Identification of inflammatory markers in eosinophilic cells of the immune system: fluorescence, Raman and CARS imaging can recognize markers but differently

AbstractEosinophils (Eos) play an important role in the immune system’s response releasing several inflammatory factors and contributing to allergic rhinitis, asthma, or atopic dermatitis. Since Eos have a relatively short lifetime after isolation from blood, usually eosinophilic cell line (EoL-1) is used to study mechanisms of their activation and to test therapies. In particular, EoL-1 cells are examined in terms of signalling pathways of the inflammatory response manifested by the presence of lipid bodies (LBs). Here we examined the differences in response to inflammation modelled by various factors, between isolated human eosinophils and EoL-1 cells, as manifested in the number and chemical composition of LBs. The analysis was performed using fluorescence, Raman, and coherent anti-Stokes Raman scattering (CARS) microscopy, which recognised the inflammatory process in the cells, but it is manifested slightly differently depending on the method used. We showed that unstimulated EoL-1 cells, compared to isolated eosinophils, contained more LBs, displayed different nucleus morphology and did not have eosinophilic peroxidase (EPO). In EoL-1 cells stimulated with various proinflammatory agents, including butyric acid (BA), liposaccharide (LPS), or cytokines (IL-1β, TNF-α), an increased production of LBs with a various degree of lipid unsaturation was observed in spontaneous Raman spectra. Furthermore, stimulation of EoL-1 cells resulted in alterations of the LBs morphology. In conclusion, a level of lipid unsaturation and eosinophilic peroxidase as well as LBs distribution among cell population mainly accounted for the biochemistry of eosinophils upon inflammation.

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0040 Relationship Between Inflammatory Markers and Sleep in Healthy Adolescents

SLEEP ◽

10.1093/sleep/zsaa056.039 ◽

2020 ◽

Vol 43 (Supplement_1) ◽

pp. A16-A16

Author(s):

A Reddy ◽

L Li

Keyword(s):

Sleep Quality ◽

Inflammatory Markers ◽

Kidney Diseases ◽

Pearson Correlation ◽

Research Center ◽

Inflammatory Factors ◽

Poor Sleep ◽

Diabetes Research ◽

Hyperactive Behavior ◽

Tnf Α

Abstract Introduction Multiple studies in different countries show a trend of adolescents having insufficient sleep. Review of literature strongly suggests role of cytokines in sleep regulation. Different inflammatory markers like tumor necrosis factor (TNF)α, C-reactive protein (CRP) and interleukins (IL) are sleep regulatory substances. Most of the studies showing relation between cytokines and sleep are seen in adults. In our study, we were interested in finding the relationship between sleep quality and inflammatory markers in healthy adolescents. Methods Twenty eight female and male, African American and White, healthy adolescents aged 15–18 completed the study. Sleep quality was measured using the Pediatric Sleep Questionnaires (PSQ), including snoring, daytime sleepiness and hyperactive behavior. Blood sample was collected from each participant for measuring the inflammatory factors. Results Partial Pearson correlation analysis showed that global PSQ score and hyperactive behavior were significantly correlated with TNF α (r=0.37 for both). Snoring was significantly correlated with leptin, CRP and IL-6 in healthy adolescents. No other correlations were observed. Conclusion Consistent with findings in adults, we have observed an association between inflammatory markers and poor sleep in healthy adolescents. Our findings suggest the importance to improve sleep quality in adolescents for better health outcomes. Support None of the authors have any conflict of interest. This research was supported by awards, P30DK056336 and P30DK079626, from the National Institute of Diabetes And Digestive And Kidney Diseases to Nutrition Obesity Research Center and Diabetes Research Center, respectively, at the University of Alabama at Birmingham.

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Curcumin Nanomicelle Improves Lipid Profile, Stress Oxidative Factors and Inflammatory Markers in Patients Undergoing Coronary Elective Angioplasty; A Randomized Clinical Trial

Endocrine Metabolic & Immune Disorders - Drug Targets ◽

10.2174/1871530321666210104145231 ◽

2021 ◽

Vol 21 ◽

Author(s):

Bijan Helli ◽

Hadis Gerami ◽

Maria Kavianpour ◽

Habib Heybar ◽

Seyed Kianoosh Hosseini ◽

...

Keyword(s):

Oxidative Stress ◽

Clinical Trial ◽

Lipid Profile ◽

Inflammatory Markers ◽

Interleukin 1 ◽

Stress Factors ◽

Inflammatory Factors ◽

Control Group ◽

Controlled Clinical Trial ◽

Tnf Α

Background: Curcumin demonstrated many pharmacological effects including antioxidants, anti-inflammation, eliminating free radicals, anti-tumor, lipid regulation, and anti-coagulation. Objective: This study aimed to assess and compare curcumin and nano-curcumin effects on lipid profile, oxidative stress, and inflammatory factors related to patients ‘heart. Method: This randomized, double-blind, placebo-controlled clinical trial was conducted on 90 patients undergoing coronary elective angioplasty which were randomly divided into 3 groups. The doses administered for 8 weeks were a 500 mg capsule of curcumin daily for the first group and an 80 mg capsule of nano-curcumin for the second group. However, the placebo group received capsules like curcumin. Lipid profile, oxidative stress factors, and inflammatory markers were measured at the baseline and end of the experiment. Results: Statistically significant changes were observed in the total cholesterol (TC), triacylglycerol (TG) and low-density lipoprotein cholesterol (LDL-C) in the intervention groups to the control group (p<0.05). Curcumin and nano-curcumin supplementation also improved significant changes in plasma levels of total antioxidant capacity (TAC), malondialdehyde (MDA), Superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), high-sensitivity C-reactive protein (hs-CRP), Interleukin 1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) in comparison to the placebo (p<0.05). Furthermore, the nano-curcumin group compared to the curcumin group demonstrated significant changes (p<0.05) in TC, TG, SOD, MDA and TNF-α levels. Conclusion: The effects of curcumin on nano formula may be better for cardiac patients due to its high bioavailability.

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Inflammatory Markers May Inform the Effects of Electroconvulsive Therapy on Cognition in Patients with Depression

Neuropsychobiology ◽

10.1159/000515931 ◽

2021 ◽

pp. 1-9

Author(s):

Jan-Baptist Belge ◽

Linda Van Diermen ◽

Bernard Sabbe ◽

Manuel Morrens ◽

Violette Coppens ◽

...

Keyword(s):

Episodic Memory ◽

Cognitive Functioning ◽

Electroconvulsive Therapy ◽

Inflammatory Markers ◽

Verbal Learning ◽

Potential Biomarker ◽

Tnf Α ◽

Autobiographic Memory ◽

Learning Test ◽

Verbal Episodic Memory

Introduction: The neurobiological mechanisms underlying the acute cognitive effects of electroconvulsive therapy (ECT) remain poorly understood. Prior research has shown that proinflammatory cytokines such as IL-6, TNF-α, IL1-β, and IL-10 may interfere with cognitive functioning. Interestingly, immunomodulation is one of the proposed modes of action of ECT. This study investigates whether changes of peripheral levels of IL-6, TNF-α, IL1-β, and IL-10 are related to changes in cognitive functioning following ECT. Methods: In the week before and 1 week after an acute course of ECT, 62 patients suffering from depression underwent a neuropsychological evaluation to assess their processing speed using the Symbol Digit Substitution Test (SDST), verbal episodic memory using the Hopkins Verbal Learning Test-Revised (HVLT-R), and their retrospective autobiographic memory using the Autobiographical Memory Interview (AMI) with the peripheral inflammatory markers being measured at the same 2 time points. Results: Patients improved drastically following ECT, while their main performance on both the HVLT-R and AMI declined and their SDST scores remained stable. The levels of IL-6 and IL1-β had both decreased, where the decrease in IL-6 was related to the decrease in HVLT-R scores. Higher baseline IL-10 levels were associated with a more limited decrease of the HVLT-R scores. Conclusion: Our findings tentatively suggest that the effects of ECT on verbal episodic memory may be related to the treatment’s immunomodulatory properties, most notably due to decreased IL-6 levels. Moreover, baseline IL-10 appears to be a potential biomarker to predict the effects of ECT on verbal episodic memory. Whilst compelling, the results of this study should be interpreted with caution as, due to its exploratory nature, no correction for multiple comparisons was made. Further, a replication in larger cohorts is warranted.

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Biomimetic nanotherapy: core–shell structured nanocomplexes based on the neutrophil membrane for targeted therapy of lymphoma

Journal of Nanobiotechnology ◽

10.1186/s12951-021-00922-4 ◽

2021 ◽

Vol 19 (1) ◽

Author(s):

Qiangqiang Zhao ◽

Duanfeng Jiang ◽

Xiaoying Sun ◽

Qiuyu Mo ◽

Shaobin Chen ◽

...

Keyword(s):

Mesoporous Silica Nanoparticles ◽

Treatment Options ◽

Inflammatory Factors ◽

Main Method ◽

Tnf Α ◽

Good Biocompatibility ◽

Inflammatory Drugs ◽

Anti Inflammatory ◽

New Treatment ◽

Lymphoma Therapy

Abstract Background Non-Hodgkin’s lymphoma (NHL) is a malignant disease of lymphoid tissue. At present, chemotherapy is still the main method for the treatment of NHL. R-CHOP can significantly improve the survival rate of patients. Unfortunately, DOX is the main cytotoxic drug in R-CHOP and it can lead to adverse reactions. Therefore, it is particularly important to uncover new treatment options for NHL. Results In this study, a novel anti-tumor nanoparticle complex Nm@MSNs-DOX/SM was designed and constructed in this study. Mesoporous silica nanoparticles (MSNs) loaded with Doxorubicin (DOX) and anti-inflammatory drugs Shanzhiside methylester (SM) were used as the core of nanoparticles. Neutrophil membrane (Nm) can be coated with multiple nanonuclei as a shell. DOX combined with SM can enhance the anti-tumor effect, and induce apoptosis of lymphoma cells and inhibit the expression of inflammatory factors related to tumorigenesis depending on the regulation of Bcl-2 family-mediated mitochondrial pathways, such as TNF-α and IL-1β. Consequently, the tumor microenvironment (TME) was reshaped, and the anti-tumor effect of DOX was amplified. Besides, Nm has good biocompatibility and can enhance the EPR effect of Nm@MSNs-DOX/SM and increase the effect of active targeting tumors. Conclusions This suggests that the Nm-modified drug delivery system Nm@MSNs-DOX/SM is a promising targeted chemotherapy and anti-inflammatory therapy nanocomplex, and may be employed as a specific and efficient anti-Lymphoma therapy.

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Mono-2-ethylhexylphthalate (MEHP) induces TNF-α release and macrophage differentiation through different signalling pathways in RAW264.7 cells

Toxicology Letters ◽

10.1016/j.toxlet.2011.11.016 ◽

2012 ◽

Vol 209 (1) ◽

pp. 43-50 ◽

Cited By ~ 31

Author(s):

Anette Kocbach Bølling ◽

Johan Ovrevik ◽

Jan Tore Samuelsen ◽

Jørn A. Holme ◽

Kirsten E. Rakkestad ◽

...

Keyword(s):

Raw264.7 Cells ◽

Signalling Pathways ◽

Macrophage Differentiation ◽

Tnf Α

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From Inflammation to the Onset of Fibrosis through A2A Receptors in Kidneys from Deceased Donors

International Journal of Molecular Sciences ◽

10.3390/ijms21228826 ◽

2020 ◽

Vol 21 (22) ◽

pp. 8826

Author(s):

Elena Guillén-Gómez ◽

Irene Silva ◽

Núria Serra ◽

Francisco Caballero ◽

Jesús Leal ◽

...

Keyword(s):

Deceased Donor ◽

Inflammatory Factors ◽

Mrna Levels ◽

A2a Adenosine Receptor ◽

A2a Receptors ◽

Tnf Α ◽

Anti Inflammatory ◽

Pka Pathway ◽

Tgf Β1 ◽

M2 Phenotype

Pretransplant graft inflammation could be involved in the worse prognosis of deceased donor (DD) kidney transplants. A2A adenosine receptor (A2AR) can stimulate anti-inflammatory M2 macrophages, leading to fibrosis if injury and inflammation persist. Pre-implantation biopsies of kidney donors (47 DD and 21 living donors (LD)) were used to analyze expression levels and activated intracellular pathways related to inflammatory and pro-fibrotic processes. A2AR expression and PKA pathway were enhanced in DD kidneys. A2AR gene expression correlated with TGF-β1 and other profibrotic markers, as well as CD163, C/EBPβ, and Col1A1, which are highly expressed in DD kidneys. TNF-α mRNA levels correlated with profibrotic and anti-inflammatory factors such as TGF-β1 and A2AR. Experiments with THP-1 cells point to the involvement of the TNF-α/NF-κB pathway in the up-regulation of A2AR, which induces the M2 phenotype increasing CD163 and TGF-β1 expression. In DD kidneys, the TNF-α/NF-κB pathway could be involved in the increase of A2AR expression, which would activate the PKA–CREB axis, inducing the macrophage M2 phenotype, TGF-β1 production, and ultimately, fibrosis. Thus, in inflamed DD kidneys, an increase in A2AR expression is associated with the onset of fibrosis, which may contribute to graft dysfunction and prognostic differences between DD and LD transplants.

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In vitro evidence for the involvement of H2S pathway in the effect of clodronate during inflammatory response

Scientific Reports ◽

10.1038/s41598-021-94228-y ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Rosangela Montanaro ◽

Alessio D’Addona ◽

Andrea Izzo ◽

Carlo Ruosi ◽

Vincenzo Brancaleone

Keyword(s):

Inflammatory Markers ◽

In Vitro Study ◽

Inos Expression ◽

Beneficial Effects ◽

Tnf Α ◽

Inflammatory State ◽

Anti Inflammatory ◽

Underlying Mechanisms ◽

Inflammatory Effect

AbstractClodronate is a bisphosphonate agent commonly used as anti-osteoporotic drug. Throughout its use, additional anti-inflammatory and analgesic properties have been reported, although the benefits described in the literature could not solely relate to their inhibition of bone resorption. Thus, the purpose of our in vitro study is to investigate whether there are underlying mechanisms explaining the anti-inflammatory effect of clodronate and possibly involving hydrogen sulphide (H2S). Immortalised fibroblast-like synoviocyte cells (K4IM) were cultured and treated with clodronate in presence of TNF-α. Clodronate significantly modulated iNOS expression elicited by TNF-α. Inflammatory markers induced by TNF-α, including IL-1, IL-6, MCP-1 and RANTES, were also suppressed following administration of clodronate. Furthermore, the reduction in enzymatic biosynthesis of CSE-derived H2S, together with the reduction in CSE expression associated with TNF-α treatment, was reverted by clodronate, thus rescuing endogenous H2S pathway activity. Clodronate displays antinflammatory properties through the modulation of H2S pathway and cytokines levels, thus assuring the control of the inflammatory state. Although further investigation is needed to stress out how clodronate exerts its control on H2S pathway, here we showed for the first the involvement of H2S in the additive beneficial effects observed following clodronate therapy.

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A study on relationship between elderly sarcopenia and inflammatory factors IL-6 and TNF-α

European Journal of Medical Research ◽

10.1186/s40001-017-0266-9 ◽

2017 ◽

Vol 22 (1) ◽

Cited By ~ 43

Author(s):

Ai-Lin Bian ◽

Hui-Ying Hu ◽

Yu-Dong Rong ◽

Jian Wang ◽

Jun-Xiong Wang ◽

...

Keyword(s):

Inflammatory Factors ◽

Tnf Α

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Tumor Necrosis Factor Alpha Inhibits Type I Collagen Synthesis through Repressive CCAAT/Enhancer-Binding Proteins

Molecular and Cellular Biology ◽

10.1128/mcb.20.3.912-918.2000 ◽

2000 ◽

Vol 20 (3) ◽

pp. 912-918 ◽

Cited By ~ 115

Author(s):

Patricia Greenwel ◽

Shizuko Tanaka ◽

Dmitri Penkov ◽

Wen Zhang ◽

Michelle Olive ◽

...

Keyword(s):

Tumor Necrosis Factor ◽

Tumor Necrosis ◽

Type I Collagen ◽

Type I ◽

Necrosis Factor Alpha ◽

Gene Coding ◽

Tnf Α ◽

Factor Alpha ◽

Necrosis Factor ◽

Stimulation Of

ABSTRACT Extracellular matrix (ECM) formation and remodeling are critical processes for proper morphogenesis, organogenesis, and tissue repair. The proinflammatory cytokine tumor necrosis factor alpha (TNF-α) inhibits ECM accumulation by stimulating the expression of matrix proteolytic enzymes and by downregulating the deposition of structural macromolecules such as type I collagen. Stimulation of ECM degradation has been linked to prolonged activation of jun gene expression by the cytokine. Here we demonstrate that TNF-α inhibits transcription of the gene coding for the α2 chain of type I collagen [α2(I) collagen] in cultured fibroblasts by stimulating the synthesis and binding of repressive CCAAT/enhancer proteins (C/EBPs) to a previously identified TNF-α-responsive element. This conclusion was based on the concomitant identification of C/EBPβ and C/EBPδ as TNF-α-induced factors by biochemical purification and expression library screening. It was further supported by the ability of the C/EBP-specific dominant-negative (DN) protein to block TNF-α inhibition of α2(I) collagen but not TNF-α stimulation of the MMP-13 protease. The DN protein also blocked TNF-α downregulation of the gene coding for the α1 chain of type I collagen. The study therefore implicates repressive C/EBPs in the TNF-α-induced signaling pathway that controls ECM formation and remodeling.

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