HMGB1 Promotes the Synthesis of Pro-IL-1β and Pro-IL-18 by Activation of p38 MAPK and NF-κB Through Receptors for Advanced Glycation End-products in Macrophages

He, Qiang; You, Hong; Li, Xinmin; Liu, Tianhui; Wang, Ping; Wang, Bao-en

doi:10.7314/apjcp.2012.13.4.1365

Cited by 105 publications

(76 citation statements)

References 20 publications

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“…In the nucleus, HMGB1 functions as a non-histone nucleosomal protein that binds DNA, contributes to stabilization of nucleosomes, and promotes DNA repair and replication (Bustin, 1999). In the extracellular milieu, HMGB1 is a pro-inflammatory cytokine that acts as an alarmin via passive release from damaged or necrotic cells (Beyer et al, 2012;He et al, 2012;Yi et al, 2013) or by active secretion from innate immune system cells in response to LPS, TNF-a or IL-1β stimulation to induce T-cell activation, cytokine production, and inflammatory responses by the transduction of cellular signals through its receptors (Akirav et al, 2012;Kang et al, 2013;Mohammad et al, 2013). Aside from these pro-inflammatory functions, HMGB1 protein also promotes regeneration processes and accelerates cell cycle progression.…”

Section: Introductionmentioning

confidence: 99%

Tax is Involved in Up-regulation of HMGB1 Expression Levels by Interaction with C/EBP

Zhang

Wang²,

ZhiGuo³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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The high mobility group box 1 (HMGB1) protein is a multifunctional cytokine-like molecule that plays an important role in the pathogenesis of tumors. In this study, real-time polymerase chain reactions and Western blot assays indicated that HMGB1 transcriptional activity and protein level are increased in Tax + -T cells (TaxP). To clarify the mechanisms, a series of HMGB1 deletion reporter plasmids (pHLuc1 to pHLuc6) were transfected into Tax --T cells (TaxN, Jurkat) and Tax + -T cells (TaxP). We found that promoter activity in Tax + -T cells to be higher than that in Tax

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Section: Introductionmentioning

confidence: 99%

Tax is Involved in Up-regulation of HMGB1 Expression Levels by Interaction with C/EBP

Zhang

Wang²,

ZhiGuo³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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“…Certain results suggested that high mobility group box-1 administration stimulates pro-IL-18 synthesis via NF-κB and p38 MAPK in THP-1 macrophages, while LPS-stimulation does not induce the expression of pro-IL-18 mRNA and protein in human primary peripheral blood mononuclear cells (7,27).…”

Section: Introductionmentioning

confidence: 99%

Adrenergic stimulation alters the expression of inflammasome components and interleukins in primary human monocytes

Horstmann

Marzi

Relja

2015

Experimental and Therapeutic Medicine

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Abstract. Prior to their release, interleukin (IL)-1β and IL-18 are cleaved to their bioactive forms by a multiprotein complex known as an inflammasome, which is comprised of a number of elements that are subject to nuclear factor-κB-dependent transcription. Catecholamines have been indicated to exert an enhancing effect on the IL-1β release. The aim of the present study was to determine whether alterations in inflammasome gene expression may be responsible for the modified IL-1β and IL-18 secretion following lipopolysaccharide (LPS) and catecholamine co-stimulation. Monocytes were isolated from the peripheral blood of 21 healthy volunteers using CD14 + microbeads. Following stimulation with LPS (2 µg/ml) and/or phenylephrine (PE; 10 µM) for 24 h, the supernatants were subjected to ELISA to evaluate the ex vivo protein expression levels of IL-1β and IL-18. In addition, the gene expression levels of inflammasome components associated with the cleavage of IL-1β and IL-18, including NLRP1, NLRP3, caspase-1 and PYCARD were determined using polymerase chain reaction. The results indicated that LPS significantly increased IL-1β expression compared with the unstimulated control samples. Co-stimulation with LPS + PE significantly enhanced IL-1β expression compared with LPS alone. Furthermore, IL-18 expression was significantly reduced by LPS and LPS + PE co-stimulation. The gene expression levels of IL-18, NLRP1, caspase-1 and PYCARD were comparable in the LPS-and LPS + PE-stimulated cells. LPS significantly induced the expression levels of IL-1β and NLRP3, and to a lesser degree, the expression of NLRP1, compared with the control. By contrast, PE markedly induced the expression levels of IL-18 and NLRP1, while LPS reduced the gene expression of IL-18. In conclusion, adrenergic stimulation suppressed NLRP3 expression and enhanced NLRP1 expression, indicating that NLRP3 may regulate IL-1β secretion and NLRP1 may regulate the release of IL-18.

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“…Cytokine patterns (increase in IL8, IL18, and MCP1 compared to vehicle control) reflected an immunomodulation in THP-1 cells cultured in tumor cell supernatants as well. IL18 is marker of inflammasome activation in THP-1 cells [48], while lipopolysaccharide-stimulated THP-1 monocytes secrete IL8 [49] and MCP1 [50]. IL8 is also released in response to oxidative stimuli [51].…”

Section: Discussionmentioning

confidence: 99%

Plasma Treatment of Ovarian Cancer Cells Mitigates Their Immuno-Modulatory Products Active on THP-1 Monocytes

Bekeschus

Wulf

Freund

et al. 2018

Plasma

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Cancers modulate their microenvironment to favor their growth. In particular, monocytes and macrophages are targeted by immuno-modulatory molecules installed by adjacent tumor cells such as ovarian carcinomas. Cold physical plasma has recently gained attention as innovative tumor therapy. We confirmed this for the OVCAR-3 and SKOV-3 ovarian cancer cell lines in a caspase 3/7 independent and dependent manner, respectively. To elaborate whether plasma exposure interferes with their immunomodulatory properties, supernatants of control and plasma-treated tumor cells were added to human THP-1 monocyte cultures. In the latter, modest effects on intracellular oxidation or short-term metabolic activity were observed. By contrast, supernatants of plasma-treated cancer cells abrogated significant changes in morphological and phenotypic features of THP-1 cells compared to those cultured with supernatants of non-treated tumor cell counterparts. This included cell motility and morphology, and modulated expression patterns of nine cell surface markers known to be involved in monocyte activation. This was particularly pronounced in SKOV-3 cells. Further analysis of tumor cell supernatants indicated roles of small particles and interleukin 8 and 18, with MCP1 presumably driving activation in monocytes. Altogether, our results suggest plasma treatment to alleviate immunomodulatory secretory products of ovarian cancer cells is important for driving a distinct myeloid cell phenotype.

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HMGB1 Promotes the Synthesis of Pro-IL-1β and Pro-IL-18 by Activation of p38 MAPK and NF-κB Through Receptors for Advanced Glycation End-products in Macrophages

Cited by 105 publications

References 20 publications

Tax is Involved in Up-regulation of HMGB1 Expression Levels by Interaction with C/EBP

Tax is Involved in Up-regulation of HMGB1 Expression Levels by Interaction with C/EBP

Adrenergic stimulation alters the expression of inflammasome components and interleukins in primary human monocytes

Plasma Treatment of Ovarian Cancer Cells Mitigates Their Immuno-Modulatory Products Active on THP-1 Monocytes

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