scholarly journals Salvadora persica protects mouse intestine from eimeriosis

2019 ◽  
Vol 28 (4) ◽  
pp. 605-612 ◽  
Author(s):  
Saleh Al-Quraishy ◽  
Felwa Abdullah Thagfan ◽  
Esam Mohamed Al-Shaebi ◽  
Mahmood Qasem ◽  
Rewaida Abdel-Gaber ◽  
...  
Keyword(s):  
B Cell Lymphoma ◽  
Interferon Γ ◽  
Salvadora Persica ◽  
Leaf Extracts ◽  
Therapeutic Value ◽  
Mouse Intestine ◽  
Apoptotic Genes ◽  
Factor Α ◽  
Necrosis Factor

Abstract Eimeriosis is a global poultry health problem. In the current study, we investigated the role of Salvadora persica leaf extracts (SE) against murine eimeriosis induced by Eimeria papillata. The infection induced an oocyst output of 6242 ± 731 oocysts/g feces. After treatment with 300 mg⁄kg SE, the oocysts expelled in feces decreased by approximately 3-fold. In addition, the total number of E. papillata in the parasitic stage decreased in the jejunum of mice after treatment with SE. In addition, SE significantly reduced the number of apoptotic cells by approximately 2-fold in the infected jejunum. SE ameliorated the changes in glutathione, malondialdehyde, and catalase due to E. papillata infection. Finally, SE regulated the cytokine genes, interleukin (IL)-1β, IL-6, interferon-γ, and tumor necrosis factor-α, and the apoptotic genes, B-cell lymphoma-2, Bax, and Caspase-3. SE protects the jejunum from E. papillata induced injury and may have potential therapeutic value as a food additive during eimeriosis.

scholarly journals HIF1α/TET1 Pathway Mediates Hypoxia-Induced Adipocytokine Promoter Hypomethylation in Human Adipocytes

Cells ◽  
2020 ◽  
Vol 9 (1) ◽  
pp. 134 ◽  
Author(s):  
Mohamed M. Ali ◽  
Shane A. Phillips ◽  
Abeer M. Mahmoud
Keyword(s):  
Dna Methylation ◽  
Interleukin 1 ◽  
Hypoxia Inducible Factor ◽  
Interferon Γ ◽  
The Body ◽  
Human Adipocytes ◽  
Protein Levels ◽  
Factor Α ◽  
Necrosis Factor

Obesity is associated with the accumulation of dysfunctional adipose tissue that secretes several pro-inflammatory cytokines (adipocytokines). Recent studies have presented evidence that adipose tissues in obese individuals and animal models are hypoxic, which may result in upregulation and stabilization of the hypoxia inducible factor HIF1α. Epigenetic mechanisms such as DNA methylation enable the body to respond to microenvironmental changes such as hypoxia and may represent a mechanistic link between obesity-associated hypoxia and upregulated inflammatory adipocytokines. The purpose of this study was to investigate the role of hypoxia in modifying adipocytokine DNA methylation and subsequently adipocytokine expression. We suggested that this mechanism is mediated via the DNA demethylase, ten-eleven translocation-1 (TET1), transcription of which has been shown to be induced by HIF1α. To this end, we studied the effect of hypoxia (2% O2) in differentiated subcutaneous human adipocytes in the presence or absence of HIF1α stabilizer (Dimethyloxalylglycine (DMOG), 500 μM), HIF1α inhibitor (methyl 3-[[2-[4-(2-adamantyl) phenoxy] acetyl] amino]-4-hydroxybenzoate, 30 μM), or TET1-specific siRNA. Subjecting the adipocytes to hypoxia significantly induced HIF1α and TET1 protein levels. Moreover, hypoxia induced global hydroxymethylation, reduced adipocytokine DNA promoter methylation, and induced adipocytokine expression. These effects were abolished by either HIF1α inhibitor or TET1 gene silencing. The major hypoxia-responsive adipocytokines were leptin, interleukin-1 (IL6), IL1β, tumor necrosis factor α (TNFα), and interferon γ (IFNγ). Overall, these data demonstrate an activation of the hydroxymethylation pathway mediated by TET1. This pathway contributes to promoter hypomethylation and gene upregulation of the inflammatory adipocytokines in adipocytes in response to hypoxia.

Multiple Inhibitory Cytokines Induce Deregulated Progenitor Growth and Apoptosis in Hematopoietic Cells From Fac−/− Mice

Blood ◽  
1998 ◽  
Vol 91 (11) ◽  
pp. 4092-4098 ◽  
Author(s):  
Laura S. Haneline ◽  
Hal E. Broxmeyer ◽  
Scott Cooper ◽  
Giao Hangoc ◽  
Madeleine Carreau ◽  
...  
Keyword(s):  
Hematopoietic Cells ◽  
Interferon Γ ◽  
Major Mechanism ◽  
Inflammatory Protein ◽  
Tnf Α ◽  
Murine Homologue ◽  
Anemia Group ◽  
Factor Α ◽  
Necrosis Factor

Abstract We used a murine model containing a disruption of the murine homologue (Fac) of Fanconi Anemia group C (FAC) to evaluate the role of Fac in the pathogenesis of bone marrow (BM) failure. Methylcellulose cultures of BM cells fromFac−/− and Fac+/+ mice were established to examine the growth of multipotent and lineage-restricted progenitors containing inhibitory cytokines, including interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α), and macrophage inflammatory protein-1α (MIP-1α). Clonogenic growth of Fac−/− progenitors was reduced by 50% at 50- to 100-fold lower concentrations of all inhibitory cytokines evaluated. We hypothesized that the aberrant responsiveness to inhibitory cytokines in clonogenic cells may be a result of deregulated apoptosis. To test this hypothesis, we performed the TUNEL assay on purified populations of primary BM cells enriched for hematopoietic progenitors or differentiated myeloid cells. After stimulation with TNF-α, accentuated apoptosis was observed in both populations of Fac−/− cells. In addition, deregulated apoptosis was also noted in the most immature phenotypic population of hematopoietic cells after stimulation with MIP-1α.Together these data suggest a role of Fac in affecting the signaling of multiple cytokine pathways and support cytokine-mediated apoptosis as a major mechanism responsible for BM failure observed in FA patients.

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