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)

Rhinovirus infection results in increased release of inflammatory mediators from airway epithelial cells in asthma. As an antioxidant, lycopene offers protection from adverse effects of inflammation. The aim of this study was to find an appropriate method of lycopene enrichment of airway epithelial cells and to determine the effects of lycopene enrichment on the inflammatory response of cells infected by rhinovirus or exposed to lipopolysaccharide. Lycopene enrichment of airway epithelial cells using solubilisation in tetrahydrofuran versus incorporation in liposomes was compared. After determining that solubilisation of lycopene in tetrahydrofuran was the most suitable method of lycopene supplementation, airway epithelial cells (Calu-3) were incubated with lycopene (dissolved in tetrahydrofuran) for 24 h, followed by rhinovirus infection or lipopolysaccharide exposure for 48 h. The release of interleukin-6, interleukin-8 and interferon-gamma induced protein-10 (IP-10) and their messenger RNA levels were measured using enzyme linked immunosorbent assay and reverse transcription polymerase chain reaction, respectively. Viral replication was measured by tissue culture infective dose of 50% assay. Lycopene concentration of cells and media were analysed using high-performance liquid chromatography. Preincubation of airway epithelial cells with lycopene (dissolved in tetrahydrofuran) delivered lycopene into the cells and resulted in a 24% reduction in interleukin-6 after rhinovirus-1B infection, 31% reduction in IP-10 after rhinovirus-43 infection and 85% reduction in rhinovirus-1B replication. Lycopene also decreased the release of IL-6 and IP-10 following exposure to lipopolysaccharide. We conclude that lycopene has a potential role in suppressing rhinovirus induced airway inflammation.
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PMID:Lycopene enrichment of cultured airway epithelial cells decreases the inflammation induced by rhinovirus infection and lipopolysaccharide. 1882 41

Obesity has been associated with an increased prevalence of asthma and poorer control of this disease. However, the mechanisms by which obesity can influence airway function and make asthma more difficult to control remain uncertain. The physiological changes associated with obesity can contribute to respiratory symptoms and these should be differentiated from those caused by asthma. Obesity can possibly influence the development of asthma through genetic, developmental, hormonal, neurogenic or mechanical influences. Breathing at low lung volumes and changes in the pattern of breathing in obese subjects may alter airway smooth muscle plasticity and airway function. The release by adipocytes of various cytokines and mediators such as Interleukin-6, TNF-alpha, eotaxin, and leptin, and the reduction of anti-inflammatory adipokines in obese subjects may possibly contribute to the development or increased clinical expression of asthma in promoting airway inflammation. Reduced asthma control and impaired response to asthma therapy have been reported in obese patients. Obesity-related co-morbidities such as Sleep Apnea and Gastro-esophageal reflux may also contribute to this poor control. Weight loss improves asthma control and reduces medication needs. Research is needed to better define the optimal management of obese asthmatic patients.
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PMID:Influence of obesity on the prevalence and clinical features of asthma. 1903 10

In the last few decades, the prevalence of allergic diseases, asthma, allergic rhinoconjunctivitis and atopic dermatitis in particular, has been observed to increase in urban settings. In addition, epidemiological data show the proportion of overweight individuals to rise in the last two decades. Obesity and overweight are a major public health problem not only in industrialized countries but also in developing ones because the morbidity and mortality rates are greater in the obese. An increased body mass index is considered a risk factor for the occurrence of myocardial infarction, stroke, atherosclerosis, hypertension, insulin resistance, dyslipidemia and some types of carcinoma. An ever greater body of available data point to the possible association of allergic diseases with obesity and overweight. Impaired immune tolerance is considered to be a sequel of immune changes due to the activity of adipokines, bioactive molecules secreted in white adipose tissue. About 50 adipokines are currently known to be secreted in adipose tissue, some of them belonging to the group of cytokines such as tumor necrosis factor alpha and interleukin-6. The association between obesity and allergic diseases has not yet been fully clarified. While the observations recorded to date should not be neglected, additional studies are necessary to help understand the complex function of adipokines involved in allergic events.
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PMID:Obesity and allergic diseases. 1911 Nov 50

A 68-year-old woman with a 4 year history of bronchial asthma developed marked myalgia in the extremities following exercise to which she was unaccustomed. Examination on admission, 11 days after onset, revealed myalgia, muscular weakness and cutaneous hemorrhagic bullae. Blood tests revealed eosinophilia (9160/mm(3)) and elevation of creatinine kinase and C-reactive protein. Muscle biopsy in the quadriceps femoris showed small vessel vasculitis and eosinophilic infiltration. Skin biopsy revealed leukocytoclastic vasculitis with neutrophilic and eosinophilic infiltration and fibrinoid necrosis. We diagnosed her as having Churg-Strauss syndrome (CSS). Corticosteroid treatment relieved her symptoms and resulted in normalization of the laboratory test results. Myositis is rare as an initial manifestation of CSS. The previous studies on immunological changes after eccentric exercise suggest that unaccustomed exercise could induce an increase in the serum level of interleukin-6 and trigger the onset of CSS.
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PMID:Churg-Strauss syndrome presenting as myositis following unaccustomed exercise. 1949 52

Respiratory syncytial virus (RSV) is the most common cause of hospitalization for respiratory tract infection in young children. It is also a significant cause of morbidity and mortality in elderly individuals and in persons with asthma and chronic obstructive pulmonary disease. Currently, no reliable vaccine or simple RSV antiviral therapy is available. Recently, we determined that the minor pulmonary surfactant phospholipid, palmitoyl-oleoyl-phosphatidylglycerol (POPG), could markedly attenuate inflammatory responses induced by lipopolysaccharide through direct interactions with the Toll-like receptor 4 (TLR4) interacting proteins CD14 and MD-2. CD14 and TLR4 have been implicated in the host response to RSV. Treatment of bronchial epithelial cells with POPG significantly inhibited interleukin-6 and -8 production, as well as the cytopathic effects induced by RSV. The phospholipid bound RSV with high affinity and inhibited viral attachment to HEp2 cells. POPG blocked viral plaque formation in vitro by 4 log units, and markedly suppressed the expansion of plaques from cells preinfected with the virus. Administration of POPG to mice, concomitant with viral infection, almost completely eliminated the recovery of virus from the lungs at 3 and 5 days after infection, and abrogated IFN-gamma (IFN-gamma) production and the enhanced expression of surfactant protein D (SP-D). These findings demonstrate an important approach to prevention and treatment of RSV infections using exogenous administration of a specific surfactant phospholipid.
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PMID:Pulmonary surfactant phosphatidylglycerol inhibits respiratory syncytial virus-induced inflammation and infection. 2008 Jul 99

Endotoxin, a component of gram-negative bacterial cell walls, is a pro-inflammatory agent that induces local and systemic inflammatory responses in normal subjects which can contribute to the risk of developing asthma and chronic obstructive lung diseases. A probabilistic approach linking models of exposure, internal dosimetry, and health effects was carried out to quantitatively assess the potential inhalation risk of airborne endotoxin in homes during the winter and summer seasons. Combining empirical data and modeling results, we show that the half-maximum effect of the endotoxin dose (ED50) was estimated to be 707.9 (95% confidence interval (CI): 308.8-1287.0) endotoxin units (EU) for body temperature change, 481.8 (95% CI: 333.2-630.3) EU for elevation of neutrophils, and 1174.5 (95% CI: 816.0-1532.9) EU for elevation of the cytokine, interleukin-6. Our study also suggests that airborne endotoxin in homes may pose potential risks, and a higher risk for elevation of neutrophils and cytokine interleukin-6 appeared in winter season than in summer. Our study offers a risk-management framework for discussion of future studies of human respiratory exposure to airborne endotoxin.
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PMID:Modeling human health risks of airborne endotoxin in homes during the winter and summer seasons. 2010 6

The combination of beta(2)-adrenoceptor agonists (beta(2)-agonists) with inhaled steroids has become the standard treatment for mild to moderate asthma. Theophylline has also been combined successfully with inhaled steroids. However, the possible interaction between theophylline and beta(2)-agonists, with regard to their anti-inflammatory effects, has not been clarified. The aim of this study was to investigate the in vitro interaction between theophylline and salbutamol on cytokine generation from human monocytes and compare it with a similar interaction between dexamethasone and salbutamol. Purified monocytes from normal donors were pretreated with the drugs (alone or in combination) and stimulated with lipopolysaccharide for 24 h. Released tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6), and their corresponding mRNA expressions, were determined and analyzed. Salbutamol (>or= 0.1 microM) significantly inhibited the release of TNF-alpha, but also significantly enhanced that of IL-6. In contrast, theophylline (50 microM) and dexamethasone (0.1 microM) strongly inhibited the generation of both cytokines. It is noteworthy that when the drugs were used in combination the effects of theophylline and salbutamol were additive in inhibiting TNF-alpha release, but theophylline blocked the IL-6-enhancing effect of salbutamol. A similar effect was seen when dexamethasone was combined with salbutamol. These results show that beta(2)-agonists have opposing effects on the generation of TNF-alpha and IL-6, but that when they were combined with clinically relevant concentrations of theophylline, theophylline, like dexamethasone, was capable of augmenting the anti-inflammatory effects of the beta(2)-agonists while at the same time preventing their proinflammatory effect. Thus, theophylline may have a potentially useful steroid-sparing effect.
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PMID:Interactions between theophylline and salbutamol on cytokine release in human monocytes. 2038 27

Mast cell-mediated allergic disease is involved in many diseases such as anaphylaxis, rhinitis, asthma and atopic dermatitis. The discovery of drugs for the treatment of allergic disease is an important subject in human health. In this study, we investigated the effect of the water extract of Clinopodium gracile Matsum var. multicaule (WECG) on the mast cell-mediated allergic inflammation and studied the possible mechanism of action. WECG inhibited compound 48/80-induced systemic anaphylaxis and immunoglobulin E-mediated cutaneous anaphylaxis in a dose-dependent manner. WECG dose-dependently reduced histamine release from rat peritoneal mast cells and human mast cells. The inhibitory effect of WECG on histamine release was mediated by the modulation of intracellular calcium. In addition, WECG attenuated the phorbol 12-myristate 13-acetate and calcium ionophore A23187-stimulated gene expression and secretion of proinflammatory cytokines such as tumor necrosis factor-alpha and interleukin-6 in human mast cells. The inhibitory effect of WECG on these proinflammatory cytokines was nuclear factor-kappaB (NF-kappaB) dependent. Our findings provide evidence that WECG inhibits mast cell-derived allergic inflammation and involvement of calcium and NF-kappaB in these effects.
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PMID:Clinopodium gracile inhibits mast cell-mediated allergic inflammation: involvement of calcium and nuclear factor-kappaB. 2046 1

Asthma is an inflammatory airway disease. The pathogenic mechanisms of asthma include the infiltration of leukocytes and release of cytokines. Mimosa pudica (Mp) has been used traditionally for the treatment of insomnia, diarrhea and inflammatory diseases. Although Mp extract has various therapeutic properties, the effect of this extract on asthma has not yet been reported. This study investigated the suppressive effects of Mp extract on asthmatic responses both in vitro and in vivo. Mp extract was acquired from dried and powdered whole plants of M. pudica using 80% ethanol. BALB/c mice were used for the mouse model of asthma induced by ovalbumin. Mp extract significantly inhibited the HMC-1 cell migration induced by stem cell factor and blocked the release of monocyte chemotactic protein-1 (MCP-1) and interleukin-6 (IL-6) in EoL-1 cells. Leukocytosis, eosinophilia and mucus hypersecretion in asthmatic lung were significantly suppressed by Mp extract. The release of ovalbumin-specific IgE in bronchoalveolar lavage fluid and serum was also decreased. Mp extract treatment resulted in no liver cytotoxicity. The Mp extract has inhibitory properties on asthma and may be used as a potent therapeutic agent for allergic lung inflammation.
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PMID:Suppression of ovalbumin-induced airway inflammatory responses in a mouse model of asthma by Mimosa pudica extract. 2062 91

Platycodon grandiflorum (Campanulaceae) is used as traditional medicine in Asian countries. In Korean traditional medicine, Platycodon root has been widely used since ancient times as a traditional drug to treat cold, cough and asthma. However, its effects on bone marrow-derived mast cell (BMMC)-mediated allergy and inflammation mechanisms remain unknown. In this study, the biological effect of Platycodon root ethanol extract (PE) was evaluated in BMMC after induction of allergic mediators by phorbol 12-myristate 13-acetate (PMA) plus calcium ionophore A23187 (A23187) stimulation. The effect of PE on the production of several allergic mediators, such as interleukin-6 (IL-6), prostaglandin D(2) (PGD(2)), leukotriene C(4) (LTC(4)), beta-Hexosaminidase (beta-Hex) and cyclooxygenase-2 (COX-2) protein, was investigated. The results demonstrate that PE inhibits PMA + A23187 induced production of IL-6, PGD(2), LTC(4), beta-Hexosaminidase and COX-2 protein. Taken together, these results indicate that PE has the potential for use in the treatment of allergy.
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PMID:Anti-allergic activity of a platycodon root ethanol extract. 2071 34


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