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)

Fifty-seven patients with amyotrophic lateral sclerosis (ALS) were randomly assigned to receive 0.5, 1, 3, 7, 10, or 30 micrograms/kg recombinant human ciliary neurotrophic factor (rHCNTF) or placebo subcutaneously 3 times a week for 2 weeks. Dose-limiting toxicity, consisting of febrile reactions in some patients, fatigue, and nonproductive cough, was observed at a dose level of 30 micrograms/kg. Dose-related changes in parameters of the acute-phase response were noted, consistent with the relationship of CNTF and its receptor system to the cytokine interleukin-6 (IL-6) and its receptor. No adverse neurologic consequences of rHCNTF administration were observed. Antibodies to rHCNTF were observed in sera of most patients tested after 2 weeks of continuous treatment and 4 weeks' withdrawal period. rHCNTF was safe and tolerated within acceptable limits when administered to patients with ALS in this study at doses of up to 30 micrograms/kg 3 times a week for 2 weeks. Further studies to explore the efficacy of rHCNTF in the treatment of human motor neuron diseases are justified.
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PMID:A phase I study of recombinant human ciliary neurotrophic factor (rHCNTF) in patients with amyotrophic lateral sclerosis. The ALS CNTF Treatment Study (ACTS) Phase I-II Study Group. 868 12

Inhalation of O3 causes airways neutrophilic inflammation accompanied by other changes including increased levels of cyclo-oxygenase products of arachidonic acid in bronchoalveolar lavage fluid (BALF). Ozone O3 exposure also causes decreased forced vital capacity (FVC) and forced expiratory volume after 1 s (FEV(1)), associated with cough and substernal pain on inspiration, and small increases in specific airway resistance (SRAW). The spirometric decrements are substantially blunted by pretreatment with indomethacin. Since the O3-induced decrement in FVC is due to involuntary inhibition of inspiration, a role for stimulation of nociceptive respiratory tract afferents has been suggested and cyclo-oxygenase products have been hypothesized to mediate this stimulation. However, the relation (if any) between the O3-induced neutrophilic airways inflammation and decreased inspiratory capacity remains unclear. We studied the effects of pharmacologic inhibition of O3-induced spirometric changes on the inflammatory changes. Each of ten healthy men was exposed twice (5-week interval) to 0.4 ppm O3 for 2 h, including 1 h of intermittent exercise (ventilation 601*min(-1)). One-and-a-half hours prior to and midway during each exposure the subject ingested 800 mg and 200 mg, respectively, of the non-steroidal anti-inflammatory drug ibuprofen (IBU), or placebo [PLA (sucrose)], in randomized, double-blind fashion. Spirometry and body plethysmography were performed prior to drug administration, and before and after O3 exposure. Immediately following postexposure testing, fiberoptic bronchoscopy with bronchoalveolar lavage (BAL) was performed. Neither IBU nor PLA administration changed pre-exposure lung function. O3 exposure (with PLA) caused a significant 17 percent mean decrement in FEV(1) (P <0.01) and a 56 percent increase in mean SRAW. Following IBU pretreatment, O3 exposure induced a significantly lesser mean decrement in FEV(1) (7 percent) but still a 50 percent increase in mean SRAW. IBU pretreatment significantly decreased post-O3 BAL levels of prostaglandin E2 (PGE2) by 60.4 percent (P <0.05) and thromboxane B(2) (TxB(2)) by 25.5 percent (P <0.05). Of the proteins, only interleukin-6 was significantly reduced (45 percent, P <0.05) by IBU as compared to PLA pretreatment. As expected, O3 exposure produced neutrophilia in BALF. There was, however, no effect of IBU on this finding. None of the major cell types in the BALF differed significantly between pretreatments. We found no association between post-exposure changes of BALF components and pulmonary function decrements. We conclude that IBU causes significant inhibition of O3-induced increases in respiratory tract PGE(2) and TxB(2) levels concomitant with a blunting of the spirometric response. This is consistent with the hypothesis that the products of AA metabolism mediate inhibition of inspiration. However, IBU did not alter the modest SRAW response to O3.
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PMID:Effects of cyclo-oxygenase inhibition on ozone-induced respiratory inflammation and lung function changes. 886 65

A 67-year-old man and a 70-year-old man were admitted to our hospital because of dyspnea and dry coughing. Chest X-ray films showed bilateral reticulonodular shadows in the middle and lower lung fields. Specimens were obtained by open lung biopsies and the findings were compatible with those of usual interstitial pneumonia. Immunoelectrophoresis revealed monoclonal gammopathy in both patients. The levels of interleukin 6 in bronchoalveolar lavage fluid were high. In these two patients, idiopathic pulmonary fibrosis was associated with multiple myeloma and monoclonal gammopathy, and the levels of interleukin-6 in bronchoalveolar lavage fluid were high. These findings may help to elucidate the pathogenesis and development of idiopathic pulmonary fibrosis.
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PMID:[Two patients with idiopathic pulmonary fibrosis and monoclonal gammopathy]. 897 78

A 31-y-old black man with neurofibromatosis, alcoholism and hypertension was admitted because of abdominal pain, hematemesis and cough. In the hospital he had prolonged fever and developed a multiorgan crisis. Despite thorough investigation, no infectious cause for fever was found. Urinary catecholamines and metabolites were markedly elevated. Computerized tomography revealed a mass abutting the left kidney. A diagnosis of pheochromocytoma was made, and as soon as treatment with phenoxybenzamine and propranolol was begun, the fever resolved. Serum interleukin-6 (IL-6) concentration was initially elevated, decreased after the start of adrenergic blockade, and gradually fell to an undetectable level after surgery. These observations suggest that interleukin-6 might have been causally related to the patient's fever and possibly the multiorgan crisis.
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PMID:Interleukin-6 in the fever and multiorgan crisis of pheochromocytoma. 957 53

Epidemiological data indicate that living or working in a moldy building is associated with increased risk of respiratory symptoms and disease related to inflammatory reactions, but biochemical evidence linking cause and effect is still scarce. The staff working in a mold-contaminated school, and a reference group without such exposure, were studied. Nasal lavage was performed and health data were collected with a questionnaire at the end of the spring term, after a 2.5-mo summer vacation, and at the end of the fall term. Here we show that concentrations of tumor necrosis factor alpha (TNF-alpha), interleukin-6 (IL-6), and nitric oxide (NO) in nasal lavage fluid were significantly higher in the exposed than in the control subjects at the end of the first exposure period. These inflammatory mediators decreased to reference group concentrations during the period when there was no exposure and the production of NO and IL-6 increased again during the reexposure in the fall term. Reports of cough, phlegm, rhinitis, eye irritation, and fatigue paralleled the changes in the measured inflammatory markers. These results point to an association between inflammatory markers in the nasal lavage fluid, the high prevalence of respiratory symptoms among the occupants, and chronic exposure to molds in the indoor environment.
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PMID:Nitric oxide and proinflammatory cytokines in nasal lavage fluid associated with symptoms and exposure to moldy building microbes. 1058 10

A 51-year-old male who had been working as a building wrecker for 20 years, was admitted to our hospital in June 1999 for proteinuria and hematuria examination. He started this work in 1978. Twelve years later, severe coughing and bloody sputum began and he was diagnosed as having silicosis in 1995. Urinalysis on admission showed proteinuria(294 mg/day), microhematuria(20-30/hpf), RBC cast and granular cast. High serum IgA(770 mg/dl) and high serum interleukin-6(IL-6) (3,280 pg/dl) were found. A renal biopsy showed mild mesangial matrix expansion and mesangial cell proliferation with IgA deposition, which was diagnosed as IgA nephropathy. Chest X-rays showed multiple small nodular lesions on both lung fields indicating silicosis. In Nov. 1999, he resigned from his job as a building wrecker because of increasing coughing and bloody sputum associated with body weight loss. Within 3 months after stopping this work, coughing and bloody sputum disappeared and the abnormal urinalysis findings returned to normal. Serum IgA and serum IL-6 data improved to 462 mg/dl and 2.5 pg/dl, respectively. It is suggested that silicon exposure might be related to the pathogenesis of IgA nephropathy in this patient.
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PMID:[A case of IgA nephropathy associated with silicosis]. 1172 60

In a man aged 34 who had been experiencing frequent coughing since November 2001, a chest radiograph showed infiltration shadows in both lung fields. Chest CT showed diffuse centrilobular nodules and multiple mediastinal lymphadenopathy. Laboratory examination revealed high values for C-reactive protein and the erythrocyte sedimentation rate, together with polyclonal hyperimmunoglobulinemia and an elevated interleukin-6 level. We suspected multicentric Castleman's disease, and so performed thoracoscopic mediastinal lymph node biopsy and lung biopsy. The former disclosed follicular hyperplasia and plasma cell infiltration in the interfollicular area, suggesting a diagnosis of Castleman's disease, plasma cell type. The lung biopsy showed heavy infiltration of plasma cells. The diagnosis was therefore multicentric Castleman's disease (MCD) with pulmonary involvement. The chest CT findings were tpical characteristics of pulmonary involvement in patients with MCD.
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PMID:[A case of multicentric Castleman's disease with pulmonary involvement]. 1269 8

Dextromethorphan (DM) is a dextrorotatory morphinan and an over-the-counter non-opioid cough suppressant. We have previously shown that DM protects against LPS-induced dopaminergic neurodegeneration through inhibition of microglia activation. Here, we investigated protective effects of DM against endotoxin shock induced by lipopolysaccharide/d-galactosamine (LPS/GalN) in mice and the mechanism underlying its protective effect. Mice were given multiple injections of DM (12.5 mg/kg, s.c.) 30 min before and 2, 4 h after an injection of LPS/GalN (20 microg/700 mg/kg). DM administration decreased LPS/GalN-induced mortality and hepatotoxicity, as evidenced by increased survival rate, decreased serum alanine aminotransferase activity and improved pathology. Furthermore, DM was also effective when it was given 30 min after LPS/GalN injection. The protection was likely associated with reduced serum and liver tumor necrosis factor alpha (TNF-alpha) levels. DM also attenuated production of superoxide and intracellular reactive oxygen species in Kupffer cells and neutrophils. Real-time RT-PCR analysis revealed that DM administration suppressed the expression of a variety of inflammation-related genes such as macrophage inflammatory protein-2, CXC chemokine, thrombospondin-1, intercellular adhesion molecular-1 and interleukin-6. DM also decreased the expression of genes related to cell-death pathways, such as the DNA damage protein genes GADD45 and GADD153. In summary, DM is effective in protecting mice against LPS/GalN-induced hepatotoxicity, and the mechanism is likely through a faster TNF-alpha clearance, and decrease of superoxide production and inflammation and cell-death related components. This study not only extends neuroprotective effect of DM, but also suggests that DM may be a novel compound for the therapeutic intervention for sepsis.
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PMID:Protective effect of dextromethorphan against endotoxic shock in mice. 1562 75

Virus-associated hemophagocytic syndrome (VAHS) triggered by HHV-8 is extremely rare and has been reported only in 9 immunocompromised patients. We report the first case of HHV-8-associated VAHS in an HIV-negative, immunocompetent patient with plasmablastic variant (plasmablastic microlymphoma) of multicentric Castleman disease (MCD). This 61-year-old man presented with fever, cough, and bilateral inguinal lymphadenopathy. Biopsy of the right inguinal lymph node revealed plasmablastic MCD with nodular aggregates of plasmablasts expressing IgM, MUM1, HHV-8 latency-associated nuclear antigen, and viral interleukin-6. These plasmablasts were monotypic for Iglambda light chain expression but not Igkappa. All the B-cell clonality assays, including IgH-FR2, IgH-FR3, DH-JH, Igkappa, and Iglambda PCR, showed a polyclonal pattern. His serum human interleukin-6 level was markedly elevated and was negative for EBV acute infection/reactivation. The marrow aspirate showed florid hemophagocytosis. His disease progressed rapidly to multisystemic illness, and he died of acute respiratory failure in 1 month. Our case showed that HHV-8 might trigger VAHS in an immunocompetent patient with plasmablastic MCD. We speculated that our patient developed VAHS under the cytokine storm associated with the proliferating HHV-8-infected plasmablasts, similar to the EBV-triggered VAHS in patients with EBV-associated T-cell lymphoma.
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PMID:Fatal HHV-8-associated hemophagocytic syndrome in an HIV-negative immunocompetent patient with plasmablastic variant of multicentric Castleman disease (plasmablastic microlymphoma). 1633 Sep 52

A 47-year-old man with pulmonary hyalinizing granuloma is herein presented. The patient, whose chief complaint was a mild cough, was found by chest radiograph to have multiple bilateral nodules. Subsequent high-resolution computed tomography demonstrated multiple slightly irregular nodules, perinodular ground-glass opacity, peribronchovascular interstitial thickening, and cysts. A mild enlargement of systemic lymph nodes was also noted. Laboratory tests disclosed a slight elevation in the C-reactive protein, gamma-globulin, interleukin-6, and soluble interleukin-2 receptor levels. A histopathologic examination of the specimen yielded from a thoracoscopic lung biopsy resulted in a definite diagnosis of pulmonary hyalinizing granuloma.
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PMID:High-resolution CT findings in pulmonary hyalinizing granuloma. 1804 99


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