Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:6.2.1.7 (BAL)
1,977 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The study was set up to evaluate the changes in broncho-alveolar lavage cell-count in asthmatics after bronchial provocation. Similarities and differences between atopic (A) and nonatopic (N) asthma were given a special concern. Twenty mild asthmatics--10 A and 10 N. There was no difference in BAL eosinophila between these groups before provocation. After provocation more eosinophils were found in A group (p = 0.06). Neutrophils were more numerous in N on both occasions--0 = 0.00003 and p = 0.006 respectively). Lymphocytes showed a similar pattern--p = 0.03, p = 0.003. A positive correlation between BAL eosinophilia and bronchial hyperreactivity was shown in both groups. Inflammation, including inflammatory cells plays a major role in bronchial asthma pathophysiology. It seems to be more expressed in nonatopic patients.
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PMID:[Evaluation of allergic inflammation parameters in bronchoalveolar lavage in patients with asthma]. 862 Jan 67

Eosinophils play a key role for the function of release inflammatory mediators and destroy epithelial tissue in the airway. Therefore, they have been accepted to be proinflammatory effector cells in the pathogenesis of the bronchial asthma. The aim of this study was to investigate the effect of the calcitonin gene-related peptide (CGRP) a 37-amino acid neuropeptide on eosinophils responsible for hypersensitivity using BAL fluids that represent the cell population in the lung tissue. For this purpose, 15 rats were divided into three groups receiving vehicle, 10(-6) M and 10(-5) M CGRP using a portable nebulizer. Nebulated exposure of CGRP resulted in both significant increases in the eosinophil numbers with 10(-6) and 10(-5) M CGRP of 18 +/- 0.913 cell/mm2 (mean +/- SEM: p < 0.01) and 31.25 +/- 1.931 (p < 0.01), respectively vs. control (12 +/- 0.408 cell/mm2). CGRP is capable of causing a eosinophilia in the lung in vivo and may contribute to airway inflammation in patients with asthma.
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PMID:The effect of human calcitonin gene-related peptide on eosinophil chemotaxis in the rat airway. 873 88

We investigated the effects of IL-12 on a murine model of allergic lung inflammation. Administration of IL-12 was timed to interfere with either allergic sensitization (early dosage) or the hypersensitivity inflammatory response in the lung (late dosage), or both (early and late dosages). Comparisons of IL-12- and PBS-treated animals within each treatment group revealed several noticeable effects of IL-12. Early dosage, and the combination of early and late dosages, strikingly decreased ragweed-specific serum IgE, tracheal ring reactivity to acetylcholine, and BAL eosinophilia following allergen challenge. In contrast, late dosage had no effect on IgE levels and only a minimal effect on tracheal ring reactivity, but had a modest effect on recruitment of eosinophils. Early dosage down-regulated IL-5 and IL-10, but did not alter IL-4 or IFN-gamma expression. Late dosage down-regulated IL-5, up-regulated IL-10 and IFN-gamma, but did not change IL-4 expression. The combination of early and late dosage down-regulated IL-4, IL-5, and IL-10 expression, but increased IFN-gamma expression and production in the BAL cells and fluids. Taken together, these results indicate that IL-12 has potent immunomodulatory effects on allergic lung inflammation that depend on the timing of IL-12 administration relative to allergic sensitization and allergen challenge.
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PMID:Immunomodulatory effects of IL-12 on allergic lung inflammation depend on timing of doses. 889 55

We have investigated the diagnostic value of (BAL) in 29 immunocompetent children (ages 1 month to 18 years) with chronic diffuse pulmonary infiltrates on chest radiograph who presented for evaluation over a 3-year period. The median age at the time of the BAL was 20 months with a range of 1-210 months. Positive results (1) diagnostic of a primary disorder; (2) consistent with a diagnosis; or (3) diagnostic of a secondary disorder, were obtained in 20/29 patients (13 with a single positive BAL finding and 7 with more than one finding). BAL was diagnostic of a primary disorder in only 5 patients (17%) with aspiration detected in 3 and infection in 2. The differential diagnosis was narrowed in 15 patients by the presence of lymphocytosis, neutrophilia, or eosinophilia. A secondary disorder was uncovered in 8 patients. Negative results were obtained in 9 additional patients. We conclude that BAL provided useful information in children with chronic diffuse infiltrates, but its ability to determine the primary cause was limited.
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PMID:The diagnostic value of bronchoalveolar lavage in immunocompetent children with chronic diffuse pulmonary infiltrates. 903 92

Cysteinyl leukotrienes are important mediators of asthma, and inhibition of their effects may represent a potential breakthrough in the therapy of allergic rhinitis and asthma. Strategies for inhibition of cysteinyl leukotriene receptors and inhibition of 5-lipoxygenase activity. The leukotrienes antagonists, with particular reference to asthma and allergic rhinitis, is reviewed in this paper. In studies in asthmatic patients, these compounds can inhibit bronchoconstriction in response to exercise, aspirin and allergen. Results from clinical studies using receptor antagonists, such as LY-171883, SK&F-104353, ICI-204219, ONO-1078, MK-751, MK-0679, demonstrate beneficial effects, with improvement in symptoms and forced expiratory volume in one second (FEV1), and a reduction in the use of beta 2-adrenergic relief medication. NZ-107 was studied for its effect on airway inflammation caused by intratracheal injection of LTB4 or IL-5, or by inhalation of PAF, and by cell activation. Analysis of the BAL fluid revealed that both induced eosinophilia and neutrophilia were suppressed. Surprisingly, although PAF and superoxide generation were inhibited in macrophages and eosinophils, NZ-107 had no effect on neutrophil activation. U-75302 was studied in guinea pigs and inhibited LTB4 induced chemotaxis of eosinophils in vitro and antigen-induced lung eosinophilia in vivo. Further studies are needed to clarify the exact mechanism by which these compounds provide beneficial effects.
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PMID:Leukotrienes and their antagonists in allergic disorders. 915 Aug 42

The effect of prior ozone (O3) exposure on airway hyperresponsiveness and inflammation induced by trimellitic anhydride (TMA) has been investigated in TMA-sensitized guinea pigs. Airway responsiveness was measured as the concentration of acetylcholine needed to increase baseline lung resistance (RL) by 300% (PC300). Ozone (3 ppm for 3 h) caused an increase in -log PC300 at 1 h after exposure, with return of -log PC300 to control levels at 8 h. Ozone also increased baseline RL at 8 h. TMA challenge increase -log PC300 in TMA-sensitized guinea pigs at 8 h after challenge from 3.85 +/- 0.09 to 4.11 +/- 0.09. Ozone exposure prior to TMA challenge prevented the induction of airway hyperresponsiveness with a mean -log PC300 of 3.51 +/- 0.20, which was not different from that of control TMA-sensitized group. Baseline RL was significantly higher in ozone-pretreated animals after TMA challenge when compared to those of either control or challenged with TMA alone. Ozone had no effect on TMA challenge-induced BAL eosinophilia and neutrophilia. We conclude that a single exposure to ozone inhibits the increase in airway responsiveness but increases the bronchoconstrictor response induced by TMA in TMA-sensitized guinea pigs; however, the inflammatory airway response to TMA is unchanged by preexposure to ozone.
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PMID:Interaction of ozone exposure with airway hyperresponsiveness and inflammation induced by trimellitic anhydride in sensitized guinea pigs. 916 62

In the guinea pig, interleukin-5 (IL-5) has been shown to induce airway hyperresponsiveness as well as eosinophilia, which are important symptoms in asthma. IL-5 seems to be a critical cytokine since it selectively affects eosinophil functions. The mechanism of action by which IL-5 leads to airway hyperresponsiveness may be important for our understanding of the pathogenesis of asthma. Neurogenic inflammation, which is mediated by nonadrenergic noncholinergic nerves (NANC), may play a role in the IL-5-induced effects in guinea pig airways. In this study, the role of neuropeptides in the IL-5-induced airway hyperresponsiveness and eosinophilia in the guinea pig was examined using selective neurokinin receptor antagonists. Intra-airway application of IL-5 (1 microgram, twice) induces a selective eosinophil migration (control: 12 [8-22] x 10(5) cells and IL-5: 90 [67-187] x 10(5) cells, p < 0.05) and activation (control: 6.3 +/- 0.9 ng eosinophil peroxidase [EPO]/ml bronchoalveolar lavage [BAL] fluid and IL-5: 29.3 +/- 4.9 ng EPO/ml BAL fluid, p < 0.05) and a pronounced airway hyperresponsiveness in vivo. The maximal responses to histamine are increased by 160 +/- 16% (p < 0.05) after IL-5. Treatment of guinea pigs with either the nonselective neurokinin (NK)-receptor antagonist, FK224, or the selective NK2-receptor antagonist, SR48968, results in a complete inhibition of the in vivo hyperresponsiveness found after application of IL-5. Vice versa, intra-airway administration of substance P (10 micrograms, twice) results in an airway hyperresponsiveness (increased maximal response after substance P: 166 +/- 15% [p < 0.05]) without inducing migration or activation of eosinophils. All examined NK-receptor antagonists do not influence the IL-5-induced eosinophil accumulation. In addition, no effect of the NK-receptor antagonists is observed on the IL-5-induced eosinophil activation, as determined by BAL fluid EPO levels. The release of NK2-receptor active tachykinins plays an important role in the development of IL-5-induced airway hyperresponsiveness. This feature appears to be a step following eosinophil infiltration and activation since there are no effects on eosinophil function by pretreatment of the used NK-receptor antagonists.
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PMID:Role for neurokinin-2 receptor in interleukin-5-induced airway hyperresponsiveness but not eosinophilia in guinea pigs. 927 11

LEAC offers a very practical means of studying the pathophysiology of asthma. Despite the local nature of the challenge, LEAC often has a significant effect on FEV1 and may cause short-term destabilization of asthma. In common with other bronchoscopic methods used to study human asthma, samples obtained by LEAC show a considerable degree of variability and it is therefore necessary to use groups of 12-15 subjects to minimize the risk of Type II statistical errors. Comparisons between different studies of allergen exposure are made difficult by a variety of technical considerations. Chief among these are subject selection, the technique used for allergen exposure, the timing of sampling, and the analysis techniques. Dose-response studies in nonasthmatic allergic subjects indicate that the degree of BAL eosinophilia is related to the dose of antigen [17] but there is as yet no agreement on how LEAC might be standardized. Notwithstanding these reservations, local endobronchial allergen challenge has already yielded valuable information on the pathophysiology of asthma and will remain a useful complement to other investigational techniques in the future exploration of this disease.
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PMID:Endobronchial allergen challenge. 958 78

Tropical Pulmonary Eosinophilia (TPE) is a severe form of allergic asthma caused by the host inflammatory response to filarial helminths in the lung microvasculature, and is characterized by pulmonary eosinophilia, increased filarial-specific IgG and IgE antibodies, and airway hyperresponsiveness. The current study examined the effect of IL-12 on pulmonary eosinophilia, deposition of eosinophil major basic protein and airway hyperresponsiveness in mice inoculated i.v. with Brugia malayi microfilariae. Injection of recombinant murine IL-12 modulated the T helper (Th) response in the lungs from Th2- to Th1-like, with elevated IFN-gamma, and decreased IL-4 and IL-5 production. Consistent with this shift in cytokine response, antigen-specific IgG2a was elevated, and IgG1 and total serum IgE were decreased. In addition, eosinophils in BAL fluid from IL-12 treated mice were reduced from 56% to 11%, and there was no detectable MBP on respiratory epithelial cells. Importantly, IL-12 suppressed airway hyperresponsiveness compared with saline-injected control animals. Taken together, these data clearly demonstrate that by modulating Th associated cytokine production, IL-12 down-regulates filaria-induced lung immunopathology.
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PMID:Interleukin-12 suppresses filaria-induced pulmonary eosinophilia, deposition of major basic protein and airway hyperresponsiveness. 979 6

Allergic sensitization in asthma develops as a consequence of complex interactions between T cells and antigen-presenting cells. We have developed several in vivo models to study allergen-specific T cell and B cell function and their relevance to allergic airway hyperresponsiveness (AHR), focusing on the role of the costimulatory molecules CD80 and CD86. Treatment of mice with anti-CD86, but not anti-CD80, significantly inhibited increased serum levels of ovalbumin (OA)-specific IgE and IgG1, airway eosinophilia, and AHR both after 10 d of OA aerosol exposure (in the absence of adjuvant) and after intraperitoneal sensitization followed by repeated airway challenges. Inhibition of AHR was associated with decreased IL-4 and IL-5 levels in the BAL fluid of sensitized mice, suggesting impaired Th2 function in anti-CD86-treated animals. This effect was not seen when mice received treatment only before allergen challenge, indicating that anti-CD86 acts through inhibition of allergic sensitization and not simply by inhibiting the influx of inflammatory cells. These data suggest that the CD86 costimulatory ligand plays a major role in the development of allergic inflammation and AHR in allergen-challenged mice. Further, this study demonstrates that T-B cell interactions during allergic sensitization are amenable to therapeutic manipulation and that selective blockade of accessory signals can be an effective means for modulating distinct T cell functions.
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PMID:Anti-CD86 (B7.2) treatment abolishes allergic airway hyperresponsiveness in mice. 1022 38


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