scholarly journals Targeting pro-inflammatory cytokines following joint injury: acute intra-articular inhibition of interleukin-1 following knee injury prevents post-traumatic arthritis

2014 ◽  
Vol 16 (3) ◽  
pp. R134 ◽  
Author(s):  
Bridgette D Furman ◽  
Daniel S Mangiapani ◽  
Evan Zeitler ◽  
Karsyn N Bailey ◽  
Phillip H Horne ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Knee Injury ◽  
Interleukin 1 ◽  
Joint Injury ◽  
Post Traumatic ◽  
Traumatic Arthritis ◽  
Pro Inflammatory Cytokines

scholarly journals Down-Regulation of MiR-150 Alleviates Inflammatory Injury Induced by Interleukin 1 via Targeting Kruppel-Like Factor 2 in Human Chondrogenic Cells

2018 ◽  
Vol 47 (6) ◽  
pp. 2579-2588 ◽  
Author(s):  
Xirui Yang ◽  
Qi Zhang ◽  
Zhaomeng Gao ◽  
Chunyan Yu ◽  
Lei Zhang
Keyword(s):  
Cell Viability ◽  
Inflammatory Cytokines ◽  
Cell Damage ◽  
Interleukin 1 ◽  
Annexin V ◽  
Cartilage Degeneration ◽  
Joint Injury ◽  
Notch Pathways ◽  
Induced Apoptosis ◽  
Pro Inflammatory Cytokines

Background/Aims: Interleukin-1 (IL-1) is known to be involved in cartilage degeneration following joint injury or due to osteoarthritis. In the present study, we explored the effects of miR-150 on IL-1-stimulated human chondrogenic cells ATDC5. Methods: ATDC5 cells were transfected with the mimic, inhibitor or negative controls specific for miR-150, and subsequently treated by IL-1. CCK8 assay, PI and FITC-conjugated Annexin V double-staining, Western blot, qRT-PCR and ELISA assay were performed to determine the changes of cell viability, apoptosis, and the release of pro-inflammatory cytokines. Targeting relationship between miR-150 and KLF2 was detected by dual luciferase activity assay. Results: IL-1 reduced cell viability, induced apoptosis, and enhanced the expression and release of pro-inflammatory cytokines (IL-6, IL-8 and TNF-α) in ATDC5 cells. IL-1 also increased the expression of miR-150. Suppression of miR-150 alleviated IL-1-induced cell damage in ATDC5 cells, while overexpression of miR-150 resulted in an opposite impact. KLF2 was negatively regulated by miR-150, and it was proved as a target gene of miR-150. KLF2 overexpression exhibited protective actions in IL-1-injured ATDC5 cells, even if miR-150 was suppressed in cell. Moreover, IL-1-induced activation of NF-kB and Notch pathways was alleviated by KLF2 overexpression. Conclusions: Suppression of miR-150 led to up-regulation of KLF2, which in turn protected ATDC5 cells against IL-1-induced injury.

Microstructural changes and immunohistological analysis of pro-inflammatory cytokines in spleens of lipopolysaccharide-induced rats

2018 ◽  
Author(s):  
Y. B. Zhong ◽  
X. L. Zhang ◽  
M. Y. Lv ◽  
X. F. Hu ◽  
Y. Li
Keyword(s):  
Inflammatory Cytokines ◽  
Optical Density ◽  
Normal Saline ◽  
Interleukin 1 ◽  
Saline Group ◽  
Control Group ◽  
Sprague Dawley ◽  
Necrosis Factor Alpha ◽  
Lymphoid Follicles ◽  
Pro Inflammatory Cytokines

This study investigated splenic status changes in weaned Sprague-Dawley rats induced by lipopolysaccharide. There were forty 26-day-old rats selected randomly and equally divided into two groups. The treatment group received daily single doses of lipopolysaccharide, and the control group was treated with normal saline. We conducted haematoxylin-eosin staining, immunohistochemical staining and semi-quantitative optical density analysis for both groups on the 29th, 32nd, 35th and 38th days after treatment. The results indicated that splenic marginal zone in the lipopolysaccharide group was thinner or disappeared compared to that of the saline group. However, the periarterial lymphoid sheath and the diameters of splenic lymphoid follicles appeared thicker and wider than those in the saline group (P less than 0.05). The expression of interleukin-1 beta, interleukin-6 and tumour necrosis factor alpha was mainly localized within the periarterial lymphoid sheath and splenic lymphoid follicles in the lipopolysaccharide treated rats. The integrated optical density and the average optical density in the lipopolysaccharide group were greater than those in the normal saline treated group (P less than 0.05). In conclusion, splenic immune function is probably strengthened by altering microstructures and releasing pro-inflammatory cytokines following lipopolysaccharide treatment.

Changes of Vascular Endothelium Adhesive Properties in Patients with Chronic Generalized Slight Periodontitis During the Treatment

2015 ◽  
Vol 22 (4) ◽  
pp. 79-82
Author(s):  
Жданова ◽  
O. Zhdanova ◽  
Широков ◽  
V. Shirokov ◽  
Говорунова ◽  
...  
Keyword(s):  
Serum Concentration ◽  
Adhesion Molecules ◽  
Inflammatory Cytokines ◽  
Interleukin 1 ◽  
Intercellular Adhesion Molecule ◽  
Immunoglobulin Superfamily ◽  
Control Group ◽  
Adhesive Properties ◽  
Endothelial Adhesion Molecules ◽  
Pro Inflammatory Cytokines

The article presents the description of the changes in the concentrations of pro‐inflammatory cytokines and soluble forms of selectins and immunoglobulin superfamily adhesion molecules in patients with chronic generalized slight periodontitis. Serum concentrations of interleukin‐1‐β, tumor necrosis factor‐ α, soluble forms of P‐ and E‐selectins, intercellular adhesion molecule (ICAM‐1), vascular adhesion molecules (VCAM‐1) and platelet‐endothelial adhesion molecules (PECAM‐1) in healthy subjects and patients with slight periodontitis before and after treatment were assessed. It was found that the serum concentration of sICAM‐1, sVCAM‐1, sP‐, sE‐ selektins and pro‐inflammatory cytokines are increased in patients with chronic generalized periodontitis. The increase of serum concentration of soluble forms of selectins is expressed more significantly than sICAM‐1 and sVCAM‐1. There are no statistically significant changes of serum sPECAM‐1 in the examined group of patients in comparison with control. Complex therapy, including etiological and pathogenetic treatment, is completely normalized the concentration of pro‐inflammatory cytokines, and soluble forms of studied endothelial adhesion molecules in patients with chronic generalized slight periodontitis. All the studied parameters in patients with chronic generalized slight periodontitis after treatment are in the range of the control group variability.

scholarly journals The effect of early resuscitation and ulinastatin on the severe acute pancreatitis in obese patients

2020 ◽  
Vol 24 (3) ◽  
pp. 449-454
Author(s):  
O. Tkachuk ◽  
A. Kebkalo
Keyword(s):  
Acute Pancreatitis ◽  
Inflammatory Response ◽  
Inflammatory Cytokines ◽  
Severe Acute Pancreatitis ◽  
Interleukin 1 ◽  
Obese Patients ◽  
Ringer’S Lactate ◽  
Bed Days ◽  
Experimental Group ◽  
Pro Inflammatory Cytokines

Annotation. Obesity is a problem of the third millennium. It is known that obesity is a major factor in the development of various diseases, including acute pancreatitis. Obesity itself is a pro-inflammatory condition with elevated levels of the following pro-inflammatory cytokines: tumor necrosis factor (TNF-a), interleukin (IL) IL-10, IL-6, IL-1b. Acute pancreatitis is also a disease based on the pathogenesis of the cytokine reaction and autolysis. Thus, against the background of the already formed inflammatory response, the inflammatory response intensifies and increases, and the level of pro-inflammatory cytokines reaches critical values. The purpose is to study the effect of ulinastatin on the severe acute pancreatitis in obese patients. To refute or confirm the hypothesis among patients with severe acute pancreatitis and obesity (BMI was 37.48±2.19 kg / m2), two groups were randomized. In the first group (experimental) of 18 patients, a step-up approach was performed. In the second group (control), the total number of which was 18 patients, a standard treatment algorithm was performed. The experimental group suggested the use of early resuscitation with Ringer’s lactate and ulinastatin in the first 5 days of the disease. The drug was administered at a dose of 200,000 IU by intravenous infusion for 1 hour 3 times a day for 5 days. In the control group, resuscitation was performed with 0.9% sodium chloride solution without the use of ulinastatin. Hypothesis was tested by monitoring procalciton and C-reactive protein, interleukin-1 and interleukin-6 over a period of 24 hours, 48 hours, 10 days, 15 days, 30 days, 45 and 60 days. The choice of procalcitonin and CRP was made by calculating the relative risk, as the level of CRP> 200mg / l indicated the preservation of severe disease (RR=2.07; 95% CI=1.65-2.59; p=0.01), and an increase in procalcitonin> 1.8 ng / mg was a predictor of infection (RR=2.27; 95% CI=1.083-4.769; p=0.02). The use of ulinastatin during the first 5 days in the experimental group reduced the level of interleukin-1 from 23.64±4.13 to 8.71±2.49 pg / ml (p=0.001; α=0.05), interleukin- 6 – from 29.72±4.27 to 12.43±2.36 pg / ml (p=0.001; α=0.05). The use of resuscitation with Ringer's lactate solution in combination with ulinastatin for 5 days helped to reduce the level of procalciton in 1.8 times (2.89±0.88 compared with 1.8±0.23 ng / mg; p=0.001; α=0.05). The level of CRP during the period of ulinastatin decreased by 41.68 (267.28±114.11 compared with 225.6±84.9 mg / l; p=0.01; α=0.05). In-hospital mortality was significantly lower in the ulinastatin group (16% vs. 69.6%; p=0.0003; α=0.05). Significantly lower proportion of patients (24% compared to 73.9%; p=0.0005; α=0.05) with multiple organ failure among the study group. Organ dysfunction was acquired on day 5 among patients taking ulinastatin. The length of hospital stay was 49.7±4.2 bed-days, while in the comparison group – 56.67±5.84 bed-days (p=0.01; α=0.05). Thus, the use of Ringer-lactate early resuscitation in combination with ulinastatin has improved the treatment of severe acute pancreatitis in obese patients.

Disturbance of pro-inflammatory cytokines in post-traumatic psychopathology

Cytokine ◽  
2003 ◽  
Vol 24 (5) ◽  
pp. 219-225 ◽  
Author(s):  
A.G Sutherland ◽  
D.A Alexander ◽  
J.D Hutchison
Keyword(s):  
Inflammatory Cytokines ◽  
Post Traumatic ◽  
Pro Inflammatory Cytokines
Sign in / Sign up

Export Citation Format

Share Document