Interferon-γ enhances phorbol myristate acetate-induced cell attachment and tumor necrosis factor production via the NF-κB pathway in THP-1 human monocytic cells

Kurihara, Yusuke; Furue, Masutaka

doi:10.3892/mmr.2013.1419

Cited by 15 publications

(17 citation statements)

References 17 publications

(21 reference statements)

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“…It has been reported that most T h 1 polarized responses are elicited by the adjuvants that behave as agonists of TLR3, TLR4, TLR7, TLR8, and TLR9, which corroborates the present study (13). Interferon-␥ (IFN-␥) is a T h 1-specific cytokine that is crucial in macrophage activation (52). TR-433 produced an appreciable amount of IgG2a titers and IFN-␥ that was further supported by the expression of T-bet transcription factors (Fig.…”

Section: A Tlr4-derived Peptide As An Adjuvantsupporting

confidence: 91%

A TLR4-derived non-cytotoxic, self-assembling peptide functions as a vaccine adjuvant in mice

Tandon

Pathak

Harioudh

et al. 2018

Journal of Biological Chemistry

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Vaccination is devised/formulated to stimulate specific and prolonged immune responses for long-term protection against infection or disease. A vaccine component, namely adjuvant, enhances antigen recognition by the host immune system and thereby stimulates its cellular and adaptive responses. Especially synthetic Toll-like receptor (TLR) agonists having selfassembling properties are considered as good candidates for adjuvant development. Here, a human TLR4-derived 20-residue peptide (TR-433), present in the dimerization interface of the TLR4 -myeloid differentiation protein-2 (MD2) complex, displayed self-assembly and adopted a nanostructure. Both in vitro studies and in vivo experiments in mice indicated that TR-433 is nontoxic. TR-433 induced pro-inflammatory responses in THP-1 monocytes and HEK293T cells that were transiently transfected with TLR4/CD14/MD2 and also in BALB/c mice. In light of the self-assembly and pro-inflammatory properties of TR-433, we immunized with a mixture of TR-433 and either ovalbumin or filarial antigen trehalose-6-phosphate phosphatase (TPP). A significant amount of IgG titers was produced, suggesting adjuvanting capability of TR-433 that was comparable with that of Freund's complete adjuvant (FCA) and appreciably higher than that of alum. We found that TR-433 preferentially activates type 1 helper T cell (T h 1) response rather than type 2 helper T cell (T h 2) response. To our knowledge, this is the first report on the identification of a short TLR4-derived peptide that possesses both self-assembling and pro-inflammatory properties and has significant efficacy as an adjuvant, capable of activating cellular responses in mice. These results indicate that TR-433 possesses significant potential for development as a new adjuvant in therapeutic application. 2 The abbreviations used are: FCA, Freund's complete adjuvant; FIA, Freund's incomplete adjuvant; TLR, Toll-like receptor; LPS, lipopolysaccharide; TPP, trehalose-6-phosphate phosphatase; MTT, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide; TEM, transmission EM; ThT, thioflavin T; TNF, tumor necrosis factor; IL, interleukin; PMA, phorbol 12-myristate 13-acetate; Ova, ovalbumin; HRP, horseradish peroxidase; IFN, interferon. Figure 8. TR-433 adjuvant activity depends on T-bet expression. mRNA expressions of T-bet and GATA-3 were analyzed in splenocytes in duplicates in two independent experiments (n ϭ 2). Mouse glyceraldehyde-3-phosphate dehydrogenase was used as an endogenous control, and relative -fold change was determined by the comparative ⌬CT method. Statistical analysis was carried out using one-way analysis of variance using Dunnett's test.

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Section: A Tlr4-derived Peptide As An Adjuvantsupporting

confidence: 91%

A TLR4-derived non-cytotoxic, self-assembling peptide functions as a vaccine adjuvant in mice

Tandon

Pathak

Harioudh

et al. 2018

Journal of Biological Chemistry

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“…TNF-β and IFN-γ are important proinflammatory cytokines generated by T cells after antigen or mitogen stimulation. They can promote macrophage activation through immunomodulation, and play important roles in strengthening and maintaining the activated state of macrophages [17]. IL-10, which is mainly secreted by Th2 cells and macrophages, is an anti-inflammatory cytokine secreted by a subset of regulatory T cells, and has an anti-hepatic fibrosis effect [18].…”

Section: Discussionmentioning

confidence: 99%

Expression of M-CSF, TNF-β, IFN-γ, and IL-10 in Rats with Liver Cirrhosis and Hypersplenism and its Significance

Lv¹,

Deng²,

Yu³

et al. 2016

J Hypertens

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Objective: This study aimed to examine the expression of M-CSF, TNF-β, IFN-γ, and IL-10 in rats with liver cirrhosis and hypersplenism, and to investigate its significance.Methods: Seventy-two healthy male SD rats were randomly divided into a model group (n=60) and a control group (n=12). The rats in the model group were first gavaged with a 40% CCL4/peanut oil solution to develop cirrhosis and hypersplenism. The expression rates and intensities of the pro-inflammatory cytokines M-CSF, TNF-β, and IFN-γ, and the anti-inflammatory cytokine IL-10 in the spleen were measured and compared with the control group. The pro-inflammatory/anti-inflammatory cytokine ratio and its role were analyzed. Results:The positive expression rates of M-CSF, TNF-β, IFN-γ, and IL-10 in the model group (cirrhosis and hypersplenism) were 61.76%, 79.41%, 64.70%, and 88.24%, respectively, which were significantly different (P<0.05) from the 25%, 33.33%, 16.67%, and 50% in the control group. The relative protein expression intensities of M-CSF, TNF-β, IFN-γ, and IL-10 in the model group were 0.63 ± 0.58, 1.06 ± 0.49, 0.99 ± 0.38, and 1.12 ± 0.42, respectively, and were significantly different (P<0.05) from the 0.18 ± 0.12, 0.52 ± 0.27, 0.38 ± 0.28, and 0.60 ± 0.32 in the control group. The relative mRNA expression levels of M-CSF, TNF-β, IFN-γ, and IL-10 in the model group were 2.06 ± 0.11, 4.07 ± 0.19, 2.98 ± 0.11, and 7.94 ± 0.27, respectively, and were significantly different (P<0.05) from the 1.01 ± 0.05, 1.06 ± 0.11, 1.00 ± 0.31, and 1.02 ± 0.08 in the control group. Conclusion:The abnormally increased expression of M-CSF, TNF-β, IFN-γ, and IL-10 in rats with liver cirrhosis and hypersplenism, as well as the abnormal pro-inflammatory/anti-inflammatory cytokine ratio and regulation may play an important role in enhancing the phagocytosis of macrophages and causing peripheral cytopenias.

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“…Activated STAT1 then dimerizes to regulate the expression of various genes, for instance VCAM-1 and ICAM-1 [7][8][9][10]. Besides, in various inflammatory and granulomatous conditions, IFN-g is critical in up-regulating ICAM-1 expression in mRNA levels, amplifying inflammatory cytokine production and enhancing monocytes or macrophages anti-microbial and anti-tumor activity [11] .…”

Section: Introductionmentioning

confidence: 99%

“…Based on these characteristics, the molecular mechanisms regarding the physiological functions of macrophages and monocytes in cardiovascular system as well as the developmental etiology and pathogenesis of the cardiovascular diseases can be widely studied in this cell line [16] . The non-adherent THP-1 cells can be differentiated into adherent macrophages in the stimulation of phorbol-12-myristate-13-acetate (PMA) [11] .…”

Section: Introductionmentioning

confidence: 99%

Lauric acid abolishes interferon-gamma (IFN-γ)-induction of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression in human macrophages

Lim

Gan

Ong

et al. 2015

Asian Pacific Journal of Reproduction

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A B S T R A C TObjective: To investigate the effect of different concentrations of lauric acid on Intercellular Adhesion Molecule-1 (ICAM-1) and Vascular Cell Adhesion Molecule-1 (VCAM-1) expression in IFN-g stimulated human monocytic THP-1 cell line. Methods: THP-1 cell were cultured using Roswell Park Memorial Institute medium supplemented with 10% fetal bovine serum. THP-1 monocytes were firstly differentiated into macrophages by using phorbol-12-myristate-13-acetate. IFN-g response test was performed and total cellular RNA was extracted using TRI Reagent ® LS before q-RT-PCR was carried out. Subsequently, IFN-g treated THP-1 macrophages were stimulated with increasing doses of lauric acid for another 24 h, before q-RT-PCR.Results: The mRNA expression levels of ICAM-1 and VCAM-1 were normalized to bactin and relatived to the untreated cells. The expressions of ICAM-1 and VCAM-1 were significantly induced in cells treated with 10 ng/mL of IFN-g. This showed that IFN-g could up-regulate inflammatory process and may cause atheroma formation. MTT assay was carried out to investigate the effect of lauric acid on undifferentiated and differentiated THP-1 cells. Although lauric acid did not have any significant impact on undifferentiated and differentiated THP-1 cell viability, the normalized fold expressions of ICAM-1 and VCAM-1 in IFN-g-treated THP-1 macrophages were decreased significantly in a dose dependent manner with the presence of increasing doses of lauric acid. Conclusions: This study successfully proved that lauric acid was able to antagonize the up-regulatory effect of IFN-g on ICAM-1 and VCAM-1 expressions in THP-1 macrophages. This indicates that lauric acid may be an anti-inflammatory therapeutic and prophylaxis agent for atherosclerosis.

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Interferon-γ enhances phorbol myristate acetate-induced cell attachment and tumor necrosis factor production via the NF-κB pathway in THP-1 human monocytic cells

Cited by 15 publications

References 17 publications

A TLR4-derived non-cytotoxic, self-assembling peptide functions as a vaccine adjuvant in mice

A TLR4-derived non-cytotoxic, self-assembling peptide functions as a vaccine adjuvant in mice

Expression of M-CSF, TNF-β, IFN-γ, and IL-10 in Rats with Liver Cirrhosis and Hypersplenism and its Significance

Lauric acid abolishes interferon-gamma (IFN-γ)-induction of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression in human macrophages

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