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Neutrophil-to-lymphocyte ratio in patients with severe tinnitus: prospective, controlled clinical study.
Ozbay, I, Kahraman, C, Balikci, HH, Kucur, C, Kahraman, NK, Ozkaya, DP, Oghan, F
The Journal of laryngology and otology. 2015;(6):544-7
Abstract
OBJECTIVE To determine the relationship between severe tinnitus and inflammation using the neutrophil-to-lymphocyte ratio as a marker of stress. METHODS A total of 107 patients who had been suffering with severe tinnitus (tinnitus handicap inventory scale grades of 3-5) for at least 2 weeks were recruited. Patients underwent detailed ENT examinations and audiometric tests to exclude a relevant pathological cause of the tinnitus. Patients with systemic diseases, malignancy or inflammatory diseases that could alter neutrophil-to-lymphocyte ratio were excluded. A total of 107 age- and sex-matched healthy control participants were also recruited. Routine laboratory test results and neutrophil-to-lymphocyte ratio were compared between the patients and controls. RESULTS Lipid profile, liver function, white blood cell count, haemoglobin level, mean corpuscular volume, and vitamin B12 and folate levels were similar among the patients and controls. However, mean neutrophil-to-lymphocyte ratio was significantly higher among the patients than the controls (p < 0.05). CONCLUSION The findings of this novel study suggest that neutrophil-to-lymphocyte ratio should be considered during the evaluation of tinnitus patients as a potential clinical marker of tinnitus. Further studies are required to verify the findings.
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Expression of mitochondrial superoxide dismutase in polymorphonuclear leukocytes from patients with type 1 diabetes with and without microvascular complications.
Wegner, M, Rawłuszko-Wieczorek, AA, Araszkiewicz, A, Pioruńska-Stolzmann, M, Zozulińska-Ziółkiewicz, D, Wierusz-Wysocka, B, Jagodziński, PP
Polskie Archiwum Medycyny Wewnetrznej. 2014;(5):239-46
Abstract
INTRODUCTION One of the causes of impaired antioxidant response in patients with type 1 diabetes might be decreased expression of mitochondrial manganese superoxide dismutase (MnSOD). OBJECTIVES The aim of this study was to evaluate the expression of MnSOD on transcript and protein levels in polymorphonuclear leukocytes (PMNLs) from patients with type 1 diabetes and analyze its association with microvascular complications. PATIENTS AND METHODS The MnSOD expression was assessed in PMNLs from 46 patients with type 1 diabetes and 12 age- and sex -matched healthy subjects. The study group was divided into 2 subgroups: with and without microvascular complications. The MnSOD expression on the transcript level was evaluated by real -time quantitative polymerase chain reaction, while that on the protein level by Western blot analysis. RESULTS A significant increase in the MnSOD transcript level was observed in all patients with diabetes with and without microvascular complications (P = 0.01, P = 0.02, respectively). The MnSOD protein level was higher in patients without microvascular complications compared with those with complications and the control group (P = 0.05, P = 0.03, respectively). The MnSOD expression was positively correlated with fasting plasma glucose and total cholesterol levels both at the transcript level (r = 0.4, P <0.05 for both correlations) and at the protein level (r = 0.3 and r = 0.4, respectively, P <0.05). CONCLUSIONS Although an increased MnSOD transcript level in patients with type 1 diabetes suggests enhanced antioxidant mobilization in all diabetic patients, decreased levels of the MnSOD protein in PMNLs from patients with microvascular complications compared with those without complications indicates that patients with microvascular complications may have impaired antioxidant response.
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High-dose oral N-acetylcysteine, a glutathione prodrug, modulates inflammation in cystic fibrosis.
Tirouvanziam, R, Conrad, CK, Bottiglieri, T, Herzenberg, LA, Moss, RB, Herzenberg, LA
Proceedings of the National Academy of Sciences of the United States of America. 2006;(12):4628-33
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Abstract
Neutrophilic airway inflammation is a hallmark of cystic fibrosis (CF). As high oxidant producers, airway neutrophils contribute largely to the systemic redox imbalance seen in CF. In turn, this chronic and profound imbalance can impact circulating neutrophils before their migration into airways. Indeed, in 18 CF patients with stable disease, blood neutrophils were readily deficient in the pivotal antioxidant glutathione (P = 0.003, compared with 9 healthy controls). In a phase 1 study, this deficiency was improved (P = 0.025) by the glutathione prodrug N-acetylcysteine, given orally in high doses (0.6 to 1.0 g three times daily, for 4 weeks). This treatment was safe and markedly decreased sputum elastase activity (P = 0.006), the strongest predictor of CF pulmonary function. Consistently, neutrophil burden in CF airways was decreased upon treatment (P = 0.003), as was the number of airway neutrophils actively releasing elastase-rich granules (P = 0.005), as measured by flow cytometry. Pulmonary function measures were not improved, as expected with short-term treatment. After excluding data from subjects without baseline airway inflammation, positive treatment effects were more pronounced and included decreased sputum IL-8 levels (P = 0.032). Thus, high-dose oral N-acetylcysteine has the potential to counter the intertwined redox and inflammatory imbalances in CF.
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Effect of diclofenac alone or in combination with alpha-tocopherol on the oxidative activity of polymorphonuclear leukocytes in healthy and osteoarthritic individuals.
Al-Arfaj, AS, Alballa, SR, Mustafa, AA, Al-Tuwaijri, AS, Al-Dalaan, AN, Al-Humayyd, MS
Saudi medical journal. 2004;(2):198-203
Abstract
OBJECTIVE To investigate the effects of diclofenac alone or when combined with alpha-tocopherol on the oxidative activity of polymorphonuclear leukocytes (PMNs) in healthy and osteoarthritic (OA) patients. METHODS The study was carried out at the College of Medicine, King Saud University, Riyadh, Kingdom of Saudi Arabia, over the period 1999 to 2000. Twelve healthy controls and 12 osteoarthritic patients were recruited to the study. Twelve healthy controls and osteoarthritic patients were given diclofenac 50 mg thrice daily orally, initially for 5 days then alpha-tocopherol at 200 mg thrice daily orally, was added for another 5 days. Blood samples were drawn before the start of the study (pre-treatment) and at 5 days following treatment with diclofenac alone and 10 days following treatment with diclofenac and alpha-tocopherol. Chemiluminescence (CL) response was measured for whole blood and isolated polymorphonuclear leukocytes (PMNs) on all samples. RESULTS Diclofenac enhanced CL response of whole blood and of PMNs of healthy controls when stimulated with phorbol myristate acetate (PMA) and opsonized zymosan (OPZ). Co-treatment with alpha-tocopherol resulted in no appreciable change in the CL response of whole blood when stimulated with PMA or OPZ but a further significant enhancement of CL response of isolated PMNs when these cells were stimulated by either PMA or OPZ. In osteoarthritic patients, diclofenac alone and when combined with alpha-tocopherol showed no significant change in CL response of whole blood. The CL response of PMNs from OA patients was decreased by diclofenac alone. However, this inhibitory effect was not observed when alpha-tocopherol was used together with diclofenac. CONCLUSION The effect of diclofenac alone or in combination with alpha-tocopherol did not produce a consistent effect on the CL response of whole blood or isolated PMNs of healthy or osteoarthritic patients.
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Mobilization and oxidative burst of neutrophils are influenced by carbohydrate supplementation during prolonged cycling in humans.
Scharhag, J, Meyer, T, Gabriel, HH, Auracher, M, Kindermann, W
European journal of applied physiology. 2002;(6):584-7
Abstract
Prolonged, strenuous exercise may lead to suppressive effects on the immune system, which might be responsible for a greater susceptibility to opportunistic infections. The aim of this study was to examine the influence of carbohydrate substitution (CHS) during prolonged, strenuous exercise on neutrophil granulocytes and their oxidative burst (intracellular oxidation of dihydrorhodamine(123) to rhodamine(123) after induction by formylized 1-methionyl-1-leucyl-1-phenylalanin) using flow cytometry. In three trials different concentrations of CHS (placebo compared to 6% and 12% CHS; 50 ml.kg(-1)) were given randomly to 14 endurance trained cyclists [mean (SD) age 25 (5) years, maximal oxygen uptake 67 (6) ml.min(-1).kg(-1)] cycling for 4 h in a steady state at 70% of their individual anaerobic threshold. Blood samples were taken before, immediately after cessation, 1 h and 19 h after exercise. A significant rise in neutrophil counts was observed immediately after cessation and 1 h after exercise with a return to normal rest values 19 h after exercise for all three conditions ( P<0.001). The relative proportions of rhodamine(123)+ neutrophils were significantly diminished in all three conditions 1 h after exercise ( P<0.01), while the mean fluorescence intensity was lowest in the placebo trial and differed significantly to the 12% CHS trial ( P=0.024) and almost significantly to the 6% CHS trial ( P=0.052). In conclusion, these data suggest a beneficial effect of CHS on the neutrophil oxidative burst and a possible attenuation of the susceptibility to infections, presumably due to the reduction of metabolic stress in prolonged, strenuous exercise.
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Plasma from aged stored red blood cells delays neutrophil apoptosis and primes for cytotoxicity: abrogation by poststorage washing but not prestorage leukoreduction.
Biffl, WL, Moore, EE, Offner, PJ, Ciesla, DJ, Gonzalez, RJ, Silliman, CC
The Journal of trauma. 2001;(3):426-31; discussion 432
Abstract
BACKGROUND Blood transfusion-particularly that of older stored red blood cells (RBCs)--is an independent risk factor for postinjury multiple organ failure. Immunomodulatory effects of RBC transfusion include neutrophil (PMN) priming for cytotoxicity, an effect exacerbated by longer RBC storage times. We have found that delayed PMN apoptosis in trauma patients is provoked by transfusion, independent of injury severity. We hypothesized that aged stored RBCs delay PMN apoptosis, but that prestorage leukodepletion or poststorage washing could abrogate the effect. METHODS Healthy volunteers each donated 1 unit of blood. One half was leukodepleted, and RBC units were processed in the usual fashion and stored at 4 degrees C. Aliquots were removed on days 1, 14, 21, and 42 and the plasma fraction isolated. Selected aliquots were washed with normal saline before plasma isolation. PMNs harvested from healthy controls were incubated (5% CO2, 37 degrees C) with unmodified, leukoreduced, or washed RBC plasma (20% plasma/80% RPMI 1640), and apoptosis assessed by morphology after 24 hours. Apoptotic index (apoptotic PMNs/total PMNs) was compared. PMN priming for superoxide release was also assessed after plasma exposure. RESULTS PMN apoptosis was delayed by RBCs stored for 21 or 42 days. Prestorage leukodepletion did not alter the effect. However, washing 42-day-old RBCs abrogated the effect. PMN priming for superoxide was provoked by stored packed RBCs in an identical pattern to delayed apoptosis. CONCLUSION Plasma from stored RBCs-even if leukoreduced-delays apoptosis and primes PMNs. The effect becomes evident at 21 days and worsens through product outdate (42 days), but may be prevented by poststorage washing. Inflammatory agents contaminating stored blood likely mediate the effect. Modification of transfusion practices (e.g., giving fresher or washed RBCs or blood substitutes) may attenuate adverse immunomodulatory effects of transfusion in trauma patients.