Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P05231 (interleukin-6)
 23,907 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

These studies attempt to understand more fully the host response and pathogenesis associated with severe acute respiratory syndrome (SARS) coronavirus (SARS-CoV) by monitoring gene expression using formalin-fixed paraffin-embedded (FFPE) pulmonary autopsy tissues. These tissues were from patients in different hospitals in Singapore who were diagnosed with various microbial infections, including SARS-CoV, that caused acute respiratory distress syndrome (ARDS). Global expression patterns showed limited correlation between end-stage ARDS and the initiating pathogen, but when focusing on a subset of genes implicated in pulmonary pathogenesis, molecular signatures of pulmonary disease were obtained and appeared to be influenced by preexisting pulmonary complications and also bacterial components of infection. Many factors detected during pulmonary damage and repair, such as extracellular matrix (ECM) components, transforming growth factor (TGF) enhancers, acute-phase proteins, and antioxidants, were included in the molecular profiles of these ARDS lung tissues. In addition, differential expression of cytokines within these pulmonary tissues were observed, including notable genes involved in the interferon (IFN) pathway, such as Stat1, IFN regulatory factor-1 (IRF-1), interleukin-6 (IL-6), IL-8, and IL-18, that are often characterized as elevated in ARDS patients.
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PMID:SARS-CoV virus-host interactions and comparative etiologies of acute respiratory distress syndrome as determined by transcriptional and cytokine profiling of formalin-fixed paraffin-embedded tissues. 1668 59

This study was performed to investigate the relationships between markers of inflammation in serum (interleukin-6 [IL-6], interleukin-10 [IL-10], and granulocyte elastase [GE]), severity of injury, and clinical outcomes, and to evaluate the predictive value of these markers for major complications and mortality. This study, which was conducted between August 2003 and May 2005, examined patients older than 16 y who were admitted to the Emergency Unit of the Uludag University Medical School within 12 h after trauma, and who had traumatic hemorrhagic shock (THS) at admission. Three groups were established: the THS group (n=20), the pure hemorrhagic shock (PHS) group (n=20), and the healthy control group (n=20). Demographic data were recorded for all subjects, and blood samples were taken for lactate, base excess, GE, IL-6, and IL-10 measurements. The Glasgow Coma Score, the Revised Trauma Score, the Injury Severity Score, the New Injury Severity Score, and the Trauma Score-Injury Severity Score were calculated; complications and final clinical outcomes were monitored. A total of 35 men and 25 women were included in the study; mean patient age was 41+/-17 y. In the THS group, scores were as follows: Revised Trauma Score, 10.2+/-2.2; Trauma Score-Injury Severity Score, 0.86+/-0.2; Injury Severity Score, 24.8+/-9.0; and New Injury Severity Score, 32.7+/-9.0. IL-6, IL-10, lactate, and base excess levels in the THS group were significantly higher than those in the PHS and healthy control groups. The serum GE level of the THS group was significantly higher than that of the healthy control group, but it did not differ significantly from that of the PHS group. Complications such as sepsis, acute respiratory distress syndrome, and multiple organ failure occurred in 50% of the THS group and in 20% of the PHS group. Mortality was 30% in the THS group and 10% in the PHS group. In the THS group, no significant differences were noted between markers of inflammation and trauma scores of patients who died and those who survived. The investigators concluded that although the levels of markers of inflammation increased in THS patients, they were inadequate for predicting mortality and the development of complications such as acute respiratory distress syndrome, multiple organ failure, and sepsis. A larger study based on the use of serial marker measurements is warranted.
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PMID:Relationships between markers of inflammation, severity of injury, and clinical outcomes in hemorrhagic shock. 1802 20

Glucocorticoids are widely used in the treatment of different inflammatory diseases. The present study was performed to investigate the effect of dexamethasone (DEX) on acute respiratory distress syndrome (ARDS) induced by the H5N1 viral infection in mice. BALB/c mice, 6-8 weeks old, were divided into three groups with 80 mice in each. The infected group and the DEX-treated infected group were inoculated intranasally with 1 x 10(2) 50% mouse infectious dose of A/Chicken/Hebei/108/2002 (H5N1) viruses, with daily intraperitoneal injections of PBS, or 2.5 mg.kg(-1) DEX at days 3-14 post inoculation, respectively. The control group received noninfectious allantoic fluid and a daily intraperitoneal injection of PBS. In H5N1-infected mice, DEX treatment did not improve the mortality (17 out of 20 versus 16 out of 20 deaths in the DEX-treated infected group versus the infected group), and did not alleviate clinical signs, including weight loss, decreased food intake and inactivity. There was no significant amelioration of the hypoxaemia and ARDS-associated pathological changes in DEX-treated infected mice, as assessed by blood gas analysis and histological score. Furthermore, DEX therapy did not inhibit inflammatory cellular infiltration and cytokine release (interleukin-6 and tumour necrosis factor-alpha) in bronchoalveolar lavage fluid induced by the H5N1 infection. In conclusion, dexamethasone treatment (2.5 mg.kg(-1)) from days 3-14 post inoculation has no beneficial effect on acute respiratory distress syndrome caused by the H5N1 infection in mice.
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PMID:Effect of dexamethasone on acute respiratory distress syndrome induced by the H5N1 virus in mice. 1912 72

The effects of the combination of a 'lowest' lung ventilation with extracorporeal elimination of carbon dioxide by interventional lung assist are described in a patient presenting with severe acute respiratory distress syndrome due to fulminant pneumonia. Reducing tidal volume to 3 ml.kg(-1) together with interventional lung assist resulted in a decrease in severe hypercapnia without alveolar collapse or hypoxaemia but with a decrease in serum levels of interleukin-6. This approach was applied for 12 days with recovery of the patient, without complications. Extracorporeal removal of carbon dioxide by interventional lung assist may be a useful tool to enable 'ultraprotective' ventilation in severe acute respiratory distress syndrome.
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PMID:Pumpless extracorporeal removal of carbon dioxide combined with ventilation using low tidal volume and high positive end-expiratory pressure in a patient with severe acute respiratory distress syndrome. 1914 99

The treatment of severely traumatic patients was changing from total care treament to the damage control surgery, as a result in the inflammatory reaction caused by trauma, in which the inflammatory marks, such as interleukin-6 and serum procalcitonin in the blood increased, and caused hypothermia, acidosis, and disturbance of blood coagulation, and resulted in the acute respiratory distress syndrome and multiple organs failure. A long-term operation as the second hit made the disease worse. In the patients, the femoral fracture was treated with external fixator; the pelvic fracture was treated with external fixator, and the uncontrolled haemorrhage in the pelvis was treated through direct hemostasis, angiography and embolism of arteries, and the tamponade of pelvis; the purpose of treatment of spinal fracture was keeping the stability of spine, avoiding the secondary injury on the spinal cord. It must pay attention to the injury of the adjacent organs and infection in the opening spinal injury. The result of operation was better in the incomplete spinal cord injury.
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PMID:[Application of damage control theory on the trauma orthopaedic treatment]. 1970 36

Although current H5N1 highly pathogenic avian influenza viruses (HPAIV) are inefficiently transmitted to humans, infected individuals can suffer from severe disease, often progressing rapidly to acute respiratory distress syndrome and multiorgan failure. This is in contrast with the situation with human influenza viruses, which in immunocompetent individuals usually cause only a respiratory disease which is less aggressive than that observed with avian H5N1 viruses. While the biological basis of inefficient transmission is well documented, the mechanisms by which the H5N1 viruses cause fatal disease remain unclear. In the present study, we demonstrate that human pulmonary microvascular endothelial cells (hPMEC) had a clearly higher susceptibility to infection by H5N1 HPAIV than to infection by human influenza viruses. This was measurable by de novo intracellular nucleoprotein production and virus replication. It was also related to a relatively higher binding capacity to cellular receptors. After infection of hPMEC, cell activation markers E-selectin and P-selectin were upregulated, and the proinflammatory cytokines interleukin-6 and beta interferon were secreted. H5N1 virus infection was also associated with an elevated rate of cell death. Reverse genetics analyses demonstrated a major role for the viral hemagglutinin in this cell tropism. Overall, avian H5N1 viruses have a particular receptor specificity targeting endothelial cells that is different from human influenza viruses, and this H5N1 receptor specificity could contribute to disease pathogenesis.
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PMID:Hemagglutinin-dependent tropism of H5N1 avian influenza virus for human endothelial cells. 1981 46

H9N2 avian influenza viruses have repeatedly caused infections in swine and humans in some countries. The purpose of the present study was to evaluate the pulmonary pathology caused by H9N2 viral infection in mice. Six- to eight-week-old BALB/c mice were infected intranasally with 1 x 10(4) MID(50) of A/Chicken/Hebei/4/2008(H9N2) virus. Clinical signs, pathological changes and viral replication in lungs, arterial blood gas, and cytokines in bronchoalveolar lavage fluid (BALF) were observed at different time points after infection. A control group was infected intranasally with noninfectious allantoic fluid. H9N2-infected mice exhibited severe respiratory syndrome, with a mortality rate of 60%. Gross observations showed that infected lungs were highly edematous. Major histopathological changes in infected lungs included diffuse pneumonia and alveolar damage, with neutrophil-dominant inflammatory cellular infiltration, interstitial and alveolar edema, hemorrhage, and severe bronchiolitis/peribronchiolitis. In addition, H9N2 viral infection resulted in severe progressive hypoxemia, lymphopenia, and a significant increase in neutrophils, tumor necrosis factor-alpha and interleukin-6 in BALF. The features described above satisfy the criteria for acute respiratory distress syndrome (ARDS). Our data show that H9N2 viral infection resulted in ARDS in mice, and this may facilitate studies of the pathogenesis of future potential H9N2 disease in humans.
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PMID:Acute respiratory distress syndrome induced by H9N2 virus in mice. 1994 15

In an attempt to treat cancer patients with ERBB2 overexpressing tumors, we developed a chimeric antigen receptor (CAR) based on the widely used humanized monoclonal antibody (mAb) Trastuzumab (Herceptin). An optimized CAR vector containing CD28, 4-1BB, and CD3zeta signaling moieties was assembled in a gamma-retroviral vector and used to transduce autologous peripheral blood lymphocytes (PBLs) from a patient with colon cancer metastatic to the lungs and liver, refractory to multiple standard treatments. The gene transfer efficiency into autologous T cells was 79% CAR(+) in CD3(+) cells and these cells demonstrated high-specific reactivity in in vitro coculture assays. Following completion of nonmyeloablative conditioning, the patient received 10(10) cells intravenously. Within 15 minutes after cell infusion the patient experienced respiratory distress, and displayed a dramatic pulmonary infiltrate on chest X-ray. She was intubated and despite intensive medical intervention the patient died 5 days after treatment. Serum samples after cell infusion showed marked increases in interferon-gamma (IFN-gamma), granulocyte macrophage-colony stimulating factor (GM-CSF), tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and IL-10, consistent with a cytokine storm. We speculate that the large number of administered cells localized to the lung immediately following infusion and were triggered to release cytokine by the recognition of low levels of ERBB2 on lung epithelial cells.
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PMID:Case report of a serious adverse event following the administration of T cells transduced with a chimeric antigen receptor recognizing ERBB2. 2035 76

Elevated concentrations of interleukin-6 (IL-6), C-reactive protein (CRP), and matrix metalloproteinase-9 (MMP-9) in fetal and neonatal compartments have been associated with an increased risk for preterm birth (PTB) and/or neonatal morbidity. The purpose of this study was to determine if the maternal serum concentration of IL-6, CRP, and MMP-9 in women at risk for PTB, who are not in labor and have intact membranes, are associated with an increased risk for PTB <32 weeks and/or neonatal morbidity. Maternal serum samples collected from 475 patients enrolled in a multicenter randomized controlled trial of single versus weekly corticosteroids for women at increased risk for preterm delivery were assayed. Serum was collected at randomization (24 to 32 weeks' gestation). Maternal serum concentrations of IL-6, CRP, and MMP-9 were subsequently determined using enzyme-linked immunoassays. Multivariate logistic regression analysis was performed to explore the relationship between maternal serum concentrations of IL-6, CRP, and MMP-9 and PTB <32 weeks, respiratory distress syndrome (RDS), chronic lung disease (CLD), intraventricular hemorrhage (IVH), necrotizing enterocolitis (NEC), and any sepsis. Maternal serum concentrations of IL-6 and CRP, but not MMP-9, above the 90th percentile at the time of randomization were associated with PTB <32 weeks. In contrast, there was no significant relationship between RDS and NEC and the maternal serum concentration of IL-6, CRP, or MMP-9 (univariate analysis). The development of CLD was associated with a high (above 90th percentile) IL-6 and CRP in maternal serum, even after adjustment for gestational age (GA) at randomization and treatment group. However, when GA at delivery was added to the model, this finding was nonsignificant. Neonatal sepsis was more frequent in neonates born to mothers with a high maternal serum concentration of CRP (>90th percentile). However, there was no significant association after adjustment for GA at randomization and treatment group. Logistic regression analysis for each analyte indicated that high maternal serum concentrations of IL-6 and CRP, but not MMP-9, were associated with an increased risk of IVH (odds ratio [OR] 4.60, 95% confidence interval [CI] 1.86 to 10.68; OR 4.07, 95% CI 1.63 to 9.50) after adjusting for GA at randomization and treatment group. Most babies (25/30) had grade I IVH. When GA at delivery was included, elevated IL-6 remained significantly associated with IVH (OR 2.77, 95% CI 1.02 to 7.09). An elevated maternal serum concentration of IL-6 and CRP are risk factors for PTB <32 weeks and subsequent development of neonatal IVH. An elevated maternal serum IL-6 appears to confer additional risk for IVH even after adjusting for GA at delivery.
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PMID:Maternal serum interleukin-6, C-reactive protein, and matrix metalloproteinase-9 concentrations as risk factors for preterm birth <32 weeks and adverse neonatal outcomes. 2019 52

Clinical and laboratory evidence suggests that alcohol consumption dysregulates immune function. Burn patients who consume alcohol before their injuries demonstrate higher rates of morbidity and mortality, including acute respiratory distress syndrome, than patients without alcohol at the time of injury. Our laboratory observed higher levels of proinflammatory cytokines and leukocyte infiltration in the lungs of mice after ethanol exposure and burn injury than with either insult alone. To understand the mechanism of the increased pulmonary inflammatory response in mice treated with ethanol and burn injury, we investigated the role of intercellular adhesion molecule (ICAM)-1. Wild-type and ICAM-1 knockout (KO) mice were treated with vehicle or ethanol and subsequently given a sham or burn injury. Twenty-four hours postinjury, lungs were harvested and analyzed for indices of inflammation. Higher numbers of neutrophils were observed in the lungs of wild-type mice after burn and burn with ethanol treatment. This increase in pulmonary inflammatory cell accumulation was significantly lower in the KO mice. In addition, levels of KC, interleukin-1beta, and interleukin-6 in the lung were decreased in the ICAM-1 KO mice after ethanol exposure and burn injury. Interestingly, no differences were observed in serum or lung tissue content of soluble ICAM-1 24 hours postinjury. These data suggest that upregulation of adhesion molecules such as ICAM-1 on the vascular endothelium may play a critical role in the excessive inflammation seen after ethanol exposure and burn injury.
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PMID:Decreased pulmonary inflammation after ethanol exposure and burn injury in intercellular adhesion molecule-1 knockout mice. 2061 55


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