scholarly journals Nrf2 suppresses macrophage inflammatory response by blocking proinflammatory cytokine transcription

2016 ◽  
Vol 7 (1) ◽  
Author(s):  
Eri H. Kobayashi ◽  
Takafumi Suzuki ◽  
Ryo Funayama ◽  
Takeshi Nagashima ◽  
Makiko Hayashi ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Proinflammatory Cytokine ◽  
Cytokine Transcription

scholarly journals The influence of sepsis as a complication after trauma on immune response to injury

2011 ◽  
Vol 139 (3-4) ◽  
pp. 179-184
Author(s):  
Maja Surbatovic ◽  
Darko Mirkovic ◽  
Sonja Radakovic ◽  
Miodrag Jevtic ◽  
Nikola Filipovic
Keyword(s):  
Immune Response ◽  
Mortality Rate ◽  
Inflammatory Response ◽  
Proinflammatory Cytokine ◽  
Inflammatory Cytokine ◽  
Elisa Test ◽  
Sepsis Group ◽  
Blood Samples ◽  
Significant Difference ◽  
Anti Inflammatory Cytokine

Introduction. Mortality rate in trauma complicated with sepsis is exceeding 50%. Outcome is not determined only by infection or trauma, but also by the intensity of immuno-inflammatory response. Objective. The aim of this study was to determine the influence of sepsis on the immuno-inflammatory response, in the group of 35 traumatized men, of which in 25 cases trauma was complicated with sepsis. Methods. Cytokines were measured by ELISA test in plasma. Blood samples were drown on the first, third and fifth day after ICU admission. Results. Proinflammatory cytokine IL-8 was 230-fold higher in trauma + sepsis group (1148.48 vs. 5.05 pg/ml; p<0.01), and anti- inflammatory cytokine IL-1ra was 4-fold higher (1138.3 vs. 310.05 pg/ml; p<0.01), whereas IL-12 and IL-4 showed no significant difference between the groups. Conclusion. We concluded that sepsis, as a complication after trauma, drastically enhances immuno-inflammatory response to insult, as indicated by IL-8 and IL-1ra, but not IL-12 and IL-4.

scholarly journals Study on the Usefulness of APR Scores from the Viewpoint of Proinflammatory Cytokines

2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
T. Nakamura ◽  
D. Hatanaka ◽  
T. Yoshioka ◽  
S. Yamada ◽  
H. Goto
Keyword(s):  
Inflammatory Response ◽  
Proinflammatory Cytokines ◽  
Proinflammatory Cytokine ◽  
Clinical Laboratory ◽  
Diagnosis And Treatment ◽  
Antibiotic Administration ◽  
Acute Phase Reactants ◽  
Group I ◽  
Cytokine Levels ◽  
Fetal Inflammatory Response

Background. Delayed diagnosis and treatment of newborn infection adversely impact outcomes. Clinical laboratory parameters have aimed to obtain the most correct and prompt diagnosis and treatment of this disease. This study simultaneously observed changes over time in APR as well as proinflammatory cytokines and anti-proinflammatory cytokines and aims to clarify usefulness of APR scores.Methods. We evaluated the usefulness of acute phase reactants (APR) in 46 newborns whose serum up to age 7 days had been stored, with comparison of three types (Group I: infection 15, Group F: fetal inflammatory response syndrome 17, and Group C: control 14) of APR-based scores, those of C-reactive protein (CRP), alpha1-acid glycoprotein (AGP), and haptoglobin (Hp), with proinflammatory cytokine levels. APR scores for CRP, AGP, and Hp and the levels of the proinflammatory cytokines IL-1β, IL-6, IL-8, IL-10, and TNFαwere determined.Results. The cytokine levels started to increase from age 0 days and then decreased rapidly. The three APR scores, CRP, AG, and Hp, were elevated at age 0 days and then gradually decreased in infection (Group I) and fetal inflammatory response syndrome (Group F). The duration of antibiotic administration according to APR scores was significantly shorter in Group F than in Group I.Conclusion. This study demonstrated APR scores to be more useful for deciding whether antibiotics should be discontinued than proinflammatory cytokine levels.

TLR-4 pathway mediates the inflammatory response but not bacterial elimination inE. colipneumonia

2005 ◽  
Vol 289 (5) ◽  
pp. L731-L738 ◽  
Author(s):  
Janet S. Lee ◽  
Charles W. Frevert ◽  
Gustavo Matute-Bello ◽  
Mark M. Wurfel ◽  
Venus A. Wong ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Proinflammatory Cytokine ◽  
Inflammatory Responses ◽  
Mutant Mice ◽  
Wild Type ◽  
Neutrophil Accumulation ◽  
E Coli ◽  
Cytokine Levels ◽  
Lower Lung ◽  
Different Strains

We examined the role of Toll-like receptor (TLR)-4 in modifying the lung inflammatory response and its effects on the bacterial recovery from the lungs following inhaled Escherichia coli in two different strains of TLR-4 mutant mice that are hyporesponsive to LPS. The C57BL/10ScN( tlr4lps-del) mice containing a deletion mutation in the TLR-4 gene showed lower proinflammatory cytokine levels, lower lung MPO activity, and less parenchymal and peribronchial inflammation compared with the C57BL/10ScSn mice, a related TLR-4 wild-type substrain. However, the C57BL/10ScN( tlr4lps-del) mutant showed lower bacterial recovery in the lungs following inhaled E. coli associated with a rapid but transient increase in air space neutrophil counts at 6 h. In comparison, the C3H/HeJ( tlr4Lps-d) mutant mice containing a Pro712His substitution in TLR-4 demonstrated lower proinflammatory cytokine levels, lower lung MPO activity, and lower neutrophil accumulation in the air spaces but showed no differences in the bacterial burden of inhaled E. coli at 6 h, when compared with the TLR-4 wild-type C3H/HeSnJ mice. Thus two different TLR-4 mutants showed attenuated inflammatory responses in the lungs, but the reduced inflammatory responses were not consistently associated with either improved or impaired bacterial elimination from the lungs. Our findings indicate that the inflammatory response to inhaled E. coli is TLR-4 dependent, but bacterial elimination depends on other factors in addition to TLR-4.

Enzymatically Inactive Eosinophil Peroxidase Inhibits Proinflammatory Cytokine Transcription and Secretion by Macrophages

1999 ◽  
Vol 196 (1) ◽  
pp. 23-33 ◽  
Author(s):  
John A. Lincoln ◽  
Doris L. Lefkowitz ◽  
Ken J. Grattendick ◽  
Stanley S. Lefkowitz ◽  
Robert C. Allen
Keyword(s):  
Proinflammatory Cytokine ◽  
Eosinophil Peroxidase ◽  
Cytokine Transcription

Low-dose inhaled carbon monoxide attenuates the remote intestinal inflammatory response elicited by hindlimb ischemia-reperfusion

2009 ◽  
Vol 296 (1) ◽  
pp. G9-G14 ◽  
Author(s):  
Jeffrey R. Scott ◽  
Mark A. Cukiernik ◽  
Michael C. Ott ◽  
Aurelia Bihari ◽  
Amit Badhwar ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Inflammatory Response ◽  
Proinflammatory Cytokine ◽  
Low Dose ◽  
Ischemia Reperfusion ◽  
Fold Increase ◽  
Leukocyte Recruitment ◽  
Leukocyte Rolling ◽  
Hindlimb Ischemia ◽  
Tnf Α

Heme oxygenase (HO) represents the rate-limiting enzyme in the degradation of heme into carbon monoxide (CO), iron, and biliverdin. Recent evidence suggests that several of the beneficial properties of HO, may be linked to CO. The objectives of this study were to determine if low-dose inhaled CO reduces remote intestinal leukocyte recruitment, proinflammatory cytokine expression, and oxidative stress elicited by hindlimb ischemia-reperfusion (I/R). Male mice underwent 1 h of hindlimb ischemia, followed by 3 h of reperfusion. Throughout reperfusion, mice were exposed to AIR or AIR + CO (250 ppm). Following reperfusion, the distal ileum was exteriorized to assess the intestinal inflammatory response by quantifying leukocyte rolling and adhesion in submucosal postcapillary venules with the use of intravital microscopy. Ileum samples were also analyzed for proinflammatory cytokine expression [tumor necrosis factor (TNF)-α and interleukin (IL)-1β] and malondialdehyde (MDA) with the use of enzyme-linked immunosorbent assay and thiobarbituric acid reactive substances assays, respectively. I/R + AIR led to a significant decrease in leukocyte rolling velocity and a sevenfold increase in leukocyte adhesion. This was also accompanied by a significant 1.3-fold increase in ileum MDA and 2.3-fold increase in TNF-α expression. Treatment with AIR + CO led to a significant reduction in leukocyte recruitment and TNF-α expression elicited by I/R; however, MDA levels remained unchanged. Our data suggest that low-dose inhaled CO selectively attenuates the remote intestinal inflammatory response elicited by hindlimb I/R, yet does not provide protection against intestinal lipid peroxidation. CO may represent a novel anti-inflammatory therapeutic treatment to target remote organs following acute trauma and/or I/R injury.

scholarly journals The role of interleukin-17 in tumor development and progression

2019 ◽  
Vol 217 (1) ◽  
Author(s):  
Junjie Zhao ◽  
Xing Chen ◽  
Tomasz Herjan ◽  
Xiaoxia Li
Keyword(s):  
Stem Cells ◽  
Wound Healing ◽  
Inflammatory Response ◽  
Proinflammatory Cytokine ◽  
Cancer Biology ◽  
Tissue Repair ◽  
Tumor Development ◽  
Interleukin 17 ◽  
Wide Range

IL-17, a potent proinflammatory cytokine, has been shown to intimately contribute to the formation, growth, and metastasis of a wide range of malignancies. Recent studies implicate IL-17 as a link among inflammation, wound healing, and cancer. While IL-17–mediated production of inflammatory mediators mobilizes immune-suppressive and angiogenic myeloid cells, emerging studies reveal that IL-17 can directly act on tissue stem cells to promote tissue repair and tumorigenesis. Here, we review the pleotropic impacts of IL-17 on cancer biology, focusing how IL-17–mediated inflammatory response and mitogenic signaling are exploited to equip its cancer-promoting function and discussing the implications in therapies.

scholarly journals TREM2 Regulates High Glucose-Induced Microglial Inflammation via the NLRP3 Signaling Pathway

2021 ◽  
Vol 11 (7) ◽  
pp. 896
Author(s):  
Yuan Li ◽  
Weihong Long ◽  
Menghan Gao ◽  
Fangtai Jiao ◽  
Zecai Chen ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Signaling Pathway ◽  
Nlrp3 Inflammasome ◽  
High Glucose ◽  
Proinflammatory Cytokine ◽  
Inflammasome Activation ◽  
Molecular Function ◽  
Nlrp3 Inflammasome Activation ◽  
Bv2 Cells ◽  
Microglial Inflammation

Background: TREM2 expressed on microglia plays an important role in modulating inflammation in neurodegenerative diseases. It remains unknown whether TREM2 modulates hyperglycemia-induced microglial inflammation. Methods: We investigated the molecular function of TREM2 in high glucose-induced microglial inflammation using western blotting, qPCR, ELISA, pulldown, and co-IP methods. Results: Our data showed that in high glucose-induced BV2 cells, TREM2 was increased, and the proinflammatory cytokine IL-1β was increased. TREM2 knockout (KO) attenuated the proinflammatory cytokine IL-1β; conversely, TREM2 overexpression (OE) exacerbated IL-1β expression. Furthermore, we found that high glucose promoted the interaction of TREM2 with NLRP3. TREM2 KO abolished the interaction of TREM2 with NLRP3, while TREM2 OE enhanced the interaction. Moreover, TREM2 KO reduced high glucose-induced NLRP3 inflammasome activation, and TREM2 OE augmented high glucose-induced NLRP3 inflammasome activation, indicating that high glucose enhances the expression of TREM2, which activates the NLRP3 inflammasome. To further clarify whether the NLRP3 signaling pathway mediates the TREM2-regulated inflammatory response, we blocked the NLRP3 inflammasome by knocking out NLRP3 and treating cells with a caspase1 inhibitor, which decreased the levels of the IL-1β proinflammatory cytokine but did not affect the high glucose-induced expression of TREM2. Conclusions: TREM2 modulates high glucose-induced microglial inflammation via the NLRP3 signaling pathway.

scholarly journals Isorhapontigenin from Traditionally used Iris Domestica Reduces the Inflammatory Response by Suppressing NF-κB and MAPK Signaling in LPS-Activated RAW 264.7 Macrophages

2021 ◽  
Author(s):  
Wen-Chung Huang ◽  
Shu-Ju Wu ◽  
Han Lo ◽  
Hui-Ling Peng ◽  
Sindy Hu ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Proinflammatory Cytokine ◽  
Protein Localization ◽  
Mapk Signaling ◽  
Raw 264.7 Cells ◽  
Heme Oxygenase 1 ◽  
Raw 264.7 ◽  
Western Blots ◽  
Pathway Activation ◽  
Species Production

Abstract BackgroundIsorhapontigenin, a resveratrol analogue, isolated from Iris domestica can induce apoptosis in tumor cells. Here, we designed to explore whether isorhapontigenin reduced inflammatory response in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells.MethodsIsorhapontigenin treated with RAW 264.7 cells, and then with LPS to stimulate inflammatory response. Proinflammatory cytokine expressions were measured using ELISA, and protein expressions were detected using western blots. ResultsIsorhapontigenin significantly inhibited the proinflammatory cytokine expressions. Isorhapontigenin also decreased cyclooxygenase-2 and inducible nitric oxide synthase productions and promoted heme oxygenase-1 expression in LPS-stimulated RAW264.7 cells. Isorhapontigenin could significantly inhibit NF-κB subunit p65 protein localization to the nucleus and reduced MAPK signal pathway activation. Isorhapontigenin also decreased reactive oxygen species production. ConclusionThus, isorhapontigenin has potential anti-inflammation and anti-oxidative stress that inhibits inflammatory mediators and cytokines expressions through suppressing the MAPK and NF-κB pathways.

scholarly journals HMGB1 translocation and release mediate cigarette smoke–induced pulmonary inflammation in mice through a TLR4/MyD88-dependent signaling pathway

2017 ◽  
Vol 28 (1) ◽  
pp. 201-209 ◽  
Author(s):  
Yao Cheng ◽  
Dan Wang ◽  
Bin Wang ◽  
Huanan Li ◽  
Junjie Xiong ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Signaling Pathway ◽  
Cigarette Smoke ◽  
Proinflammatory Cytokine ◽  
Cytokine Production ◽  
Pulmonary Inflammation ◽  
High Mobility ◽  
Lung Epithelial Cells ◽  
Proinflammatory Cytokine Production ◽  
Tnf Α

We performed studies to determine the role of high-mobility group box 1 (HMGB1) in cigarette smoke (CS)–induced pulmonary inflammation. After mice were exposed to five cigarettes four times a day for 3 d, toll-like receptor 4 (TLR4) expression and TLR4-mediated signaling were significantly up-regulated, and HMGB1 had translocated from the nucleus to the cytoplasm in lung epithelial cells and then been released into the extracellular lung space. On CS exposure, inflammatory cell recruitment and proinflammatory cytokine production were significantly increased in lung tissue and bronchoalveolar lavage, and these effects depended on the TLR4 signaling pathway. HMGB1 inhibition decreased the CS-induced inflammatory response, whereas treatment with exogenous HMGB1 aggravated the damage and increased the phosphorylation of JNK, p38, and IκBα in the lungs of wild-type mice but not in TLR4-knockout mice. Blockade of TLR4 action or TLR4 knockout significantly inhibited HMGB1-induced proinflammatory cytokine production in mouse tracheal epithelial (MTE) cells and lung tissues. In addition, a MyD88 deficiency inhibited JNK, p38, and IκBα phosphorylation, and this effect was associated with the suppressed production of TNF-α and IL-1β in MTE cells and lung tissues in response to CS stimulation. Thus HMGB1 activates the NF-κB and JNK/p38 pathways through TLR4/MyD88-dependent signaling and induces an inflammatory response in lungs exposed to CS.

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