scholarly journals Observations on diffuse cellular inflammation, with some remarks on contagion

1836 ◽  
Vol 8 (3) ◽  
pp. 416-431
Author(s):  
Charles Lendrick
Keyword(s):  
Cellular Inflammation

scholarly journals Atorvastatin treatment does not abolish inflammatory mediated cardiovascular risk in subjects with chronic kidney disease

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Renate M. Hoogeveen ◽  
Simone L. Verweij ◽  
Yannick Kaiser ◽  
Jeffrey Kroon ◽  
Hein J. Verberne ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Cardiovascular Risk ◽  
Kidney Disease ◽  
Arterial Wall ◽  
Ldl Cholesterol ◽  
Statin Treatment ◽  
Receptor Expression ◽  
Disease Stage ◽  
Cellular Inflammation

AbstractIndividuals with chronic kidney disease are at an increased risk for cardiovascular disease. This risk may partially be explained by a chronic inflammatory state in these patients, reflected by increased arterial wall and cellular inflammation. Statin treatment decreases cardiovascular risk and arterial inflammation in non-CKD subjects. In patients with declining kidney function, cardiovascular benefit resulting from statin therapy is attenuated, possibly due to persisting inflammation. In the current study, we assessed the effect of statin treatment on arterial wall and cellular inflammation. Fourteen patients with chronic kidney disease stage 3 or 4, defined by an estimated Glomerular Filtration Rate between 15 and 60 mL/min/1.73 m2, without cardiovascular disease were included in a single center, open label study to assess the effect of atorvastatin 40 mg once daily for 12 weeks (NTR6896). At baseline and at 12 weeks of treatment, we assessed arterial wall inflammation by 18F-fluoro-deoxyglucose positron-emission tomography computed tomography (18F-FDG PET/CT) and the phenotype of circulating monocytes were assessed. Treatment with atorvastatin resulted in a 46% reduction in LDL-cholesterol, but this was not accompanied by an attenuation in arterial wall inflammation in the aorta or carotid arteries, nor with changes in chemokine receptor expression of circulating monocytes. Statin treatment does not abolish arterial wall or cellular inflammation in subjects with mild to moderate chronic kidney disease. These results imply that CKD-associated inflammatory activity is mediated by factors beyond LDL-cholesterol and specific anti-inflammatory interventions might be necessary to further dampen the inflammatory driven CV risk in these subjects.

Cyclophilin D deficiency protects against the development of mitochondrial ROS and cellular inflammation in aorta

2019 ◽  
Vol 508 (4) ◽  
pp. 1202-1208 ◽  
Author(s):  
Xiaojing Liu ◽  
Heng Du ◽  
Dan Chen ◽  
Hai Yuan ◽  
Wenbin Chen ◽  
...  
Keyword(s):  
Cyclophilin D ◽  
Cellular Inflammation ◽  
Mitochondrial Ros

Chronic Sinusitis with Nasal Polyps: Staphylococcal Exotoxin Immunoglobulin E and Cellular Inflammation

2004 ◽  
Vol 18 (5) ◽  
pp. 273-278 ◽  
Author(s):  
David B. Conley ◽  
Anju Tripathi ◽  
Anne M. Ditto ◽  
Kathryn Reid ◽  
Leslie C. Grammer ◽  
...  
Keyword(s):  
Nasal Polyps ◽  
Chronic Sinusitis ◽  
Immunoglobulin E ◽  
Cellular Inflammation

scholarly journals Redox Balance and Cellular Inflammation in the Diaphragm, Limb Muscles, and Lungs of Mechanically Ventilated Rats

2010 ◽  
Vol 112 (2) ◽  
pp. 384-394 ◽  
Author(s):  
Judith Marín-Corral ◽  
Leticia Martínez-Caro ◽  
José A. Lorente ◽  
Marta de Paula ◽  
Lara Pijuan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mechanical Ventilation ◽  
Lung Injury ◽  
Protein Adducts ◽  
Organ Injury ◽  
Mechanically Ventilated ◽  
Ventilator Induced Lung Injury ◽  
Cellular Inflammation ◽  
Cell Counts ◽  
Limb Muscles

Background High tidal volume (VT) mechanical ventilation was shown to induce organ injury other than lung injury and systemic inflammation in animal models of ventilator-induced lung injury. The authors aimed to explore whether high VT mechanical ventilation per se induces early oxidative stress and inflammation in the diaphragm, limb muscles, and lungs of healthy rats exposed to ventilator-induced lung injury. Methods Protein carbonylation and nitration, antioxidants (immunoblotting), and inflammation (immunohistochemistry) were evaluated in the diaphragm, gastrocnemius, soleus, tibialis anterior, and lungs of mechanically ventilated healthy rats and in nonventilated control animals (n = 8/group) for 1 h, using two different strategies (moderate VT [VT = 9 ml/kg] and high VT [VT = 35 ml/kg]). Results The main findings are summarized as follows: compared with controls, (1) the diaphragms and gastrocnemius of high-VT rats exhibited a decrease in reactive carbonyls, (2) the soleus and tibialis of high- and moderate-VT rodents showed a reduction in reactive carbonyls and malondialdehyde-protein adducts, (3) the lungs of high-VT rats exhibited a significant rise in malondialdehyde-protein adducts, (4) the soleus and tibialis of both high- and moderate-VT rats showed a reduction in protein nitration, (5) the lungs of high- and moderate-VT rats showed a reduction in antioxidant enzyme levels, but not in the muscles, and (6) the diaphragms and gastrocnemius of all groups exhibited very low inflammatory cell counts, whereas the lungs of high-VT rats exhibited a significant increase in inflammatory infiltrates. Conclusions Although oxidative stress and inflammation increased in the lungs of rats exposed to high VT, the diaphragm and limb muscles exhibited a decline in oxidative stress markers and very low levels of cellular inflammation.

scholarly journals Autophagy Facilitates IFN-γ-induced Jak2-STAT1 Activation and Cellular Inflammation

2010 ◽  
Vol 285 (37) ◽  
pp. 28715-28722 ◽  
Author(s):  
Yu-Ping Chang ◽  
Cheng-Chieh Tsai ◽  
Wei-Ching Huang ◽  
Chi-Yun Wang ◽  
Chia-Ling Chen ◽  
...  
Keyword(s):  
Cellular Inflammation ◽  
Ifn Γ

Abstract 529: Statin Therapy Decreases Vascular Inflammation and Prolongs Patency in Murine Arteriovenous Fistula

2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Jie Cui ◽  
Harkamal S Jhajj ◽  
Chase W Kessinger ◽  
Jason McCarthy ◽  
Farouc A Jaffer
Keyword(s):  
Blood Flow ◽  
Statin Therapy ◽  
Inflammatory Cell ◽  
Vascular Inflammation ◽  
Neointimal Hyperplasia ◽  
Venous Outflow ◽  
Statin Group ◽  
Cellular Inflammation ◽  
Anti Inflammatory

Background: AVFs are the lifeline of dialysis patients, but can often occlude. The most common cause of AVF failure is inflammation-driven neointimal hyperplasia and thrombosis. Here, we investigated whether statin therapy with well-recognized anti-inflammatory properties can improve murine AVF patency, and further assessed the anti-inflammatory effects. Methods: One week prior to AVF creation, mice were randomized to oral atorvastatin 1.14mg/kg/day or control 100ul PBS (both n=10), administered by daily gavage. AVF were created using an end-to-side internal jugular vein and carotid artery anastomosis. AVF blood flow was measured (Transonic blood flow probe) at day 0 and weekly thereafter until occlusion (blood flow < 0.1ml/min). On day 6, CLIO-VT680, an inflammatory cell-targeted fluorescent nanoparticle, was injected intravenously (10mg/kg). 24 hours later, in vivo survival epifluorescence molecular imaging was performed to visualize inflammatory cell in the AVF venous outflow limb. Histopathological assessment of AVF was performed in on day 7 and 14 mice (6 statin each, 6 control each) to assess venous outflow area, AVF scarring via collagen, and adventitial macrophage content. Results: At day 7, the in vivo venous outflow cellular inflammation signal (CLIO-VT680 TBR) was significantly lower in statin-treated mice (3.5±0.16 vs 4.5±0.5 PBS, p=0.02). Adventitial macrophage content was significantly lower in statin group at day 14 (p=0.01). Positive AVF remodeling, a desirable feature for clinical AVF patency, was higher in the statin group as compared to the PBS group (p=0.02 at week 1, p=0.002 at week 2). In vivo, statin-treated animals exhibited greater AVF blood flow (BF) preservation from day 7 to day 14 (ΔAVF BF +0.14±0.2 ml/min vs. -0.79±0.32 ml/min PBS, p=0.02). The ΔAVF BF from day 7 to day 14 correlated inversely and significantly with the day 7 CLIO-VT680 cellular inflammation (r=-0.56, p=0.02), indicating that baseline inflammation may predict AVF failure. Kaplan Meier survival analysis showed median AVF patency in mice treated with statin was 28 days compared to 14 days in PBS treated group (p<0.05). Conclusion: Statin therapy prolongs AVF patency and preserves AVF blood flow in association with diminished AVF cellular inflammation.

scholarly journals The ORMDL3 Asthma Gene Regulates ICAM1 and Has Multiple Effects on Cellular Inflammation

2019 ◽  
Vol 199 (4) ◽  
pp. 478-488 ◽  
Author(s):  
Youming Zhang ◽  
Saffron A. G. Willis-Owen ◽  
Sarah Spiegel ◽  
Clare M. Lloyd ◽  
Miriam F. Moffatt ◽  
...  
Keyword(s):  
Cellular Inflammation
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