• The Journal of the Korean Society for Microbiology
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• v.35 no.2
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• pp.149-157
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• 2000

Mycobacterium tuberculosis is capable of growing and survival within macrophage. The purpose of this study was to identify the genes regulated by infection of mycobacteria in human monocytic THP-1 cells. We used the differential display reverse transcriptase polymerase chain reaction (DD RT-PCR) and nothern blot analysis to confirm the differentially expressed genes from THP-1 cells infected with live Mycobacterium tuberculosis H37Rv, heat-killed Mycobacterium tuberculosis H37Rv and live Mycobacterium bovis BCG. Among many up or down-regulated clones, 27 clones were sequenced and compared with known genes on GenBank. Thirteen of over-expressed clones from THP-1 cells infected with live Mycobacterium tuberculosis H37Rv were identical to human prothymosin alpha, eight were novel clones and six clones showed homology with Human ferritin H chain, Esherichia coli bgl, Mouse RNA-dependent EIF-2 alpha kinase, E. coli htrL, Hyaluronan receptor and T cell receptor. Our result suggests that Mycobacterium tuberculosis might regulate prothymosin alpha gene transcription in monocytic THP-1 cell.

• Korean Journal of Pharmacognosy
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• v.43 no.2
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• pp.157-162
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• 2012

In order to investigate the immunostimulating effect of mycelia extract of Phellinus linteus (PLM) on human monocyte THP-1 and rat peritoneal macrophage cell, we examined measuring cytokine secretion (IL-6 and TNF-${\alpha}$). The production of IL-6 and TNF-a in human monocyte THP-1 was slight increased dose-dependently when the cells were challenged with PLM for 72 hrs. It was also observed that the treatment of PLM with LPS augmented the production of IL-6 and TNF-a in human monocyte THP-1. It was also observed that the treatment of PLM with LPS augmented the production of IL-6 and TNF-${\alpha}$ in human monocyte THP-1. The production of IL-6 and TNF-${\alpha}$ in rat peritoneal macrophage was significantly enhanced when the cells were treated PLM with LPS for 72 hrs. Moreover, the proliferation rate of rat spleen cells was increased in a dose dependent manner as the cells were treated with PLM and Concanavalin A.

• Journal of Periodontal and Implant Science
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• v.39 no.2
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• pp.177-184
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• 2009

Purpose: Interleukin-8 (IL-8) is an important mediator of immune and inflammatory reactions and is produced by a variety of different cell types. This study was undertaken to investigate the effects of lipopolysaccharides (LPSs) from Prevotella intermedia and Prevotella nigrescens, the major causes of inflammatory periodontal disease, on the production of IL-8 and the expression of IL-8 mRNA in differentiated THP-1 cells, a human monocytic cell line. Methods: LPSs from P. intermedia ATCC 25611 and P. nigrescens ATCC 33563 were prepared by the standard hot phenol-water method. THP-1 cells were incubated in the medium supplemented with phorbol myristate acetate to induce differentiation into macrophage-like cells. Results: We found that LPS preparations from P. intermedia and P. nigrescens can induce IL-8 mRNA expression and stimulate the release of IL-8 in differentiated THP-1 cells without additional stimuli. Conclusions: There are no previous reports of the ability of P. intermedia and P. nigrescens LPS to stimulate the release of IL-8, and the present study clearly shows, for the first time, that LPSs from P. intermedia and P. nigrescens fully induced IL-8 mRNA expression and IL-8 production in differentiated human monocytic cell line THP-1. The ability of P. intermedia and P. nigrescens LPS to promote the production of IL-8 may be important in the pathogenesis of inflammatory periodontal disease.

• Journal of Yeungnam Medical Science
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• v.20 no.2
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• pp.129-141
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• 2003

Background: Leptin is a 16-KDa non-glycosylated peptide hormone synthesized almost exclusively by adipocytes. The well-known function of leptin is regulation of food intake and energy expenditure. Leptin also plays a regulatory role in immune and inflammatory process including cytokine production. The purpose of this study was to investigate the effect of leptin on the expression of several chemokine genes(RANTES, IL-8, MCP-1, IP-10, Mig, MIP-$1{\alpha}$, MIP-$1{\beta}$, and GRO-${\alpha}$) in THP-1 cells. Materials and Methods: Total RNA of THP-1 cells were prepared by Trizol method, and then stimulated with the leptin(250 ng/$m{\ell}$) or LPS(100 ng/$m{\ell}$). We examined the expression patterns of various chemokine mRNAs in THP-1 cell lines by RT-PCR and Northern blot. Results: Leptin did not induce the expression of chemokine mRNAs in THP-1 cells. The expression patterns of RANTES, IL-8, MCP-1, IP-10, and Mig mRNAs in THP-1 cells stimulated with leptin and LPS simultaneously was almost same to the patterns of LPS alone-induced chemokine mRNAs. RANTES mRNA expression was independent on the concentrations of leptin. Although leptin did not have strong effect on the expression of RANTES, IL-8, MCP-1, IP-10, Mig, MIP-$1{\alpha}$, MIP-$1{\beta}$, and GRO-${\alpha}$ mRNAs in THP-1 cells, leptin could induce the expression of long isoform of leptin receptor(OB-RL) mRNA, and its expression was elevated in simultaneous stimulation of leptin and LPS. Conclusion: These data suggest that leptin is able to induce OB-RL in THP-1 cells, however, leptin has little effect on the expression of pro-inflammatory chemokine genes.

• Journal of Life Science
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• v.18 no.7
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• pp.952-957
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• 2008

We evaluated the effects of various factors (e.g., serum, inhibitors of protein synthesis, and cytoskeleton and protein kinases) on early PMA-induced THP-1 cell adhesion using an adhesion assay with Sulforhodamine B (SRB) staining, which was used to assess the proliferation of the attached cells. THP-1 cell adhesion to a plastic substrate was detected 1 hr after exposure to Phorbol 12-Myristate 13-Acetate (PMA) and peaked after 18 hr. At concentrations > 25 nM PMA, the level of adhesion did not change. Based on our preliminary results, we used 25 nM PMA and 5 hr of culture as standard assay conditions. Early PMA-induced cell adhesion was not affected by the presence of serum or PD 98059 in the culture medium, but was affected by the addition of PKC inhibitors and cycloheximide. In the presence of actin inhibitor with PMA, the cell adhesion increased when comparing with PMA treatment only. Thus, early PMA-induced adhesion of THP-1 cells does not require serum in the culture medium, MAP-kinase activation, or actin polymerization, but does require de novo protein synthesis and PKC activation. Our SRB-based cell adhesion assay may be used to screen other PKC inhibitors.

• IMMUNE NETWORK
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• v.5 no.4
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• pp.193-198
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• 2005

Background: Protease-activated receptor 2 (PAR2) belongs to a family of G protein coupled receptors activated by proteolytic cleavage. Trypsin-like serine proteases interact with PAR2 expressed by a variety of tissues and immune cells. The aim of our study was to investigate whether PAR2 stimulation can lead to the activation of human mac rophages. Methods: PAR2-mediated proliferation of human macrophage cell line THP-1 was measured with MTT assay. We also examined the extracellular regulated kinase (ERK) phosphorylation and cytokine production induced by trypsin and PAR2-agonist using western blot and enzyme-linked immunosorbent assay (ELISA), respectively. Results: Treatment of trypsin or PAR2-activating peptide increased cell proliferation in a dose-dependent manner, and induced the activation of ERK1/2 in THP-1 cells. In addition, trypsin-induced cell proliferation was inhibited by pretreatment of an ERK inhibitor (pD98059) or trypsin inhibitor (SBTI). Moreover, PAR2 activation by trypsin increased the secretion of TNF-${\alpha}$ in THP-1 cells. Conclusion: There results suggest that P AR2 activation by trypsin-like serine proteases can induce cell proliferation through the activation of ERK in human macrophage and that PAR2 may playa crucial role in the cell proliferation and cytokine secretion induced by trypsin-like serine proteases.

• The Journal of the Korean Society for Microbiology
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• v.35 no.1
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• pp.9-18
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• 2000

Immunological mechanisms involving the release of inflammatory factors by HIV-1 infected microglia in the brain have been implicated in the pathogenesis of HIV dementia (HIVD). Since the regulation of matrix metalloproteinases (MMPs) activity can be influenced by variety of inflammatory mediators, this study was undertaken to look for a correlation between the MMP-9 release and the production of TNF-${\alpha}$ in response to HIV-1 p24 in the human monocyte cell line THP-1 as a model for microglia. First, it was shown that HIV-l core p24 antigen induced THP-1 to secrete MMP-9 in a dose response manner while it elicited a little effect on MMP-2 release in human astroglial cell line T98G. Next, it was found that p24 induced THP-1 to secrete TNF-${\alpha}$ without prior differentiation into macrophages by phorbol myristate acetate (PMA) treatment. Furthermore, anti-TNF-${\alpha}$ neutralizing antibodies significantly blocked p24-induced MMP-9 release in a dose dependent manner. Our data indicate that p24 antigen induces monocytic MMP-9 release by triggering up-regulation of TNF-${\alpha}$ secretion.

• IMMUNE NETWORK
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• v.10 no.5
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• pp.173-180
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• 2010

Background: APRIL, originally known as a cytokine involved in B cell survival, is now known to regulate the inflammatory activation of macrophages. Although the signal initiated from APRIL has been demonstrated, its role in cellular activation is still not clear due to the presence of BAFF, a closely related member of TNF superfamily, which share same receptors (TACI and BCMA) with APRIL. Methods: Through transfection of siRNA, BAFF-deficient THP-1 cells (human macrophage-like cells) were generated and APRIL-mediated inflammatory activities were tested. The expression patterns of APRIL were also tested in vivo. Results: BAFF-deficient THP-1 cells responded to APRIL-stimulating agents such as monoclonal antibody against APRIL and soluble form of TACI or BCMA. Furthermore, co-incubation of the siBAFF-deficient THP-1 cells with a human B cell line (Ramos) resulted in an activation of THP-1 cells which was dependent on interactions between APRIL and TACI/BCMA. Immunohistochemical analysis of human pathologic samples detected the expression of both APRIL and TACI in macrophage-rich areas. Additionally, human macrophage primary culture expressed APRIL on the cell surface. Conclusion: These observations indicate that APRIL, which is expressed on macrophages in pathologic tissues with chronic inflammation, may mediate activation signals through its interaction with its counterparts via cell-to-cell interaction.

• Korean Journal of Food Science and Technology
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• v.48 no.4
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• pp.378-383
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• 2016

The glasswort is an edible halophyte demonstrating various physiological effects including anti-inflammatory activity. In the present study, the effects of glasswort extracts on inflammatory events and interactions of THP-1 monocytes with intestinal epithelial cells were investigated. Five solvent fractions, including the ethylether fraction (Fr.E), were prepared from a 70% methanol extract of glasswort. THP-1 monocytes underwent differentiation by phorbol 12-myristate 13-acetate treatment and were then activated by lipopolysaccharide (LPS), which induced cyclooxygenase (COX)-2 expression. None of the glasswort fractions tested alone induced COX-2 in differentiated THP-1 cells. Fr.E, however, enhanced LPS-induced COX-2 expression in differentiated THP-1 cells. Culture media of THP-1 cells treated with each fraction stimulated the growth of normal intestinal INT-407 cells more prominently than that of HT-29 colon cancer cells. COX-2 expression in HT-29 cells was inhibited when the cells were exposed to the THP-1 culture medium treated with Fr.E. Thus, glasswort could modulate the interaction between immune cells and intestinal cells.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.12
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• pp.6409-6413
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• 2012

The innate immune system coordinates the inflammatory response to pathogens. To do so, its cells must discriminate self from non-self utilizing receptors that identify molecules synthesized exclusively by microbes. Toll-like receptors have a crucial role in the detection of microbial infection in mammals and insects. In mammals, they have evolved to recognize conserved products unique to microbial metabolism. These include lipopolysaccharide (LPS), lipotechoic acids, and peptidoglycans (PGN). We show here that TLRs, including TLR2, are expressed on the THP-1 human leukemia cell line. Activation of TLR2 signaling in THP-1 by PGN induces the synthesis of various soluble factors and proteins including interleukin-$1{\beta}$, interleukin-8 and TNF-${\alpha}$ and apoptosis of THP-1 with PGN dose and time dependence. Moreover, in this study we show that PGN induces apoptosis of THP-1 cells in a TNF-${\alpha}$-dependent manner. These findings indicate that TLR2 signaling results in a cascade leading to tumor apoptosis and differentiation, which may suggest new clinical prospects using TLR2 agonists as cytotoxic agents in certain cancers.