scholarly journals Hyperbaric oxygen enhances neutrophil apoptosis and their clearance by monocyte-derived macrophages

2015 ◽  
Vol 93 (4) ◽  
pp. 405-416 ◽  
Author(s):  
Anwar J. Almzaiel ◽  
Richard Billington ◽  
Gary Smerdon ◽  
A. John Moody
Keyword(s):  
Mrna Expression ◽  
Hyperbaric Oxygen ◽  
Inflammatory Cytokine ◽  
Cytokine Gene Expression ◽  
Neutrophil Apoptosis ◽  
Normobaric Hyperoxia ◽  
Tnf Α ◽  
Pre Treatment ◽  
Bovine Neutrophils ◽  
Anti Inflammatory Cytokine

Neutrophil apoptosis and clearance by macrophages are essential for wound healing. Evidence suggests that hyperbaric oxygen (HBO) exposure may enhance neutrophil apoptosis, but HBO effects leading to neutrophil clearance by macrophages are still unclear. In the current study, bovine neutrophils and monocyte-derived macrophages (MDMΦ) were co-cultured under HBO (97.9% O2, 2.1% CO2 at 2.4 atm absolute (ATA)) (1 atm = 101.325 kPa), hyperbaric normoxia (8.8% O2 at 2.4 ATA), normobaric hyperoxia (95% O2, 5% CO2), normoxia (air), and normobaric hypoxia (5% O2, 5% CO2). Phagocytosis of fresh and 22 h aged neutrophils by MDMΦ was increased after HBO pre-treatment, assessed using flow cytometry and light microscopy. Enhanced clearance of neutrophils was accompanied by an increase in H2O2 levels following HBO pre-treatment with upregulation of IL-10 (anti-inflammatory cytokine) mRNA expression in LPS-stimulated MDMΦ that had ingested aged neutrophils. TNF-α (pro-inflammatory cytokine) gene expression did not change in LPS-stimulated MDMΦ that had ingested fresh or aged neutrophils after HBO, pressure, and hyperoxia. These findings suggest that HBO-activated MDMΦ participate in the clearance of apoptotic cells. Uptake of neutrophils by MDMΦ exposed to HBO may contribute to resolution of inflammation, because HBO induced up-regulation of IL-10 mRNA expression.

scholarly journals Impact of Smoking Cigarette on the mRNA Expression of Cytokines in Mucosa of Inflammatory Bowel Disease

2019 ◽  
pp. S183-S192 ◽  
Author(s):  
Z. VRABLICOVA ◽  
K. SOLTYS ◽  
A. KRAJCOVICOVA ◽  
K. STUCHLIKOVA ◽  
I. STURDIK ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Mrna Expression ◽  
Inflammatory Cytokine ◽  
Clinical Course ◽  
Response To Therapy ◽  
The Other ◽  
Other Hand ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Anti Inflammatory Cytokine

It is well known that smoking is the risk factor in the development and clinical course of Crohn´'s disease (CD), but on the other hand, smoking is a protective factor against ulcerative colitis (UC). The pathways that are influenced by smoking in CD and UC are poorly understood. The aim of our study was to analyse the influence of smoking on the mRNA expression of cytokines in mucosa in patients with CD and UC. We performed a cross-sectional study. The cohort consisted of 86 IBD patients (48 CD patients and 38 UC patients) and took place at the IBD Centre at the University Hospital Bratislava-Ružinov. We took the demographic and clinical data of each patient, including information about their smoking habits. We performed a colonoscopy on each patient and took biopsies from both inflamed and non-inflamed sigma (CD, UC) and terminal ileum (CD). mRNA was extracted from mucosal biopsy samples for each cytokine and was normalized to a housekeeping gene (GAPDH). Finally, we compared the mRNA expression of target cytokines in the mucosa of smokers and non-smokers in IBD patients. Smokers with Crohn's disease have a significantly higher mRNA expression of pro-inflammatory cytokine TNF α (p=0.003) in inflamed mucosa in sigma compared with non-smokers. In smokers with ulcerative colitis, we observed significantly higher mRNA expression of anti-inflammatory cytokine IL 10 (p=0.022) in non-inflamed mucosa of sigma. Similarly, smokers with UC have a significantly decreased mRNA expression of cytokine TLR 2 (p=0.024) and CCR1(p=0.049) in non-inflamed mucosa of sigma. Based on our results, smoking has a positive influence on cessation and the clinical course of UC due to the stimulation of anti-inflammatory cytokine IL 10 in mucosa. On the other hand, smokers with CD have a higher expression of pro-inflammatory cytokine TNF α, which could be associated with a worsening of the disease and response to therapy.

scholarly journals Effects of prepartum oilseed supplements on subclinical endometritis, pro- and anti-inflammatory cytokine transcripts in endometrial cells and postpartum ovarian function in dairy cows

2017 ◽  
Vol 29 (4) ◽  
pp. 747 ◽  
Author(s):  
Reza Salehi ◽  
Marcos G. Colazo ◽  
Mohanathas Gobikrushanth ◽  
Urmila Basu ◽  
Divakar J. Ambrose
Keyword(s):  
Dairy Cows ◽  
Sunflower Seed ◽  
Inflammatory Cytokine ◽  
Ovarian Function ◽  
Cytokine Gene Expression ◽  
Cytokine Gene ◽  
Endometrial Cells ◽  
Anti Inflammatory ◽  
Subclinical Endometritis ◽  
Anti Inflammatory Cytokine

Postpartum uterine infections affect ovarian function and delay ovulation in cattle. As dietary fats can affect immune cell function, we investigated the influence of prepartum diets on postpartum uterine inflammatory status (UIS) as assessed 25 ± 1 days postpartum by endometrial cytology (normal: ≤8% polymorphonuclear cells (PMN) vs subclinical endometritis (SCE): >8% PMN) and associations between SCE, pro- and anti-inflammatory cytokine gene expression and ovarian function. During the last 5 weeks of gestation, dairy cows received a diet supplemented with 8% rolled sunflower (n = 10) or canola seed (n = 9) or no oilseed (n = 9). Ovaries were scanned until 35 days postpartum. Prepartum diets did not influence SCE, but a preovulatory-size follicle developed sooner (P ≤ 0.05), the interval to first ovulation was shorter and the proportion of cows ovulating within 35 days postpartum was greater in the sunflower seed group. Although mRNA expression of cytokines was not affected by diet, cows with SCE had higher (P ≤ 0.05) expression of interleukin-1β (IL1B), interleukin-8 (CXCL8), IL10 and tumour necrosis factor-α (TNF) than normal cows. The interval (mean ± s.e.m.) from calving to preovulatory-size follicle was shorter (P ≤ 0.05) in normal (13.2 ± 0.9 days) than SCE cows (18.7 ± 1.4 days). In summary, a prepartum diet supplemented with sunflower seed positively influenced postpartum ovarian function without affecting UIS or pro- and anti-inflammatory cytokine gene expression in endometrial cells.

scholarly journals P0527AROLE OF PROMOTING INFLAMMATION OF KLF6 IN ACUTE KIDNEY INURY

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Dan Li ◽  
Chenyu Li ◽  
Yan Xu
Keyword(s):  
Inflammatory Cytokines ◽  
Inflammatory Cytokine ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Tnf Α ◽  
Public Dataset ◽  
Anti Inflammatory ◽  
Anti Inflammatory Cytokine ◽  
Pro Inflammatory Cytokines

Abstract Background and Aims Acute kidney injury (AKI), commonly appeared in cardiac arrest, surgery and kidney transplantation which involved in ischemia-reperfusion (IR) injury of kidney. However, the mechanisms underlying inflammatory response in IR AKI is still unclear. Method Public dataset showed kruppel-like factor 6 (KLF6) was significantly highly expressed (P<0.05) in AKI, implies KLF6 might be associated with AKI. To evaluate the mechanism of KLF6 on IR AKI, 30 rats were randomly divided into sham and IR group, and were sacrificed at 0 h, 3 h, 6 h, 12 h or 24 h after IR. Results The results showed KLF6 expression was peaking at 6 h after IR, and the expression of pro-inflammatory cytokines MCP-1 and TNF-α were increased both in serum and kidney tissues after IR, while anti-inflammatory cytokine IL-10 was decreased after IR. Furthermore, in vitro results showed KLF6 knock-down reduced the pro-inflammatory cytokines expression and increased the anti-inflammatory cytokines expression. Conclusion These results suggest that (1) KLF6 might be a novel biomarker for early diagnosis of AKI and (2) targeting KLF6 expression may offer novel strategies to protect kidneys from IR AKI Figure KLF6, AKI, Control Inflammation

scholarly journals Microneme Proteins 1 and 4 From Toxoplasma gondii Induce IL-10 Production by Macrophages Through TLR4 Endocytosis

2021 ◽  
Vol 12 ◽  
Author(s):  
Rafael Ricci-Azevedo ◽  
Flavia Costa Mendonça-Natividade ◽  
Ana Carolina Santana ◽  
Juliana Alcoforado Diniz ◽  
Maria Cristina Roque-Barreira
Keyword(s):  
Toxoplasma Gondii ◽  
Host Cell ◽  
Inflammatory Cytokine ◽  
Early Stage ◽  
Protozoan Parasite ◽  
Cell Responses ◽  
Tnf Α ◽  
Host Inflammatory Response ◽  
Anti Inflammatory Cytokine ◽  
Microneme Proteins

The protozoan parasite Toxoplasma gondii modulates host cell responses to favor its success in the early stage of infections by secreting proteins from its apical organelles. Some of these proteins, including microneme proteins (MICs) 1 and 4, trigger pro-inflammatory host cell responses. The lectins MIC1 and MIC4 interact with N-linked glycans on TLR2 and TLR4, activating NF-κB and producing IL-12, TNF-α, and IL-6. Interestingly, MIC1 and MIC4 also trigger secretion of the anti-inflammatory cytokine IL-10 through mechanisms as yet unknown. Herein, we show that the ability of these MICs to induce macrophages to produce IL-10 depends on TLR4 internalization from the cell surface. Macrophages subjected to blockade of endocytosis by Dynasore continued to release TNF-α, but failed to produce IL-10, in response to MIC1 or MIC4 exposure. Similarly, IL-10 was not produced by Dynasore-conditioned T. gondii-infected macrophages. Furthermore, MIC1- or MIC4-stimulated macrophages gained transient tolerance to LPS. We report a previously undiscovered mechanism by which well-defined T. gondii components inhibit a host inflammatory response.

scholarly journals Pro- and Anti-Inflammatory Cytokine Expression Levels in Macrophages; An Approach to Develop Indazolpyridin-methanones as Novel Inflammation Medication

2020 ◽  
Vol 19 (4) ◽  
pp. 425-435 ◽  
Author(s):  
Manikandan Alagumuthu ◽  
Vanshika Srivastava ◽  
Manisha Shah ◽  
Sivakumar Arumugam ◽  
Mohandoss Sonaimuthu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Inflammatory Cytokine ◽  
Cancer Cell Lines ◽  
Tnf Α ◽  
Anti Cancer ◽  
Cox 2 ◽  
Anti Inflammatory ◽  
Anti Inflammatory Cytokine

Background: Macrophages play a serious part in the instigation, upkeep, and resolution of inflammation. They are activated or deactivated during inflammation progression. Activation signals include cytokines (IF-γ, granulocyte-monocyte colonystimulating factor (GM-CSF), and TNF-α), extracellular matrix proteins, and other chemical mediators. Activated macrophages are deactivated by anti-inflammatory cytokines (IL- 10 and TGF-β (transforming growth factor-beta) and cytokine antagonists that are mainly produced by macrophages. Based on this, the present study aimed to develop novel (E)- Benzylidene-indazolpyridin methanones (Cpd-1-10) as effective anti-inflammatory agents by analyzing pro- and anti-inflammatory cytokine levels in macrophages. Objectives: To determine the anti-inflammatory effect of indazolpyridin-methanones by examining pro- and anti-inflammatory interleukin levels in J77A.1 macrophages. Methods: Expression of cytokines such as TNF-α, IL-1β, IL-6 and IL-10 serum levels measured by ELISA method. Anti-cancer and cytotoxicity studies were carried out by MTT assay. COX-2 seems to be associated with cancers and atypical developments in the duodenal tract. So, a competitive ELISA based COX-2 inhibition assay was done. To validate the inhibitory potentials and to get more insight into the interaction of COX-2 with Cpd1-10, molecular docking was performed. Results: Briefly, the COX-2 inhibitory relative activity was found to be in between the range of 80-92% (Diclofenac showed 84%, IC50 0.95 μM). Conclusion: Cytotoxicity effect of the compounds against breast cancer cell lines found excellent and an extended anticancer study ensured that these compounds are also alternative therapeutic agents against breast cancer. Among all the tested cancer cell lines, the anti- cancer effect on breast cancer was exceptional for the most active compounds Cpd5 and Cpd9.

scholarly journals Immune Cell–Conditioned Media Suppress Prostate Cancer PC-3 Cell Growth Correlating With Decreased Proinflammatory/Anti-inflammatory Cytokine Ratios in the Media Using 5 Selected Crude Polysaccharides

2016 ◽  
Vol 15 (4) ◽  
pp. NP13-NP25 ◽  
Author(s):  
Hsiao-Chien Lin ◽  
Jin-Yuarn Lin
Keyword(s):  
Prostate Cancer ◽  
Cell Growth ◽  
Inflammatory Cytokine ◽  
Immune Cell ◽  
Direct Action ◽  
Conditioned Media ◽  
Tnf Α ◽  
The Media ◽  
Anti Inflammatory ◽  
Anti Inflammatory Cytokine

Five different crude polysaccharides from guava seed (GSPS), bitter buckwheat (BBPS), common buckwheat (CBPS), red Formosa lambsquarters (RFLPS), and yellow Formosa lambsquarters (YFLPS) were isolated to treat human prostate cancer PC-3 cells via direct action or tumor immunotherapy. The splenocyte- and macrophage-conditioned media (SCM and MCM) were prepared using individual selected polysaccharides, and then SCM or MCM was further collected to treat PC-3 cells. The relationship between PC-3 cell growth and Th1/Th2 cytokines in SCM as well as proinflammatory/anti-inflammatory cytokine secretion profiles in MCM were delineated. The results showed that all 5 selected polysaccharides did not significantly inhibit PC-3 cell growth via direct action. However, SCM or MCM cultured in the absence or presence of 5 selected polysaccharides significantly ( P < .05) inhibited PC-3 cell growth. MCM cultured with 5 polysaccharides dose dependently enhanced their inhibitory effects on the viabilities of PC-3 cells than those cultured without polysaccharides. There was a significant ( P < .05) negative correlation between PC-3 cell viabilities and (interleukin [IL]-6 + tumor necrosis factor [TNF]-α)/IL-10 level ratios in the corresponding MCM, implying that macrophages suppress PC-3 cell growth through decreasing secretion ratios of proinflammatory/anti-inflammatory cytokines in a tumor microenvironment.

scholarly journals Pre-Treatment with Curcumin Ameliorates Cisplatin-Induced Kidney Damage by Suppressing Kidney Inflammation and Apoptosis in Rats

Drug Research ◽  
2018 ◽  
Vol 69 (02) ◽  
pp. 75-82 ◽  
Author(s):  
Vivian Soetikno ◽  
Shinta Sari ◽  
Lulu Ul Maknun ◽  
Nielda Sumbung ◽  
Deliana Rahmi ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Molecular Mechanisms ◽  
Histopathological Examination ◽  
Kidney Injury ◽  
Kidney Damage ◽  
Protective Effects ◽  
Protection Effect ◽  
Tnf Α ◽  
Pre Treatment ◽  
Damage Protection

Abstract Objective In addition to oxidative stress, inflammation and apoptosis have an important role in the pathogenesis of cisplatin-induced kidney damage. This study aimed to investigate the molecular mechanisms of protective effects of curcumin against cisplatin-induced kidney inflammation and apoptosis in rats. Materials and Methods Eighteen rats were equally divided into three groups; normal (0.5% CMC-Na), cisplatin (CDPP) (7 mg/kg i.p.), and cisplatin+curcumin (CMN100) groups. Curcumin was given at a dose of 100 mg/kg orally for nine days, starts one week before giving a single dose of cisplatin. Kidney and plasma were taken for analysis. Results Cisplatin challenged rats demonstrated kidney injury as shown by reduced creatinine clearance, increased of plasma BUN, plasma creatinine, and kidney MDA, decreased of kidney GSH levels, and kidney histopathology alterations. Also, cisplatin increased ERK1/2 phosphorylation and NF-κB expression, which subsequently increased mRNA expression of TNF-α, IL-6, KIM-1, NGAL, and Bax/Bcl-2 ratio as well as decreased mRNA expression of IL-10 in kidney tissues. Pre-treatment with curcumin significantly ameliorated inflammation and apoptosis induced by cisplatin. In addition, curcumin downregulated Ctr1 and OCT2 drug transporters as compared to cisplatin group. Histopathological examination furthers confirmed the kidney damage protection effect of curcumin. Conclusions These data indicate that curcumin has nephroprotective properties against cisplatin-induced kidney damage in rats and this effect is associated with its anti-inflammatory and anti-apoptosis profiles, in addition to its antioxidant. Hence, curcumin may be useful for preventing kidney damage against cisplatin administration.

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