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mTOR signaling promotes foam cell formation and inhibits foam cell egress through suppressing the SIRT1 signaling pathway.

Atherosclerosis (AS) is a chronic immuno‑inflammatory disease accompanied by dyslipidemia. The authors previously demonstrated that sirtuin 1 (SIRT1) may prevent atherogenesis through influencing the liver X receptor/C‑C chemokine receptor type 7/nuclear factor‑κB (LXR‑CCR7/NF‑κB) signaling pathway. Previous studies have suggested a role for mammalian target of rapamycin (mTOR) signaling in the pathogenesis of cardiovascular diseases. The present study investigated the potential association between mTOR signaling and SIRT1‑LXR‑CCR7/NF‑κB signaling (SIRT1 signaling) in AS pathogenesis. To induce foam cell formation, U937 cells were differentiated into macrophages by exposure to phorbol 12‑myristate 13‑acetate (PMA) for 24 h, followed by treatment with palmitate and oxidized low density lipoprotein for a further 24 h. Oil red O staining revealed a large accumulation of lipid droplets present in foam cells. Western blot analysis demonstrated increased protein levels of phosphorylated (p)‑mTOR and its downstream factor p‑ribosomal protein S6 kinase (p70S6K). Reverse transcription‑quantitative polymerase chain reaction and western blot analyses additionally revealed decreased expression of SIRT1, LXRα and CCR7 and increased expression of NF‑κB and its downstream factor tumor necrosis factor‑α (TNF‑α) in an atherogenetic condition induced by lysophosphatidic acid (LPA). In addition, abundant lipid droplets accumulated in U937‑LPA‑treated foam cells. Rapamycin, an mTOR inhibitor, suppressed the expression and activity of mTOR and p70S6K, however enhanced expression of SIRT1, LXRα, and CCR7. Conversely, rapamycin deceased TNF‑α and NF‑κB activity, the latter of which was further confirmed by immunofluorescence analysis demonstrating increased levels of NF‑κB present in the cytoplasm compared with the nucleus. The findings of the present study suggest that mTOR signaling promotes foam cell formation and inhibits foam cell egress via suppression of SIRT1 signaling.

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Apoptosis‑independent cleavage of RhoGDIβ at Asp19 during PMA‑stimulated differentiation of THP‑1 cells to macrophages.

Rho GDP-dissociation inhibitor β (RhoGDIβ), a regulator of the Rho family of proteins, is expressed abundantly in the hematopoietic cell lineage. During apoptosis of hematopoietic cells, RhoGDIβ is cleaved by caspase‑3 at Asp19 and this cleaved form (Δ19‑RhoGDIβ) has been implicated in the apoptotic pathway. To clarify the role of RhoGDIβ in hematopoietic cells, the present study performed immunoblotting and immunofluorescence staining to examine the expression of RhoGDIβ and ∆19‑RhoGDIβ during phorbol 12‑myristate 13‑acetate (PMA)‑stimulated differentiation of human THP‑1 monocytic cells to macrophages. During differentiation of the THP‑1 cells to macrophages, the expression of RhoGDIβ remained stable; however, the expression of Δ19‑RhoGDIβ increased, particularly in well‑spreading, non‑apoptotic cells, which differentiated into macrophages. These results suggested that Δ19‑RhoGDIβ has an apoptosis‑independent role in the PMA‑induced differentiation of THP‑1 cells to macrophages.

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Mangiferin inhibits macrophage classical activation via downregulating interferon regulatory factor 5 expression.

Mangiferin is a natural polyphenol and the predominant effective component of Mangifera indica Linn. leaves. For hundreds of years, Mangifera indica Linn. leaf has been used as an ingredient in numerous traditional Chinese medicine preparations for the treatment of bronchitis. However, the pharmacological mechanism of mangiferin in the treatment of bronchitis remains to be elucidated. Macrophage classical activation is important role in the process of bronchial airway inflammation, and interferon regulatory factor 5 (IRF5) has been identified as a key regulatory factor for macrophage classical activation. The present study used the THP‑1 human monocyte cell line to investigate whether mangiferin inhibits macrophage classical activation via suppressing IRF5 expression in vitro. THP‑1 cells were differentiated to macrophages by phorbol 12‑myristate 13‑acetate. Macrophages were polarized to M1 macrophages following stimulation with lipopolysaccharide (LPS)/interferon‑γ (IFN‑γ). Flow cytometric analysis was conducted to detect the M1 macrophages. Reverse transcription‑quantitative polymerase chain reaction was used to investigate cellular IRF5 gene expression. Levels of proinflammatory cytokines and IRF5 were assessed following cell culture and cellular homogenization using enzyme‑linked immunosorbent assay. IRF5 protein and nuclei co‑localization was performed in macrophages with laser scanning confocal microscope immunofluorescence analysis. The results of the present study demonstrated that mangiferin significantly inhibits LPS/IFN‑γ stimulation‑induced classical activation of macrophages in vitro and markedly decreases proinflammatory cytokine release. In addition, cellular IRF5 expression was markedly downregulated. These results suggest that the inhibitory effect of mangiferin on classical activation of macrophages may be exerted via downregulation of cellular IRF5 expression levels.

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Sesamin attenuates mast cell-mediated allergic responses by suppressing the activation of p38 and nuclear factor-κB.

Establishing therapeutic agents for the treatment of allergic diseases is an important focus of human health research. Sesamin, a lignan in sesame oil, exhibits a diverse range of pharmacological properties. However, to the best of our knowledge, the effect of sesamin on mast cell‑mediated allergic responses has not yet been investigated. Thus, the aim of the present study was to investigate the effect of sesamin on mast cell‑mediated allergic responses and the underlying mechanisms by which it produces this effect. In rats, oral administration of sesamin inhibited passive cutaneous anaphylaxis. Sesamin exposure attenuated immunoglobulin E‑induced histamine release from rat peritoneal mast cells, which was indicated to be mediated by the modulation of intracellular calcium. In human mast cells, sesamin reduced the stimulatory effects of phorbol 12‑myristate 13‑acetate and calcium ionophore A23187 on the production and secretion of pro‑inflammatory cytokines, including tumor necrosis factor‑α and interleukin‑6. The inhibitory effect of sesamin on pro‑inflammatory cytokine production was dependent on nuclear factor κ‑light‑chain‑enhancer of activated B cells (NF‑κB) and p38 mitogen‑activated protein kinase (MAPK). The present study demonstrates that sesamin inhibits mast cell‑derived inflammatory allergic reactions by blocking histamine release, and pro‑inflammatory cytokine production and secretion. In addition, the findings indicate that the effect of sesamin is mediated by its effect on p38 MAPK/NF‑κB signaling. Furthermore, the in vivo and in vitro anti‑allergic effects of sesamin reported in the present study suggest that it is a promising therapeutic agent for the treatment of inflammatory allergic diseases.

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Arazyme inhibits cytokine expression and upregulates skin barrier protein expression.

In the present study, the inhibitory effect of arazyme on allergic inflammation was investigated by evaluating the alteration of cytokine production and expression of skin barrier proteins in immune and HaCaT human keratinocyte cells. THP‑1 human monocytic and EoL‑1 human eosinophilic cells were treated with Dermatophagoides pteronissinus extract (DpE). Monocyte chemotactic protein‑1 (MCP‑1)/CCL2, interleukin (IL)‑6 and IL‑8 increased following DpE treatment and arazyme significantly blocked the increase of MCP‑1, IL‑6 and IL‑8 expression in cell types. Secretion of MCP‑1, IL‑6 and IL‑8 induced by lipopolysaccharide in THP‑1 cells was also inhibited by arazyme treatment. Arazyme inhibited the secretion of IL‑6 and IL‑8 due to phorbol 12‑myristate 13‑acetate and calcium ionophores in human mast cells. Arazyme blocked the secretion of thymus and activation‑regulated chemokine (TARC)/CCL17, MCP‑1, IL‑6 and IL‑8 due to tumor necrosis factor‑α (TNF‑α) and interferon‑γ (IFN‑γ) in HaCaT cells. TNF‑α and IFN‑γ suppressed the expression of skin barrier proteins, including filaggrin, involucrin and loricrin. By contrast, arazyme increased the expression of filaggrin, involucrin and loricrin. These results may contribute to the development of a therapeutic drug for the treatment of allergic diseases, including atopic dermatitis.

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CD4+ cells proliferate after peanut-extract-specific and CD8+ cells proliferate after polyclonal stimulation of PBMC of children with atopic dermatitis.

Few studies describe in vitro food-allergen induced proliferative responses and cytokine production of PBMC of children with atopic dermatitis. This is especially true for peanut-allergen.

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A new role for interleukin-7 in the induction of LFA-1 and VLA-4 adhesion molecules in Phorbol 12myristate 13acetate activated CD4+ CD23+ T-cell subset.

The low affinity receptor for IgE, CD23, has been described in several pathological conditions. However, the factors involved in the upregulation or downregulation of this receptor are still debated.

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The induction kinetics of Il-8 messenger RNA in HL60 cells demonstrate the participation of negative-acting gene(s).

Interleukin-8 (IL-8) mRNA was rapidly, but not permanently, induced at high levels by phorbol-12myristate-13acetate (PMA) in HL60 cells. Ongoing protein synthase does not seem to be required for the initial induction of IL-8 gene expression. However, the rate of transient induction kinetics was modulated by cycloheximide (CHX) indicating that secondary response genes are involved in the regulation of IL-8 RNA levels. Repression of the induced IL8 mRNA by 21 h PMA-treatment was due to reduced transcriptional activity of the gene. In HL60 cells stimulated for 1.5 and 21 h the half-lives of the lL-8 transcripts were markedly increased, suggesting the presence of negatively-acting transcriptional regulator(s).

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CD23/Fc epsilon RII expression on phytohemagglutinin-A- or phorbol-12myristate-13acetate-Ca(2+)-activated human tonsil T cells.

The low-affinity Fc receptor for IgE, CD23/Fc epsilon RII, has been expressed in T cell lines and pathologic T cells, but its presence on normal human T cells is still debated. We studied the expression of CD23/Fc epsilon RII on purified T cells from normal peripheral blood mononuclear cells (PBMC) or tonsil T cells stimulated with 10 micrograms/ml phytohemagglutinin A (PHA) or phorbol-12myristate- 13acetate (PMA) Ca2+. Using two-dimensional flow cytometry, the tonsil T-cell-enriched population showed > 10% of CD23/Fc epsilon RII expression when coexpressed with the CD3 antigen. CD4+ T cells appear to be principally involved in the expression of CD23/Fc epsilon RII, although we were unable to detect a clear expression of CD23/Fc epsilon RII in PBMC that were activated with either PHA or PMA Ca2+. PHA stimulation resulted in the release of IgE binding factor (IgEBF). The induction of CD23/Fc epsilon RII expression in PHA- and PMA-Ca(2+)-activated T cells was enhanced by IL-4, but not by IgE or IL-6. IL-4 also augmented the PHA- and PMA-Ca(2+)-induced release of IgEBF. The addition of supernatant from the Epstein-Barr virus (EBV)-infected cell line to PHA- or PMA-Ca(2+)-stimulated tonsil T cells did not increase CD23/Fc epsilon RII expression. The expression of CD23/Fc epsilon RII mRNA was detected in RNA prepared from a tonsil T-cell-enriched population by Northern blot analysis.

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