Interleukin-1 beta (IL-1β) induces tumor necrosis factor alpha (TNF-α) expression on mouse myeloid multipotent cell line 32D cl3 and inhibits their proliferation

Ledesma, Edgar; Martı́nez, Ignacio; Córdova, Yolanda; Rodrı́guez-Sosa, Miriam; Monroy, Alberto; Mora, Lucy; Soto, Isabel; Ramos, G; Weiss, Benny; Santiago‐Osorio, Edelmiro

doi:10.1016/j.cyto.2003.12.009

Cited by 22 publications

(15 citation statements)

References 26 publications

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“…Proinflammatory cytokines, such as TNF-␣, IL-6, and IL-1␤, have been reported to induce necrotic and apoptotic cell death and decrease locomotor function after SCI, while suppression of these cytokines promotes neuronal survival and attenuates the severity of SCI (Sharma et al, 2003;Ledesma et al, 2004;Allan et al, 2005;Nakamura et al, 2005;Simi et al, 2007;Sheikpranbabu et al, 2009;Tolosa et al, 2011;Burke et al, 2014;Amini Pishva et al, 2016). Our results showed that following SRT1720 administration to WT mice, there was a significant reduction in the levels of proinflammatory cytokines, including TNF-␣, IL-6 and IL-1␤, in the early postinjury stages and that the SIRT1 KO mice exhibited increased levels of these inflammatory cytokines compared with those of WT mice (Fig.…”

Section: Discussionmentioning

confidence: 99%

“…SIRT1 has been shown to play a critical role in regulating various metabolic and pathophysiological processes, such as inflammation, apoptosis, stress resistance, differentiation, and aging (Bordone and Guarente, 2005;He et al, 2010;Busch et al, 2012;Lim et al, 2012;Xie et al, 2013;Shinozaki et al, 2014). In addition, SIRT1 is directly implicated in the modulation of inflammatory responses by deacetylation of histones and critical transcription factors, such as nuclear factor B, resulting in the transcriptional repression of various genes related to inflammation (Yeung et al, 2004;Kauppinen et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

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An Agonist of the Protective Factor SIRT1 Improves Functional Recovery and Promotes Neuronal Survival by Attenuating Inflammation after Spinal Cord Injury

Chen¹,

Ji²,

Zhang

et al. 2017

J. Neurosci.

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Targeting posttraumatic inflammation is crucial for improving locomotor function. SIRT1 has been shown to play a critical role in disease processes such as hepatic inflammation, rheumatoid arthritis, and acute lung inflammation by regulating inflammation. However, the role of SIRT1 in spinal cord injury (SCI) is unknown. We hypothesized that SIRT1 plays an important role in improving locomotor function after SCI by regulating neuroinflammation. In this study, we investigate the effect of SIRT1 in SCI using pharmacological intervention (SRT1720) and the Mx1-Cre/loxP recombination system to knock out target genes. First, we found that SIRT1 expression at the injured lesion site of wild-type (WT) mice (C57BL/6) decreased 4 h after SCI and lasted for 3 d. Moreover, administration of SRT1720, an agonist of SIRT1, to WT mice significantly improved functional recovery for up to 28 d after injury by reducing the levels of proinflammatory cytokines, the number of M1 macrophages, the number of macrophages/microglia, and the accumulation of perivascular macrophages. In contrast, administration of SRT1720 to SIRT1 knock-out (KO) mice did not improve locomotor recovery or attenuate inflammation. Furthermore, SIRT1 KO mice exhibited worse locomotor recovery, increased levels of inflammatory cytokines, and more M1 macrophages and perivascular macrophages than those of WT mice after SCI. Together, these findings indicate that SRT1720, an SIRT1 agonist, can improve functional recovery by attenuating inflammation after SCI. Therefore, SIRT1 is not only a protective factor but also an anti-inflammatory molecule that exerts beneficial effects on locomotor function after SCI.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

An Agonist of the Protective Factor SIRT1 Improves Functional Recovery and Promotes Neuronal Survival by Attenuating Inflammation after Spinal Cord Injury

Chen¹,

Ji²,

Zhang

et al. 2017

J. Neurosci.

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“…15 Moreover, we demonstrated that quercetin treatment reduced ROS production and inhibited NLRP3 inflammasome activation with decrease in IL-1β, IL-18 and TNF-α levels and alleviation of histopathology 72 h after SCI. IL-1β has a key role in spinal cord damage, 24,25 which is involved in increasing other proinflammatory cytokines such as TNF-α, 26,27 enhancing vascular permeability 28 and induction of neuron apoptosis. 29 Absence of IL-1β inhibits lesion development and axonal plasticity and exerts positive effects on neurological outcome.…”

Section: Discussionmentioning

confidence: 99%

Quercetin suppresses NLRP3 inflammasome activation and attenuates histopathology in a rat model of spinal cord injury

et al. 2016

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Study design: Randomized experimental study. Objectives: To investigate the molecular mechanisms of quercetin in spinal cord injury (SCI) rats. Setting: China. Methods: One hundred female Sprague-Dawley rats were randomly assigned into four groups: sham group, SCI group, SCI+Vehicle (Veh) group, and the SCI+Quercetin (Que) group. The influences of quercetin on proinflammatory cytokine levels, histological changes and locomotion scale were estimated. Results: SCI significantly promoted nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome activation and increased proinflammatory cytokine productions in the SCI group as compared with the sham group. Quercetin administration significantly decreased reactive oxygen species production, inhibited NLRP3 inflammasome activation and reduced inflammatory cytokine levels. Moreover, quercetin administration attenuated histopathology and promoted locomotion recovery. Conclusion: Quercetin can attenuate tissue damage and improve neurological function recovery, and the mechanism may be related to the inhibition of NLRP3 inflammasome activation.

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“…Moreover, by inducing the COX-2 expression at the tumor site, IL-1β together with PGE2 was shown to inhibit the maturation and immune functions of antigen-presenting cells by mediating an accumulation of MDSCs and TAMs and promoting tumor thereby progression [69,70]. Furthermore, IL-1β has been found to up-regulate TNF-α concentrations in the tumor microenvironment through induction of the production of latter cytokine by myeloid and/or tumor cells [71,72]. In addition, IL-1β has been shown to stimulate the production of IL-10, IL-5 and IL-13, which induced type 2 immune reactions and attracted MDSCs to the tumor site [73,74].…”

Section: General Characteristic Of Mdscsmentioning

confidence: 99%

Tumor Microenvironment and Myeloid-Derived Suppressor Cells

Umansky

Sevko

2012

Cancer Microenvironment

116

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Tumor progression has been demonstrated to be supported by chronic inflammatory conditions developed in the tumor microenvironment and characterized by the longterm secretion of various inflammatory soluble factors (including cytokines, chemokines, growth factors, reactive oxygen and nitrogen species, prostaglandins etc.) and strong leukocyte infiltration. Among leukocytes infiltrating tumors, myeloid-derived suppressor cells (MDSCs) represent one of the most important players mediating immunosuppression. These cells may not only strongly inhibit an anti-tumor immune reactions mediated by T cells but also directly stimulate tumorigenesis, tumor growth and metastasis by enhancing neoangiogenesis and creating a suitable environment for the metastatic formation. This review provides an overview of interactions between MDSCs and tumor cells leading to MDSC generation, activation and migration to the tumor site, where they can strongly enhance tumor progression. Better understanding of the MDSC-tumor interplay is critical for the development of new strategies of tumor immunotherapy.

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Interleukin-1 beta (IL-1β) induces tumor necrosis factor alpha (TNF-α) expression on mouse myeloid multipotent cell line 32D cl3 and inhibits their proliferation

Cited by 22 publications

References 26 publications

An Agonist of the Protective Factor SIRT1 Improves Functional Recovery and Promotes Neuronal Survival by Attenuating Inflammation after Spinal Cord Injury

An Agonist of the Protective Factor SIRT1 Improves Functional Recovery and Promotes Neuronal Survival by Attenuating Inflammation after Spinal Cord Injury

Quercetin suppresses NLRP3 inflammasome activation and attenuates histopathology in a rat model of spinal cord injury

Tumor Microenvironment and Myeloid-Derived Suppressor Cells

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