Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P10145 (IL-8)
 23,849 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sepsis causes more than with 215,000 deaths per year in the United States alone. Death can be caused by multiple system organ failure, with the lung, in the form of the acute respiratory distress syndrome (ARDS), often being the first organ to fail. We developed a chronic porcine model of septic shock and ARDS and hypothesized that blocking the proteases neutrophil elastase (NE) and matrix metalloproteinases (MMP-2 and MMP-9) with the modified tetracycline, COL-3, would significantly improve morbidity in this model. Pigs were anesthetized and instrumented for hemodynamic monitoring and were then randomized to one of three groups: control (n = 3), laparotomy only; superior mesenteric artery occlusion (SMA) + fecal blood clot (FC; n = 7), with intraperitoneal placement of a FC; and SMA + FC + COL (n = 5), ingestion of COL-3 12 h before injury. Animals emerged from anesthesia and were monitored and treated with fluids and antibiotics in an animal intensive care unit continuously for 48 h. Serum and bronchoalveolar lavage fluid (BALF) were sampled and bacterial cultures, MMP-2, MMP-9, NE, and multiple cytokine concentrations were measured. Pigs were reanesthetized and placed on a ventilator when significant lung impairment occurred (PaO2/FiO2 < 250). At necropsy, lung water and histology were assessed. All animals in the SMA + FC group developed septic shock evidenced by a significant fall in arterial blood pressure that was not responsive to fluids. Lung injury typical of ARDS (i.e., a fall in lung compliance and PaO2/FiO2 ratio and a significant increase in lung water) developed in this group. Additionally, there was a significant increase in plasma IL-1 and IL-6 and in BALF IL-6, IL-8, IL-10, NE, and protein concentration in the SMA + FC group. COL-3 treatment prevented septic shock and ARDS and significantly decreased cytokine levels in plasma and BALF. COL-3 treatment also significantly reduced NE activity (P < 0.05) and reduced MMP-2 and MMP-9 activity in BALF by 64% and 34%, respectively, compared with the SMA + FC group. We conclude that prophylactic COL-3 prevented the development of ARDS and unexpectedly also prevented septic shock in a chronic insidious onset animal model of sepsis-induced ARDS. The mechanism of this protection is unclear, as COL-3 inhibited numerous inflammatory mediators. Nevertheless, COL-3 significantly reduced the morbidity in a clinically applicable animal model, demonstrating the possibility that COL-3 may be useful in reducing the morbidity associated with sepsis and ischemia/reperfusion injury in patients.
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PMID:Chemically modified tetracycline prevents the development of septic shock and acute respiratory distress syndrome in a clinically applicable porcine model. 1620 20

To investigate the effect of signal transducers and activators of transcription 1 (STAT1) antisense oligonucleotides (ASON) on concentrations of TNF-alpha, IL-8, NO secreted by alveolar macrophages (AMs) in bleomycin-induced rat pulmonary fibrosis, five adult female Wistar rats were intratracheally instilled with bleomycin. After 7 days, the rats were killed by right ventricle of heart exsanguinations under ketamine anaesthesia and bronchoalveolar lavage (BAL) was performed to obtain AMs. AMs were divided into four groups, treated with STAT1 ASON, STAT1 sense oligonucleotides (SON), dexamethasone (DEX) and medium alone (control), respectively. AMs and media were collected after culture for 36 h. The mRNA and protein expressions of STAT1 and ICAM-1 in AMs were detected by RT-PCR and ELISA, respectively. The concentrations of TNF-alpha, IL-8, NO in cultured medium were detected. The STAT1 mRNA expression by AMs in the STAT1 ASON group was lower than those of AMs in the STAT1 SON group, the DEX group and the control group (p<0.05). Moreover, the STAT1 mRNA expression by AMs in the DEX group was also lower than those of AMs in the STAT1 SON group and the control group (p<0.05), but the STAT1 mRNA expression by AMs in the STAT1 SON group was not different from that of the control group (p>0.05). The protein expressions of STAT1 and ICAM-1 and the mRNA expression of ICAM-1 showed similar changes to the STAT1 mRNA expression by AMs. The concentrations of TNF-alpha, IL-8, NO in cultured medium from STAT1 ASON group were lower than those from STAT1 SON, DEX and the control groups (p<0.05). Moreover, the concentrations of TNF-alpha, IL-8, NO in cultured medium from DEX group were also lower than those from the control and STAT1 SON group (p<0.05), but no difference between STAT1 SON group and the control (p>0.05). The results suggest that STAT1 ASON could inhibit the secretion of TNF-alpha, IL-8, NO in AMs, and STAT1 could become a target of treating pulmonary fibrosis.
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PMID:STAT1 antisense oligonucleotides attenuate the proinflammatory cytokine release of alveolar macrophages in bleomycin-induced fibrosis. 1621 89

Immune system dysfunction in the perioperative period, with its combined pro-inflammatory and immuno-suppressive effects, can influence long term disease progression, morbidity, and mortality. Literature on postoperative immune response in schistosomiasis patients is scarce. The aim of this study was to assess the impact of isoflurane anesthesia on pro- and anti-inflammatory cytokine balance in schistosomal patients undergoing minor procedures. The study was conducted on 24 patients (ASA class I-II) scheduled for elective urologic endoscopic procedures. Patients were divided into two groups 12 patients each: control group (n=12) and patient group (n=12). Anaesthesia was induced by a bolus dose of sufentanil 0.2 microg x kg(-1), thiopentone sodium 5 mg x kg(-1), vecuronium 0.1 mg x kg(-1) and maintained by isoflurane 1-1.5 MAC with additional sufentanil bolus of 0.15 microg x kg(-1) when indicated. Venous blood samples were obtained from each patient: before induction, fifteen minutes, one hr after induction and 24 hrs after surgery. Plasma levels of IL-1beta, TNF-alpha, IL-8, IFN-gamma, IL-1ra and TNF-BP1, as well as stress hormones (cortisol and prolactin) were measured. As for pro- and anti-inflammatory cytokine balance, the overall end-result was a rise at 24 hr postoperatively, in the level of TNF-alpha (a key pro-inflammatory cytokine) and IFN-gamma, as well as both anti-inflammatory cytokines (IL-Ira & sTNF-R1). The anti-inflammatory response was more conspicuous in the patients than controls.
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PMID:Does isoflurane anesthesia alter immuno-modulatory response in schistosomal patients? Assessment of serum pro- and anti-inflammatory cytokine balance. 1692 76

Cardiopulmonary bypass (CPB) is believed to cause postoperative lung dysfunction. To more closely examine the inflammatory processes occurring in the airways during CPB, we serially measured inflammatory mediators, with the assistance of a new bronchoscopic microsample probe, in 11 patients undergoing repair of aortic arch aneurysms. Epithelial lining fluid (ELF) and arterial blood were sampled simultaneously after induction of anesthesia, at the time of pulmonary reperfusion, and at the end of surgery. A decrease in the PaO2/FiO2 ratio was observed at the end of surgery (P = 0.029). Although the ELF concentrations of interleukin (IL)-8, IL-6, and neutrophil elastase had increased significantly at the end of surgery (median = 23,200, 1818, and 12,900 microg/mL, respectively), they did not correlate with the degree of hypoxemia. Neutrophil elastase increased significantly at the time of pulmonary reperfusion, before IL-8 and IL-6, and independently of blood transfusions. At the end of surgery, IL-6 in ELF correlated with total blood transfusion volume (rho = 0.731, P = 0.011). These results indicate that a neutrophil-derived inflammatory response is activated in the airway in the early phase of CPB.
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PMID:Activation of a neutrophil-derived inflammatory response in the airways during cardiopulmonary bypass. 1712 9

Lung injury after cardiac surgery is believed to result from cardiopulmonary bypass and its pro-inflammatory effects. To test this hypothesis, we compared the oxygenation ratios, extravascular lung water indices and systemic and pulmonary tumour necrosis factor alpha (TNF-alpha) and interleukin (IL)-8 at predetermined intervals in coronary artery surgery patients with or without cardiopulmonary bypass. No differences in oxygenation ratios or extravascular lung water indices were found. Serum values of TNF-alpha and IL-8 increased in both groups but were higher in the cardiopulmonary bypass group (end of surgery: mean (SD) TNF-alpha 3.68 (2.5) vs 2.20 (1.2) pg.ml(-1) (p = 0.043 (CI 0.05-2.9)) and mean (SD) IL-8 19.45 (10.8) vs 6.31 (5.3) pg.ml(-1) (p = 0.001 (CI 6.9-19.3)). In broncho-alveolar lavage fluid, TNF-alpha and IL-8 increased in both groups with no differences between the groups.
Anaesthesia 2007 Dec
PMID:Pulmonary function and inflammatory markers in patients undergoing coronary revascularisation with or without cardiopulmonary bypass. 1799 Dec 59

Irreversibly inflamed pulp (IIP) constitutes both a pathophysiologic and a diagnostic challenge. Gingival crevicular fluid (GCF) samples were obtained with Periopaper strips from IIP and adjacent and contralateral teeth for interleukin-8 (CXCL8) and tumor necrosis factor-alpha (TNF-alpha) measurements. Pain intensity was reported by using a verbal numeric scale (1-10). TNF-alpha (n = 25) was not detectable in GCF, whereas CXCL8 (n = 17) was significantly greater in IIP (302.1 +/- 164.9 pg/mL) compared with adjacent (139 +/- 138.58 pg/mL; P = .0072) or contralateral (173.8 +/- 166.4 pg/mL; P = .0231) teeth. A subgroup of high pain (>5) patients (n = 7) had CXCL8 IIP levels (323.6 +/- 148.4 pg/mL) that were significantly different from the contralateral teeth (P = .0262); however, they did not differ from the adjacent teeth (P = .1649), suggesting that neighboring teeth might also have inflammation. Another group of patients (n = 7) who had received local anesthesia before sampling had very low IIP CXCL8 levels. GCF CXCL8 levels might be a useful measurement for staging patients with acute pulpitis.
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PMID:Interleukin-8 is increased in gingival crevicular fluid from patients with acute pulpitis. 1821 70

A 75-year-old previously healthy man presented for elective resection of rectal cancer under general anesthesia. Six days before the operation, he had a high-grade fever, and elevated leukocyte count and C-reactive protein concentration, but this was resolved by an intravenous antibiotic. His condition was well controlled before the operation. Soon after the operation started, severe hypoxemia emerged, with low arterial pressure. Fiberoptic bronchoscopy demonstrated a massive amount of plasma-like edema fluid; the total amount of suctioned fluid was approximately 800 ml at the end of the surgery. This acute pulmonary edema appeared to be due to increased permeability rather than pulmonary congestion as indicated by chest radiography, pulmonary artery occlusion pressure, echocardiogram, and the protein-rich edema fluid. Elevated concentrations of the proinflammatory cytokines, interleukin (IL)-6 and IL-8, in both plasma and the pulmonary edema fluid, suggested a possible role of systemic and pulmonary inflammation in the development of this acute pulmonary capillary leak. According to the "two-hit" hypothesis, the bacterial infection preceding the operation may have primed the immune cells, and the following surgical stress may have then triggered rapid progression of acute respiratory distress syndrome. We should keep in mind that, especially following sepsis, sudden massive pulmonary capillary leak can occur during elective surgery, even though the patient's condition is well controlled.
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PMID:Acute pulmonary capillary leak syndrome during elective surgery under general anesthesia. 1830 21

Cardiopulmonary bypass may cause acute lung injury and can seriously affect postoperative outcome, especially in younger patients. A synthesized neutrophil elastase inhibitor, sivelestat sodium, may be most effective when used during cardiopulmonary bypass. After anesthesia induction, sivelestat (2 mg/kg/h) was given to the SS group (n=7), and 0.9% saline solution to the placebo group (n=7). Piglets were placed on hypothermic cardiopulmonary bypass and subjected to myocardial ischemia (2 h) induced by cold crystalloid cardioplegia. At 24 h after surgery, PaO(2)/FiO(2) ratio and alveolar-arterial oxygen difference were significantly better in the SS group (379.1+/-93.9 mmHg and 250.5+/-89.3 mmHg) than the placebo group (232.4+/-105.3 mmHg, and 378.3+/-90.8 mmHg, P<0.05). Interleukin-8 level in the epithelial lining fluid was above the lowest standard in 6 out of 7 (4.5, 12.9, 24.6, 27.7, 37.7, and 159.8; mean=44.5+/-57.6 g/l) in the placebo group, and in 2 out of 7 (36.1 and 67.8 g/l) in the SS group (P<0.05). The median histological score of acute lung injury in the harvested lung was 3 (2-5) in the placebo group and 1 (1-5) in the SS group (P<0.05). Intraoperative administration of sivelestat effectively reduced neutrophil induction and activation in the lung and improved oxygenation after cardiopulmonary bypass in a piglet model.
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PMID:The effect of sivelestat sodium on post-cardiopulmonary bypass acute lung injury in a neonatal piglet model. 1859 53

Inflammation induced by inhalation of air pollutant particles has been implicated as a mechanism for the adverse health effects associated with exposure to air pollution. The inflammatory response is associated with upregulation of various pro-inflammatory cytokines and chemokines. We have previously shown that diesel exhaust particles (DEP), a significant constituent of air pollution particulate matter in many urban areas, bind and concentrate IL-8, an important human neutrophil-attracting chemokine, and that the chemokine remains biologically active. In this report, we examine possible mechanisms of this association and the effects on clearance of the chemokine. The binding appears to be the result of ionic interactions between negatively charged particles and positively charged chemokine molecules, possibly combined with intercalation into small pores in the particles. The association is not limited to diesel exhaust particles and IL-8: several other particle types also adsorb the chemokine and several other cytokines are adsorbed onto the diesel particles. However, there are wide ranges in the effectiveness of various particle types and various cytokines. Finally, male Fisher 344 rats were intratracheally instilled with chemokine alone or combined with diesel exhaust or silica particles under isofluorane anesthesia. In contrast to silica particles, which do not bind the chemokine, the presence of diesel exhaust particles, which bind the chemokine, prolonged the retention of the chemokine.
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PMID:Mechanisms and implications of air pollution particle associations with chemokines. 1875 6

This study examined the hypothesis that curcumin supplementation decreases blood levels of IL-6, MCP-1, TNF-alpha, hyperglycemia, and oxidative stress by using a cell-culture model and a diabetic rat model. U937 monocytes were cultured with control (7 mM) and high glucose (35 mM) in the absence or presence of curcumin (0.01-1 microM) at 37 degrees C for 24 h. Diabetes was induced in Sprague-Dawley rats by injection of streptozotocin (STZ) (i.p., 65 mg/kg BW). Control buffer, olive oil, or curcumin (100 mg/kg BW) supplementation was administered by gavage daily for 7 weeks. Blood was collected by heart puncture with light anesthesia. Results show that the effect of high glucose on lipid peroxidation, IL-6, IL-8, MCP-1, and TNF-alpha secretion was inhibited by curcumin in cultured monocytes. In the rat model, diabetes caused a significant increase in blood levels of IL-6, MCP-1, TNF-alpha, glucose, HbA(1), and oxidative stress, which was significantly decreased in curcumin-supplemented rats. Thus, curcumin can decrease markers of vascular inflammation and oxidative stress levels in both a cell-culture model and in the blood of diabetic rats. This suggests that curcumin supplementation can reduce glycemia and the risk of vascular inflammation in diabetes.
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PMID:Curcumin supplementation lowers TNF-alpha, IL-6, IL-8, and MCP-1 secretion in high glucose-treated cultured monocytes and blood levels of TNF-alpha, IL-6, MCP-1, glucose, and glycosylated hemoglobin in diabetic rats. 1897 14


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