Cytokine

Our medical research library holds 9 studies published in Cytokine (2000–2022). Each entry links to the study's record on PubMed and, where there is one, to the publisher's page and a free full text. 8 have an abstract, the authors' own summary as PubMed records it: open "Abstract" to read it.

About the journal

• Publisher: Elsevier Science Ltd
• Published: 1989 to the present, England
• Language: English
• ISSN: 1043-4666 (print), 1096-0023 (electronic)
• Its record in the NLM Catalog

2020s

• Molecular and immunological changes in blood of rats exposed to various doses of asbestos dust. G. Ainagulova, O. Bulgakova, O. Ilderbayev, et al. 2022;159:156016. PubMed · Publisher

  Abstract

  Background: Asbestos-related diseases are a group of diseases resulting from the inhalation of asbestos fibres and their subsequent deposition in the lung parenchyma, which causes the development of inflammatory and fibrotic processes in the respiratory system. Cases of the disease often occur in the practice of doctors.

  Aims: The purpose of the study was to examine the level of circulating-free mitochondrial DNA (cf mtDNA), pro-inflammatory cytokines, immunological status and structural changes in the lung of rats exposed to various doses of asbestos dust.

  Methods: Immune monitoring was performed using the peripheral blood samples of 40 male Wistar rats exposed and unexposed to asbestos dust. cf mtDNA copy numbers were detected using quantitative real-time polymerase chain reaction (qRT-PCR) and cytokines were determined using a rat Enzyme Linked Immuno Sorbent Assay (ELISA) kit.

  Results: A comprehensive assessment of the histopathological study performed under exposure to asbestos at a dose of 25 mg and 50 mg showed the presence of pronounced structural defects in the lung tissue of laboratory rats. The level of cf mtDNA in plasma of rats exposed to asbestos at a dose of 25 mg was reliably higher than that of control rats, and animals exposed to asbestos at a dose of 50 mg. The highest levels of pro-inflammatory cytokines IL-6 and TNF-a were also observed after asbestos dusting at a dose of 25 mg.

  Conclusions: According to the results of the immunological status obtained, the decrease in the levels of pro-inflammatory cytokines in the blood plasma at 50 mg is due to the immunosuppressive effect in the rat immune system at this dose. A positive correlation was found between TNF-a level and copy numbers of cf mtDNA at a dose of 25 mg.

  Copyright © 2022 Elsevier Ltd. All rights reserved.

• Detection of circulating immunosuppressive cytokines in malignant pleural mesothelioma patients for prognostic stratification. L. Urso, M. Silic-Benussi, A. Boscolo, et al. 2021;146:155622. PubMed · Publisher

  Abstract

  Background: No data on circulating biomarkers for the prognostic stratification of Malignant Pleural Mesothelioma (MPM) patients are available. We prospectively explored the prognostic role of circulating monocyte and cytokine levels and their dynamic change during chemotherapy.

  Patients And Methods: MPM patients receiving a first line treatment based on a platinum compound plus pemetrexed were eligible. Blood samples were collected at the baseline and at the end of induction chemotherapy. CCL-2, IL-10 and TGF-β levels in plasma were quantified by Enzyme-Linked Immunosorbent Assay (ELISA); white blood cells, monocytes and platelets were evaluated by blood count test.

  Results: Thirty-one patients were included in the study. Median overall survival (OS) was 12.13 months versus 9.6 months in patients with lower and higher monocytes count, respectively (p value = 0.02). We further stratified patients according to a combined score based on the association of IL-10, TGF-β levels and monocytes count. High combined score was associated with shorter OS and PFS in univariate and multivariate analysis. Chemotherapy induced an increase in monocytes, IL-10, but not TGF-β levels.

  Conclusion: The prognostic value of circulating levels of multiple immunosuppressive cytokines and inflammatory cells should be confirmed in a wider validation set of MPM patients.

  Copyright © 2021 The Author(s). Published by Elsevier Ltd.. All rights reserved.

2010s

• Role of angiopoietins in mesothelioma progression. S. Magkouta, A. Kollintza, C. Moschos, et al. 2019;118:99-106. PubMed · Publisher

  Abstract

  Background And Objective: Anti-angiogenic treatment has been recently shown to be clinically beneficial for mesothelioma patients. Angiopoietins-1 and -2 are key regulators of tumor angiogenesis. Ang-1 is mainly known to promote angiogenesis and vessel stability, while Ang-2 could serve as an antagonist of Ang-1 causing vessel regression and destabilization or enhance angiogenesis in a context-dependent manner. We hypothesized that Ang-1 would promote and Ang2 would halt experimental mesothelioma by affecting tumor angiogenesis.

  Methods: To examine the effects of angiopoietins in mesothelioma angiogenesis and in vivo growth we constructed Ang-1 or Ang-2 overexpressing AE17 and AB1 mesothelioma cells and implanted them in the respective syngeneic animals. We also explored the clinical relevance of our observations using the human tumoral mRNAseq data available in the TCGA database.

  Results And Conclusions: Ang-1 promotes mesothelioma angiogenesis and growth while the effect of Ang-2 is context-dependent. Low Ang-1 levels in human mesotheliomas are associated with the epitheloid subtype. Tumors of high Ang-1, or concurrent high Ang-2 and VEGF expression present high PECAM-1 and CDH5 expression, markers of vascularity and vascular stability, respectively. Our results highlight the importance of angiopoietins in mesothelioma pathophysiology and pave the way for the clinical development of novel anti-angiogenic strategies.

  Copyright © 2018 Elsevier Ltd. All rights reserved.

• Corrigendum for "Differential activation of the inflammasome in THP-1 cells exposed to chrysotile asbestos and Libby "Six-Mix" amphiboles and subsequent activation of BEAS-2B cells" [Cytokine 60 (3) (2012) 718-730]. M. Li, M.E. Gunter, N.K. Fukagawa. 2017;94:59. PubMed · Publisher

• Involvement of IL-1 genes in the cellular responses to carbon nanotube exposure. Y.J. Arnoldussen, A. Skogstad, V. Skaug, et al. 2015;73(1):128-37. PubMed · Publisher

  Abstract

  The interleukin-1 (IL-1) family has been implicated in cellular responses to nanoparticles including carbon nanotubes (CNTs). IL-1α and β are key proinflammatory cytokines important in inflammatory and oxidative stress responses. The aim of this study was to characterize the role of IL-1 in cellular responses of CNTs in cells from IL-1α/β wild type (IL1-WT) mice and cells with reduced inflammatory potential from IL-1α/β deficient (IL1-KO) mice. Two multi-walled CNTs, CNT-1 containing long and thick fibers and CNT-2 containing short and thin fibers, were compared to UICC crocidolite asbestos fibers. Upon CNT exposure toxicity and apoptosis were affected differently in IL1-WT and IL1-KO cells. Upregulation of TNFα and IL-1α mRNA expression in IL1-WT cells was dependent on the type of CNT. On the contrary precursor IL-1α protein was downregulated after 24h. The mitogen-activated protein kinase (MAPK) c-Jun N-terminal kinase (JNK) was activated in IL1-KO cells and regulated by CNTs, whereas no significant changes of extracellular regulated kinase (ERK) were observed when comparing IL1-WT and IL1-KO cells. In summary, the results presented here indicate that IL-1 contributes to the cellular and molecular effects of CNT exposure and that the type of CNT has an important effect on the cellular response.

  Copyright © 2015 Elsevier Ltd. All rights reserved.

• Differential activation of the inflammasome in THP-1 cells exposed to chrysotile asbestos and Libby "six-mix" amphiboles and subsequent activation of BEAS-2B cells. M. Li, M.E. Gunter, N.K. Fukagawa. 2012;60(3):718-30. PubMed · Publisher

  Abstract

  Inflammatory responses of THP-1 cells (macrophage cell line) exposed to chrysotile asbestos (Chry) and Libby six-mix (LIB) and the subsequent impact on bronchial epithelial cells were determined. Direct treatment of THP-1 cells with Chry caused cell death, activation of caspase-1 and release of IL-1β, while the addition of caspase-1 inhibitor, Z-YVAD-FMK, reduced IL-1β, suggesting that Chry activated the caspase-1 mediated Nod-like receptor protein 3 (NLRP3) inflammasome; by comparison, LIB had less effects on all of these parameters. Expression of antioxidant enzymes, protein oxidation and nitration, and lipid peroxides in THP-1 cells treated with the two particles suggest that LIB generated more reactive oxygen species (ROS) than the same dose of Chry. Differences in fiber length and surface area suggest a possible role for particulate size in the differential activation of the inflammasome. BEAS-2B cells, representing the bronchial epithelium, treated with supernatants of medium from Chry- or LIB-treated THP-1 cells (conditioned medium) activated the MAPK cascade, increased phosphorylation of ERK and Cot (MAP3K8), increased AP-1 binding activity and induced IL-6 release. To verify that IL-1β from THP-1 cells was responsible for activation of BEAS-2B, conditioned medium with added IL-1Ra, an IL-1β antagonist, was applied to BEAS-2B. Results show that IL-1Ra attenuated effects of conditioned medium, supporting a role of IL-1β, as a secondary mediator, in the transduction of inflammatory signaling from the macrophage to epithelial cells. The effects of LIB-conditioned medium appeared to be less dependent on IL-1β. In conclusion, Chry and LIB induce differential inflammatory responses in THP-1 cells that subsequently lead to differential effects in epithelial cells.

  Copyright © 2012 Elsevier Ltd. All rights reserved.

2000s

• The microbial and danger signals that activate Nod-like receptors. S. Benko, D.J. Philpott, S.E. Girardin. 2008;43(3):368-73. Review PubMed · Publisher

  Abstract

  Nod-like receptors (NLRs) are a family of intracellular sensors that play key roles in innate immunity and inflammation. While some NLRs, including Nod1, Nod2, NAIP and IPAF, detect conserved bacterial molecular signatures from within the host cytosol, other members of this family seem to have evolved the capacity to sense danger signals perhaps independently of a microbial trigger. This is illustrated by the discovery that Nalp3 and Nalp1 are specifically activated by low concentrations of intracellular potassium. The fact that several stimuli, including bacterial toxins and some viruses, but also sterile crystals made of uric acid, asbestos or aluminium hydroxide, can trigger the Nalp3 inflammasome illustrate the fascinating prospect that microbial infections and certain danger signals may be perceived similarly by host recognition systems. Gaining insight into the function of NLR proteins in general will impact considerably on our understanding of the mechanisms underlying immunity to infection, adjuvanticity and auto-inflammatory disorders. In this review, we summarize the current knowledge on the microbial- and danger-derived signals that activate NLRs.

• Polycyclic aromatic hydrocarbons induce IL-8 expression through nuclear factor kappaB activation in A549 cell line. X.H. Pei, Y. Nakanishi, H. Inoue, et al. 2002;19(5):236-41. PubMed

  Abstract

  Air pollution causes increased cardiopulmonary morbidity and mortality. Airway inflammation plays a major role in the pathophysiology of many lung diseases. Proinflammatory cytokines, such as interleukin-8 (IL-8), are responsible in part for the initiation and maintenance of airway inflammation. Asbestos exposure and particulate air pollution have been reported to stimulate the expression of IL-8 and to induce NF-kappaB activation. However, it is unknown whether polycyclic aromatic hydrocarbons (PAH), mainly existed in most airborne particulates, can separately induce IL-8 expression. In the present study, we investigated the effect of benzo(a)pyrene (B[a]P) and 1-nitropyrene (1-NP), two representative PAH, on IL-8 expression using ELISA and Northern blot analysis. Gel shift assay was performed to study the NF-kappaB activation. We have assessed the effect of adenovirus-mediated overexpression of the NF-kappaB inhibitor, IkappaBalpha on PAH-induced IL-8 expression in A549 cell line. Both B[a]P and 1-NP stimulated IL-8 gene expression in A549 cells. This effect was associated with induction of NF-kappaB activation. Overexpression of IkappaBalpha inhibited 1-NP-induced transcription of IL-8. This suggests that PAH-induced IL-8 gene regulation may be mediated by NF-kappaB. These data indicate that PAH alone, either B[a]P or 1-NP, is sufficient to stimulate NF-kappaB activation and IL-8 transcription.

• Cytokine and free radical responses of alveolar macrophages in vitro to asbestos fibres. L.C. Mongan, T. Jones, G. Patrick. 2000;12(8):1243-7. PubMed · Publisher

  Abstract

  A method for culturing primary rat alveolar macrophages (AMs) for 14 days was used to compare their responses to crocidolite and chrysotile asbestos fibres. Exposure to crocidolite increased production of tumour necrosis factor-alpha (TNF-alpha) and interleukin 1beta (IL-1beta), whereas exposure to chrysotile did not; neither fibre altered the production of interleukin 6 (IL-6). IL-1beta production increased progressively, while TNF-alpha was fully elevated from day 1. Conversely, chrysotile, but not crocidolite, increased production of superoxide anion and nitric oxide (NO) radicals. These differential responses were only observed by extending the culture beyond the usual 1-3 days.

  Copyright 2000 Academic Press.

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