Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Overall 111 healthy children aged 3 to 7 years, 71 children with ARVI and those aged 2 to 14 years with ARVI complicated by bronchitis and pneumonia were examined. The level and rate of IL-1 production by peripheral blood monocytes in response to lipopolysaccharide (LPS) were determined. It has been established that 98.7% of the healthy children responded to LPS by marked production of IL-1. In 3 children, there was po synthesis of IL-1, in 26.1% of the healthy children, peripheral blood monocytes produced IL-1 without addition of LPS. In children with respiratory bacterial infections, there was a significant increase of IL-1 production as compared to the control. IL-1 production in ARVI was lowered.
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PMID:[Production of interleukin-1 by peripheral blood monocytes in children with respiratory diseases]. 204 81

The features of the cotton dust syndrome which need to be considered when formulating a hypothesis on mechanism(s) are: 1) the presence of fever, 2) the "Monday effect," 3) the slow onset of forced expiratory volume in 1 second (FEV1) changes, and 4) the presence of bronchitis in chronic sufferers but the absence of emphysema or fibrosis. The main hypotheses concerning the mechanisms are direct release of histamine triggered by cotton dust components, immune reactions (principally antibody mediated) to cotton dust antigens, and inflammatory response(s) triggered by endotoxins released from bacterial contaminants on the dust. While histamine release and immune reactions may occur as a result of cotton dust inhalation, it is suggested that they are of secondary importance in comparison to inflammation. Evidence is reviewed that implicates bacterial lipopolysaccharide (LPS) present in the dust as the principal etiologic agent in this process. It is postulated that LPS inhalation stimulates a secretory response by lung macrophages, involving the release of effector molecules which trigger coagulation, bronchoconstriction, fever, and mucus production. LPS-induced macrophage secretory products also promote the local sequestration and activation of both neutrophils and platelets, which serve to amplify the inflammatory response. Evidence is presented implicating both interstitial and alveolar macrophages in this process. The problems associated with the identification of "high risk" groups of cotton workers will be discussed, from a number of viewpoints; consideration will be given to the role of a variety of environmental factors (including tobacco smoking) in this context, as well as possible genetic factors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Current trends in research on the etiology and pathogenesis of byssinosis. 332 57

Airway inflammation in acute and chronic bronchitis includes a prominent neutrophil influx. Using a rat model of sulfur dioxide (SO2)-induced bronchitis, we investigated the role of the polymorphonuclear leukocyte (PMN) chemokines macrophage inflammatory protein-2 (MIP-2) and KC. Adult female rats were exposed to 230 ppm SO2 for 5 h/day for periods of 1 day to 5 wk. Immunohistochemical identification of rat PMNs in trachea cryostat sections allowed quantitation of a marked neutrophil influx into airways of bronchitic rats (PMNs/trachea ring = 55 +/- 26.2 [1 day SO2] versus 3.6 +/- 2.7 [air]; n = 5, P < or = 0.05). Northern analysis of trachea homogenates demonstrated induction of KC and MIP-2 mRNA expression after 1 day of SO2 and persistence of increased expression after longer exposure periods examined. Pretreatment of rats with dexamethasone (0.5 mg/kg) prior to a 1-day acute SO2 exposure prevented induction of chemokine mRNA and abrogated neutrophil influx completely (PMNs/trachea ring = 6.6 +/- 8.8 versus air controls; n = 5, P = 0.96). To determine if chemokine inhibition by dexamethasone could be further studied in vitro, the rat alveolar macrophage cell line NR8383 was treated with dexamethasone (10(-7) M) before stimulation with lipopolysaccharide (10 micrograms/ml). Pretreatment with dexamethasone substantially decreased induction of both MIP-2 and KC mRNA in response to lipopolysaccharide, indicating the potential utility of in vitro systems to identify additional anti-inflammatory agents. These studies support the hypothesis that the chemokines MIP-2 and KC mediate airway neutrophil influx in both acute and chronic SO2-induced bronchitis in the rat.
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PMID:Airway neutrophilia and chemokine mRNA expression in sulfur dioxide-induced bronchitis. 787 1

Two experiments were designed to determine the effects of dietary (n-3) fatty acids and grain source on the growth-suppressive effects of the inflammatory response and indices of specific immunity. In Experiment 1, chicks were fed diets containing 0.5, 1, or 2 g/100 g of either corn oil or fish oil. In Experiment 2, chicks were fed diets containing up to 2 g/100 g of either fish oil, linseed oil or corn oil as the source of dietary fat, in either cereal grain- or corn-based diets. In each experiment, subsets of chicks within each dietary treatment were either vaccinated with infectious bronchitis virus (IBV) vaccine, injected with Salmonella typhimurium lipopolysaccharide (LPS), heat-killed Staphylococcus aureus, or remained noninjected. Increasing dietary fish oil, but not corn oil increased body weight and lessened the growth-suppressing effect of heat-killed S. aureus or S. typhimurium LPS. Increasing the concentration of dietary fish oil decreased febrile response, circulating hemopexin and metallothionein concentrations. Dietary fish oil resulted in decreased release relative to dietary corn oil of interleukin-1 by peritoneal macrophages. Although IBV titers were not significantly affected by dietary oil treatment, phytohemagglutination-induced wattle swelling was greater among chicks fed fish oil. In Experiment 2, the modulating effects of fish oil on the immune system were dependent on the type of grain used in the diet, with fish oil/cereal diets resulting in greater cell-mediated immunity and lower indices of inflammation than fish oil/corn diets. Inclusion of increasing amounts of fish oil in the diet improved performance, decreased indices of the inflammatory response and either improved or did not change indices of the specific immune response of growing chicks.
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PMID:Dietary fish oil alters specific and inflammatory immune responses in chicks. 931 62

Leukemia inhibitory factor (LIF) exhibits multiple biological activities in various tissues, and we have shown that LIF activates POMC gene transcription in response to immune signals. As higher serum levels of LIF have been reported in septicemia, we measured LIF values in biological fluids by RIA. Immunoreactive LIF was detected in 303 of 428 human serum samples. Circulating LIF detection rates were 69% in acute inflammatory diseases, 83% in chronic inflammatory diseases, 61% in noninflammatory diseases, and 90% in cancer patients. Serum concentrations of human LIF was higher in patients with inflammatory disease than in noninflammatory disease (0.80 +/- 0.10 vs. 0.53 +/- 0.02 ng/mL; P < 0.05) or in cancer patients (0.44 +/- 0.06; P < 0.05). Higher serum human LIF levels were found in septicemia (0.78 +/- 0.14 ng/mL), pneumonia (0.80 +/- 0.10 ng/mL), acute bronchitis (0.88 +/- 0.09 ng/mL), other infections (1.01 +/- 0.17 ng/mL), and systemic lupus erythematosus (SLE; 0.79 +/- 0.06 ng/mL). In 7 septicemia patients, Gram-negative infection was associated with higher LIF levels (1.06 +/- 0.16 ng/mL) than was Gram-positive infection (0.58 +/- 0.14 ng/mL). In patients with acute inflammatory disease, serum LIF levels decreased within several days after hospitalization. To test circulating mouse (m) LIF changes in response to inflammatory stress, lipopolysaccharide (LPS) was injected ip to mice. LPS increased serum mLIF values concordantly with ACTH levels. After i.p. injection of 80 microg LPS, serum mLIF increased by 144% (P < 0.05), 173% (P < 0.05), and 134% at 30, 90, and 120 min respectively. In vitro, however, LPS did not increase ACTH and mLIF secretion from dispersed mouse primary pituitary cells. These results suggest that LIF is an important participant in the pathogenesis of the acute inflammatory response. The elevated serum LIF levels observed in inflammation do not appear to originate from the pituitary.
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PMID:Measurement of leukemia inhibitory factor in biological fluids by radioimmunoassay. 954 56

Increased morbidity in persons suffering from inflammatory lung diseases, such as asthma and bronchitis, has been associated with air pollution particles. One hypothesis is that particles can cause an amplification of the pulmonary inflammation associated with these diseases, thus worsening affected individuals' symptoms. This hypothesis was tested in a murine model of asthma by inhalation exposure to (1) concentrated air particles (CAPs), (2) the leachate of residual oil fly ash (ROFA-S), and (3) lipopolysaccharide (LPS). Allergen-sensitized mice (ip ovalbumin, OVA) were 21 days old when challenged with an aerosol of 3% OVA in phosphate-buffered saline (PBS) for 10 min (controls were challenged with PBS only) for 3 days. On the same days, mice were further exposed to 1 of 3 additional agents: CAPs (or filtered air) for 6 h/day; LPS (5 microg/ml, or PBS) for 10 min/day; or ROFA-S (leachate of 50 mg/ml, or PBS) for 30 min on day 2 only. At 24 h later, mice challenged with OVA aerosol showed airway inflammation and airway hyperresponsiveness (AHR) to methacholine (Mch), features absent in mice challenged with PBS alone. Both OVA- and PBS-challenged mice subsequently exposed to ROFA-S showed increased AHR to Mch when compared to their respective controls (OVA only or PBS only). In contrast, when OVA-challenged mice were further exposed to CAPs or LPS, no changes in AHR were seen in comparison to mice challenged with OVA only. Bronchoalveolar lavage (BAL) analysis and histopathology 48 h postexposure showed OVA-induced allergic inflammation. No significant additional effects were caused by CAPs or ROFA-S. LPS, in contrast, caused significant increases in total cell, macrophage, and polymorphonuclear cell numbers. The data highlight discordance between airway inflammation and hyperresponsiveness.
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PMID:Effects of environmental aerosols on airway hyperresponsiveness in a murine model of asthma. 1056 93

1. Granulocyte/macrophage colony-stimulating factor (GM-CSF) is a pro-inflammatory cytokine secreted by cells of the monocyte/macrophage lineage and has been implicated in the pathogenesis of bronchitis and asthma. 2. In the present study we have evaluated the effect of several cyclic AMP-elevating agents on lipopolysaccharide (LPS)-induced GM-CSF release from human monocytes and the extent to which the anti-inflammatory cytokine, interleukin (IL)-10, is involved. 3. LPS evoked a concentration-dependent generation of GM-CSF from human monocytes that was inhibited, at the mRNA and protein level, by 8-Br-cyclic AMP, cholera toxin, prostaglandin E2 (PGE2) and a number of structurally dissimilar phosphodiesterase (PDE) 4 inhibitors. 4. Pre-treatment of monocytes with a concentration of an anti-IL-10 monoclonal antibody that abolished the inhibitory action of a maximally effective concentration of exogenous human recombinant IL-10, significantly augmented LPS-induced GM-CSF generation. This effect was associated with a parallel upwards displacement of the concentration-response curves that described the inhibition of GM-CSF by PGE2, 8-Br-cyclic AMP and the PDE4 inhibitor, rolipram, without significantly changing the potency of any drug. Consequently, the maximum percentage inhibition of GM-CSF release was reduced. Further experiments established that the reduction in the maximum inhibition of GM-CSF release seen in anti-IL-10-treated cells was not due to functional antagonism as rolipram, PGE2 and 8-Br-cyclic AMP were equi-effective at all concentrations of LPS studied. 5. These data indicate that cyclic AMP-elevating drugs attenuate the elaboration of GM-CSF from LPS-stimulated human monocytes by a mechanism that is not mediated via IL-10. Suppression of GM-CSF from monocytes may explain, at least in part, the efficacy of PDE4 inhibitors in clinical trials of chronic obstructive pulmonary disease.
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PMID:Suppression of granulocyte/macrophage colony-stimulating factor release from human monocytes by cyclic AMP-elevating drugs: role of interleukin-10. 1152 97

The relationship between the dietary level of vitamin E (VE) and the immune response of broilers was studied in three experiments. Immunity was assessed as antibody production to infectious bronchitis virus (IBV), SRBC, and Brucella abortus (BA) antigens, mitogenic response to phytohemagglutinin A (PHA) and concanavalin A (Con A), cutaneous basophil hypersensitivity (CBH) to PHA, and lipopolysaccharide induction of acute-phase proteins (APP) and heterophilia. A range of VE (0, 10, 17.5, 25, 37.5, 50, 100, and 200 IU/kg) levels were supplemented to a basal diet (corn-soy) containing 10.2 IU of VE/kg. We found a dose-dependent increase in antibody production in response to attenuated IBV between 0 and 25 IU/kg of supplemented VE and no further increase at higher levels. Antibody levels to SRBC were higher in birds supplemented with 50 IU of VE/kg compared to those supplemented with 0 or 200 IU/kg of VE. Antibody production in response to BA antigens was not influenced by VE. Mitogenic responses were suppressed by supplemented VE in Experiment 1 for PHA (25 IU/kg diet) and Con A (25 and 50 IU/kg diets). CBH and APP levels were not affected by VE. Heterophilia was lowest at 50 IU/kg 6 h after lipopolysaccharide injection (Experiment 1). Our study showed that moderate (25 to 50 IU/kg) levels of VE supplementation were most immunomodulatory and that high levels were less effective.
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PMID:Relationship between the level of dietary vitamin E and the immune response of broiler chickens. 1173 76

Chronic bronchitis is a significant cause of morbidity and mortality. Chronic irritation of the conducting airways by inhaled substances, most importantly cigarette smoke, air pollution, and occupational exposures, is thought to be a key factor in the pathogenesis of chronic bronchitis. Microbial infections have been implicated in acute exacerbations of bronchitis and in its progression. Several animal models of chronic bronchitis have been developed. This review examines similarities and dissimilarities among commonly used animal models of bronchitis and the human disease. The most commonly used animal models of chronic bronchitis are those employing SO2, tobacco smoke, lipopolysaccharide (endotoxin), proteases, and secretagogues. Bronchiolitis induced by nickel and nitric acid have also been reported. Rats, hamsters, and dogs are the species most frequently used; sheep and monkeys have been used less frequently. These models vary in the extent or location of mucous-cell hyperplasia and metaplasia, airway inflammation, chronicity, ease of induction, and reproducibility. Frequently, the deficiencies in these models are attributable to anatomic differences between human and animal airways, differences in the severity or chronicity of inflammation or fibrosis, or lack of complete characterization of the responses and their time course in the animal model. These animal models may be useful for investigating how, and under what exposure conditions, ambient pollutants might exacerbate airway inflammation, mucus hypersecretion, and airflow limitation.
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PMID:Animal models of chronic bronchitis and their relevance to studies of particle-induced disease. 1288 90

In this study, the authors describe a new technique enabling the rapid assessment of mucociliary clearance (MCC) in rats and characterize this aspect of innate host defense in 2 animal models of bronchitis. Following instillation into the airways, fluorescent microspheres were rapidly cleared over 24 hours, with 60% to 80% of clearance occurring within 4 hours. On a background of airway neutrophilia and mucus hypersecretion, induced by either lipopolysaccharide or cigarette smoke, MCC was significantly enhanced. This reserve capacity in the MCC system will need to become overwhelmed in order to model the clinically observed impairment of lung mucus clearance in an animal system.
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PMID:Mucociliary clearance is enhanced in rat models of cigarette smoke and lipopolysaccharide-induced lung disease. 1496 4


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