced IL-6 cytokine production in influenza virus-infected cells, suggesting its potential anti-inflammatory properties during the infection. Overall, these results demonstrate the synergic and innovative antiviral efficacy of A5+ mixture, although further studies are needed to clarify the mechanisms underlying its inhibitory effect.

In Vitro Inhibitory Effect of Protopanaxadiol Ginsenosides on Tumor Necrosis Factor (TNF)-α Production and its Modulation by Known TNF-α Antagonists

Planta Medica ◽  
2001 ◽  
Vol 67 (3) ◽  
pp. 213-218 ◽  
Author(s):  
Jae Youl Cho ◽  
Eun Sook Yoo ◽  
Kyong Up Baik ◽  
Myung Hwan Park ◽  
Byung Hoon Han
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Inhibitory Effect ◽  
Tnf Α ◽  
Necrosis Factor

scholarly journals Mechanism of Entry Determines the Ability of Toxoplasma gondii To Inhibit Macrophage Proinflammatory Cytokine Production

2002 ◽  
Vol 70 (9) ◽  
pp. 5216-5224 ◽  
Author(s):  
Barbara A. Butcher ◽  
Eric Y. Denkers
Keyword(s):  
Toxoplasma Gondii ◽  
Cytokine Production ◽  
Parasitophorous Vacuole ◽  
Interleukin 12 ◽  
Proinflammatory Cytokine Production ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Infected Cells ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT Macrophages (Mφ) infected with tachyzoites of the opportunistic protozoan Toxoplasma gondii are blocked in production of the proinflammatory cytokines tumor necrosis factor alpha (TNF-α) and interleukin-12 (IL-12) in response to lipopolysaccharide (LPS) triggering, and this is associated with parasite-induced inhibition of NFκB translocation. Here, we demonstrate a requirement for active invasion in the ability of the parasite to mediate suppression. Neither soluble tachyzoite antigen nor secreted products were suppressive, and heat-inactivated, antibody-coated tachyzoites, which efficiently entered the cell through receptor-mediated uptake, failed to inhibit LPS responses. Cytochalasin D, a drug blocking tachyzoite invasion of, but not adherence to, Mφ, severely curtailed Toxoplasma-induced suppression. In addition, parasite-induced nonresponsiveness, as measured by TNF-α production, was reversed by treating infected cells with the toxoplasmastatic drugs pyrimethamine and 6-thioxanthine prior to LPS stimulation. A divergence in IL-12 and TNF-α responses was found during extended incubation of tachyzoites and Mφ in that 24 h of incubation of infected Mφ resulted in IL-12, but not TNF-α, secretion, and production of the latter cytokine remained suppressed when these cells were subjected to LPS triggering. Our results demonstrate that active invasion and survival of the parasite within the parasitophorous vacuole are required to induce and maintain Mφ cytokine-specific nonresponsiveness to LPS. They also show that the effects of Toxoplasma on IL-12 and TNF-α production are nonidentical, with the parasite exerting a longer-lasting suppression of the latter.

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