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)

An 88-year-old woman was admitted with generalized lymphadenopathy, anemia, and thrombocytopenia. On admission, a peripheral blood examination showed a red blood cell count of 146 x 10(6)/microliter, a hemoglobin concentration of 6.9 g/dl, and a platelet count of 5.0 x 10(4)/microliter. Blood examination detected polyclonal hypergammaglobulinemia; the results of the direct/indirect Coombs' test were positive; and an elevated cold agglutinin titer and high platelet associated IgG (PA-IgG) level indicated the existence of autoantibodies. Serum cytokine measurements disclosed an elevated level of interleukin-6 (IL-6). Immunoblastic lymphadenopathy-like T cell lymphoma was diagnosed on the basis of lymph node biopsy specimens. VP-16 and steroid therapy alleviated the patient's lymphadenopathy, anemia, thrombocytopenia, and hypergammaglobulinemia. These findings suggest that tumor cells with a T cell phenotype produced IL-6 in large quantities, thus provoking B-cell and plasmacytic histologic changes and humoral disease manifestations, including hypergammaglobulinemia.
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PMID:[Immunoblastic lymphadenopathy-like T cell lymphoma with high levels of serum interleukin-6, cold agglutinin disease, and immune thrombocytopenia]. 986 23

The aim of this study was to see if a short-term period of exposure to cold in young healthy subjects causes changes in hematological factors known to be associated with the promotion of thrombogenesis. Over a period of 48 hours, changes in the distribution of erythrocytes, granulocytes, and blood platelets, as well as several coagulation, inflammatory, and fibrinolytic parameters, were monitored in 11 young healthy male subjects following a short period (1 hour) of cold exposure (CE) (ambient temperature, 11 degrees C) or exposure to thermoneutral conditions (ambient temperature, 26 degrees C) in winter (November). The major findings were: (1) a CE-induced hemoconcentration as indicated by an increase in erythrocyte count (3.2% increase); (2) after appropriate adjustments for changes in hemoconcentration, a cold-induced mobilization of granulocytes (14.5% increase) and a cold-induced decrease in lymphocytes (7% decrease); (3) thromboxane B2 release following endotoxin stimulation of whole blood was increased by 27.4% in the CE experiments; (4) diurnal rhythms were observed in granulocytes, blood platelets, middle plate volume, tissue plasminogen activator, and plasma activator inhibitor; and (5) CE caused no significant changes in lipopolysaccharide-induced tissue factor, nor in the blood coagulation factor VII or cytokines, interleukin-6, and tumor necrosis factor. It is concluded that short-term cold exposure in young healthy subjects initiates a mild inflammatory reaction and a tendency for an increased state of hypercoagulability.
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PMID:The effect of short-term cold exposure on risk factors for cardiovascular disease. 1041 98

This study examined the immunological responses to cold exposure together with the effects of pretreatment with either passive heating or exercise (with and without a thermal clamp). On four separate occasions, seven healthy men [mean age 24.0 +/- 1.9 (SE) yr, peak oxygen consumption = 45.7 +/- 2.0 ml. kg(-1). min(-1)] sat for 2 h in a climatic chamber maintained at 5 degrees C. Before exposure, subjects participated in one of four pretreatment conditions. For the thermoneutral control condition, subjects remained seated for 1 h in a water bath at 35 degrees C. In another pretreatment, subjects were passively heated in a warm (38 degrees C) water bath for 1 h. In two other pretreatments, subjects exercised for 1 h at 55% peak oxygen consumption (once immersed in 18 degrees C water and once in 35 degrees C water). Core temperature rose by 1 degrees C during passive heating and during exercise in 35 degrees C water and remained stable during exercise in 18 degrees C water (thermal clamping). Subsequent cold exposure induced a leukocytosis and granulocytosis, an increase in natural killer cell count and activity, and a rise in circulating levels of interleukin-6. Pretreatment with exercise in 18 degrees C water augmented the leukocyte, granulocyte, and monocyte response. These results indicate that acute cold exposure has immunostimulating effects and that, with thermal clamping, pretreatment with physical exercise can enhance this response. Increases in levels of circulating norepinephrine may account for the changes observed during cold exposure and their modification by changes in initial status.
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PMID:Immune changes in humans during cold exposure: effects of prior heating and exercise. 1044 30

Rhinoviruses are the major cause of the common cold and a trigger of acute asthma exacerbations. Whether these exacerbations result from direct infection of the lower airway or from indirect mechanisms consequent on infection of the upper airway alone is currently unknown. Lower respiratory infection was investigated in vitro by exposing primary human bronchial epithelial cells to rhinoviruses and in vivo after experimental upper respiratory infection of human volunteers. Bronchial infection was confirmed by both approaches. Furthermore, rhinoviruses induced production of interleukin-6, -8, and -16 and RANTES and were cytotoxic to cultured respiratory epithelium. This evidence strongly supports a direct lower respiratory epithelial reaction as the initial event in the induction of rhinovirus-mediated asthma exacerbations. The frequency of infection and the nature of the inflammatory response observed are similar to those of the upper respiratory tract, suggesting that rhinovirus infections may be one of the most important causes of lower in addition to upper respiratory disease.
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PMID:Rhinoviruses infect the lower airways. 1083 65

Common colds are associated with exacerbations of chronic obstructive pulmonary disease (COPD). However, the role of the common cold virus (human rhinovirus) in the production of symptoms and lower airway inflammation at COPD exacerbation is unknown. Thirty three patients with moderate-to-severe COPD were seen at baseline, when the number of chest infections in the previous year was noted, and acutely at COPD exacerbation. Within 48 h after the onset of the exacerbation and at baseline, nasal aspirates and induced sputum were taken for rhinovirus reverse transcriptase polymerase chain reaction (RT-PCR) analysis and determination of cytokine levels. Symptoms, recorded on diary cards, were noted and forced expiratory volume in one second (FEV1) and forced vital capacity (FVC) measured. At exacerbation, mean FEV1 and FVC fell significantly from baseline (p<0.001). Ten of 43 exacerbations were associated with rhinovirus infection, detected in induced sputum. In four of these, nasopharyngeal samples contained no detectable rhinovirus. All baseline samples were negative for rhinovirus. The simultaneous presence of increased nasal discharge/nasal congestion (in 26 of the 43 exacerbations) and increased sputum (29 exacerbations) was strongly associated with the presence of rhinovirus (odds ratio 6.15; p=0.036). Total symptom scores were greater for rhinovirus as compared to nonrhinovirus exacerbations (p=0.039). Median baseline sputum interleukin-6 levels rose from 90.2 to 140.3 pg x mL(-1) at exacerbation (p=0.005); the change was greater in the presence of rhinovirus infection (p=0.008). Rhinovirus infection can be detected at chronic obstructive pulmonary disease exacerbation. This is associated with elevation of lower airway interleukin-6 levels, which may mediate lower airway symptom expression during chronic obstructive pulmonary disease exacerbations.
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PMID:Detection of rhinovirus in induced sputum at exacerbation of chronic obstructive pulmonary disease. 1110 12

The effects of respiratory viral infection on the time course of chronic obstructive pulmonary disease (COPD) exacerbation were examined by monitoring changes in systemic inflammatory markers in stable COPD and at exacerbation. Eighty-three patients with COPD (mean [SD] age, 66.6 [7.1] yr, FEV(1), 1.06 [0.61] L) recorded daily peak expiratory flow rate and any increases in respiratory symptoms. Nasal samples and blood were taken for respiratory virus detection by culture, polymerase chain reaction, and serology, and plasma fibrinogen and serum interleukin-6 (IL-6) were determined at stable baseline and exacerbation. Sixty-four percent of exacerbations were associated with a cold occurring up to 18 d before exacerbation. Seventy-seven viruses (39 [58.2%] rhinoviruses) were detected in 66 (39.2%) of 168 COPD exacerbations in 53 (64%) patients. Viral exacerbations were associated with frequent exacerbators, colds with increased dyspnea, a higher total symptom count at presentation, a longer median symptom recovery period of 13 d, and a tendency toward higher plasma fibrinogen and serum IL-6 levels. Non-respiratory syncytial virus (RSV) respiratory viruses were detected in 11 (16%), and RSV in 16 (23.5%), of 68 stable COPD patients, with RSV detection associated with higher inflammatory marker levels. Respiratory virus infections are associated with more severe and frequent exacerbations, and may cause chronic infection in COPD. Prevention and early treatment of viral infections may lead to a decreased exacerbation frequency and morbidity associated with COPD.
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PMID:Respiratory viruses, symptoms, and inflammatory markers in acute exacerbations and stable chronic obstructive pulmonary disease. 1171 91

Some patients with COPD are prone to frequent exacerbations, which are an important determinant of health status. Such patients have elevated airway cytokine levels, suggesting the presence of increased inflammation that may increase their susceptibility to exacerbation. The inflammatory response during a COPD exacerbation is variable, but increases in interleukin-6 levels during the exacerbation are related to the presence of a common cold. Rhinovirus infection is the most important etiologic factor in COPD exacerbations and is an important target for preventive therapy. The reduction of COPD exacerbations will have an important impact on the considerable morbidity and mortality associated with COPD.
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PMID:Exacerbations: etiology and pathophysiologic mechanisms. 1201 Aug 42

Heat shock proteins (HSPs) are necessary in the synthesis, degradation, folding, transport, and translocation of different proteins. It is well known that the increased expression of HSPs may have a protective effect against cerulein-induced pancreatitis in rats or against choline-deficient ethionine-supplemented diet model pancreatitis in mice. The aim of this study was to investigate the potential effects of HSP preinduction by cold or hot water immersion on trypsin-induced acute pancreatitis in rats. Trypsin was injected into the interlobular tissue of the duodenal part of the pancreas at the peak level of HSP synthesis, as determined by Western blot analysis. The rats were sacrificed by exsanguination through the abdominal aorta 6 h after the trypsin injection. The serum amylase activity, the tumor necrosis factor-alpha, interleukin-1, and interleukin-6 levels, the pancreatic weight/body weight ratio, and the pancreatic contents of DNA, protein, amylase, lipase, and trypsinogen were measured. A biopsy for histology was taken. Hot water immersion significantly elevated the HSP72 expression, while cold water immersion significantly increased the HSP60 expression. Cold water immersion pretreatment ameliorated the pancreatic edema in trypsin-induced pancreatitis, however this was not due to the HSP60. Hot water immersion pretreatment did not have any effect on the measured parameters in trypsin-induced pancreatitis. The findings suggest that the induction of HSP60 or HSP72 are not enough to protect rats against the early phase of this localized necrohemorrhagic pancreatitis model.
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PMID:Induction of heat shock proteins fails to produce protection against trypsin-induced acute pancreatitis in rats. 1214 32

Forty barrows (TR4 x C22) were weaned at 17 d of age (BW = 6.27 +/- 0.30 kg), housed (two pigs/pen) in a thermal-neutral environment (TN; constant 26.7 degrees C), and fed diets with or without 7% (as-fed basis) spray-dried plasma (SDP). On d 7, one pig/ pen was moved into a cold environment (CE; constant 15.6 degrees C). Pigs were fitted with jugular catheters on d 11. On d 12, 16 pigs per environment (eight pigs per dietary treatment) were challenged i.v. with 75 microg of lipopolysaccharide (LPS)/kg of BW. Blood samples were collected over a 4.5-h period. Pigs were then killed and tissue samples were harvested for messenger RNA (mRNA) analysis. From d 0 to 7, pigs fed SDP diets had a lower gain:feed ratio (G/F) than pigs fed no SDP (533 +/- 14 vs. 585 +/- 17 g/kg; P < 0.03). Pigs housed in the CE consumed more feed and had a lower G/F than pigs housed in TN from d 7 to 11 (P < 0.001). There were no environment x diet interactions from d 7 to 11 (P > 0.78). Baseline concentrations of serum ACTH and cortisol were lower in the TN pigs than in the CE pigs (P < 0.001). Pigs fed diets without SDP had lower serum cortisol concentrations over the 4.5-h period than pigs fed SDP (time x diet, P < 0.001). Serum concentrations of tumor necrosis factor-alpha (TNF-alpha) were highest for pigs consuming SDP in the CE, whereas there were no differences among the other treatments (time x diet x environment, P < 0.02). Pigs housed in the CE had higher serum interleukin-1beta (IL-1beta) (P < 0.001) and interleukin-6 (IL-6; P < 0.001) than TN pigs. Pigs fed SDP also had slightly higher serum IL-1beta concentrations (P < 0.10) and higher (P < 0.001) IL-6 concentrations than pigs fed no SDP. Pigs fed SDP had 9% lower liver and 13% lower thymus mRNA expression of tumor necrosis factor-alpha (TNF-alpha) than pigs that consumed no SDP (P < 0.06). Liver IL-1beta, IL-6, and LPS-binding protein mRNA were higher in the CE than in the TN (P < 0.03, P < 0.001, and P < 0.05; respectively). In addition, spleen TNF-alpha (P < 0.03) and IL-6 (P < 0.01) mRNA levels were higher in the CE than in the TN. Pigs consuming SDP and challenged with LPS responded with elevated serum concentrations of cortisol and cytokines compared with pigs fed diets with no SDP. Housing pigs in a CE increased the baseline concentrations of ACTH and cortisol, and when coupled with an LPS challenge, resulted in elevated serum and tissue mRNA levels of cytokines. Cold stress and feeding SDP during a LPS challenge may result in increased stress and immune responses in young pigs.
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PMID:The effects of thermal environment and spray-dried plasma on the acute-phase response of pigs challenged with lipopolysaccharide. 1277 43

Carbon monoxide (CO), a byproduct of heme catalysis by heme oxygenases, has been shown to exert anti-inflammatory effects. This study examines the cytoprotective efficacy of inhaled CO during intestinal cold ischemia/reperfusion injury associated with small intestinal transplantation. Orthotopic syngenic intestinal transplantation was performed in Lewis rats after 6 hours of cold preservation in University of Wisconsin solution. Three groups were examined: normal untreated controls, control intestinal transplant recipients kept in room air, and recipients exposed to CO (250 ppm) for 1 hour before and 24 hours after surgery. In air grafts, mRNA levels for interleukin-6, cyclooxygenase-2, intracellular adhesion molecule (ICAM-1), and inducible nitric oxide synthase rapidly increased after intestinal transplant. Histopathological analysis revealed severe mucosal erosion, villous congestion, and inflammatory infiltrates. CO effectively blocked an early up-regulation of these mediators, showed less severe histopathological changes, and resulted in significantly improved animal survival of 92% from 58% in air-treated controls. CO also significantly reduced mRNA for proapoptotic Bax, while it up-regulated anti-apoptotic Bcl-2. These changes in CO-treated grafts correlated with well-preserved CD31(+) vascular endothelial cells, less frequent apoptosis/necrosis in intestinal epithelial and capillary endothelial cells, and improved graft tissue blood circulation. Protective effects of CO in this study were mediated via soluble guanylyl cyclase, because 1H-(1,2,4)oxadiazole (4,3-alpha) quinoxaline-1-one (soluble guanylyl cyclase inhibitor) completely reversed the beneficial effect conferred by CO. Perioperative CO inhalation at a low concentration resulted in protection against ischemia/reperfusion injury to intestinal grafts with prolonged cold preservation.
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PMID:Carbon monoxide inhalation protects rat intestinal grafts from ischemia/reperfusion injury. 1450 65


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