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)

We investigated the kinetics of allergen-induced eotaxin expression and its relationship to eosinophil accumulation and activation in the airways of patients with allergic asthma. Twenty-four patients with allergic asthma and late asthmatic responses to allergen inhalation were randomly allocated into three groups of eight patients each, who received bronchoscopy with bronchial biopsies and BAL at 2, 4 and 24 h, respectively, after the inhalation of the diluent and the allergen. The expression of eotaxin mRNA and protein and eotaxin release were evaluated by in situ hybridization, immunohistochemistry, immunocytochemistry, and radioimmunoassay. Increased transcription from the eotaxin gene preceded the appearance of the late asthmatic response and the influx of activated eosinophils in bronchial tissue and BAL fluid (BALF). This was followed by increased cell expression of eotaxin protein (P<0.001) and increased eotaxin release (P<0.001), which correlated with the numbers of total and activated eosinophils and the level of airflow obstruction at 4 h after allergen exposure (P<0.05 for all correlations). At 24 h after allergen inhalation, enhanced eotaxin expression declined without a similar reduction in the numbers of eosinophils in bronchial biopsies and when there was a further increase in the number of these cells in BALF (P<0.05). These results indicate that eotaxin contributes to the early phase of allergen-induced recruitment of activated eosinophils into the airways of patients with allergic asthma and that other factors are implicated in the persistence of eosinophil infiltration.
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PMID:Kinetics of eotaxin expression and its relationship to eosinophil accumulation and activation in bronchial biopsies and bronchoalveolar lavage (BAL) of asthmatic patients after allergen inhalation. 982 68

The immunomodulatory role of the chemokine C10 was explored in allergic airway responses during experimental allergic bronchopulmonary aspergillosis (ABPA). The intratracheal delivery of Asperigillus fumigatus Ag into A. fumigatus-sensitized mice resulted in significantly increased levels of C10 within the bronchoalveolar lavage, and these levels peaked at 48 h after A. fumigatus challenge. In addition, C10 levels in BAL samples were greater than 5-fold higher than levels of other chemokines such as monocyte-chemoattractant protein-1, eotaxin, and macrophage-inflammatory protein-1alpha. From in vitro studies, it was evident that major pulmonary sources of C10 may have included alveolar macrophages, lung fibroblasts, and vascular smooth muscle cells. Experimental ABPA was associated with severe peribronchial eosinophilia, bronchial hyperresponsiveness, and augmented IL-13 and IgE levels. The immunoneutralization of C10 with polyclonal anti-C10 antiserum 2 h before the intratracheal A. fumigatus challenge significantly reduced the airway inflammation and hyperresponsiveness in this model of ABPA, but had no effect on IL-10 nor IgE levels. Taken together, these data suggest that C10 has a unique role in the progression of experimental ABPA.
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PMID:Immunomodulatory role of C10 chemokine in a murine model of allergic bronchopulmonary aspergillosis. 1022 48

A variety of studies have demonstrated that organ-to-organ communication circuits are established during various disease states. For example, an activated liver may release high levels of cytokines, which are carried to the lung and activate this organ. In the present study, we have examined the inflammation occurring as the liver-lung interact during the initiation of acetaminophen-induced toxicity. An overnight fast followed by an intraperitoneal acetaminophen challenge was required to elicit liver injury. In these animals, lung injury was most pronounced at 24 h post-challenge and was characterized by necrosis, edema and inflammation. Interestingly, the non-fasted/fed animals that received acetaminophen had only minor liver injury, but still presented with significant pathologic changes of the lung. BAL fluid contained increased neutrophils after acetaminophen challenge in the fasted (26%) and the fed (35%) animal groups. A significant vascular leak was found in the fasted, but not the fed, acetaminophen challenged animals. However, lung levels of the chemokine, eotaxin, and the cytokine, IL-12, were significantly elevated in the acetaminophen challenged animals that were fed, but not in the fasted group. The immunoneutralization of eotaxin, but not IL-12 or TNF-alpha, improved the histological appearance of the lung in fed mice challenged with acetaminophen.
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PMID:Alterations in cytokine/chemokine expression during organ-to-organ communication established via acetaminophen-induced toxicity. 1461 9

IL-13 is a mediator of allergen-induced airway hyperresponsiveness (AHR). The aim of this study was to evaluate whether eotaxin and IL-5 were implicated in the effects of IL-13 on allergen-induced AHR or whether IL-13 may exert its effects through direct actions on airway smooth muscle (ASM). To study this question airway inflammation and AHR were induced in mice by sensitization and subsequent challenge on three successive days with ovalbumin. A monoclonal anti-IL-13 antibody administered before each challenge significantly reduced AHR without affecting airway eosinophilia. No changes of mRNA in BAL and lung tissues or protein levels in BAL of IL-5 or eotaxin were found following anti-IL-13 treatment. Combined injection of monoclonal anti-IL-5 and antieotaxin antibodies before each antigen challenge blocked airway eosinophilia but failed to reduce AHR. IL-13 induced calcium transients in cultured murine ASM cells and augmented the calcium and contractile responses of these cells to leukotriene D4. These results suggest that IL-13 plays an important role in allergen-induced AHR and is important in the early phases of the inflammatory process. Its effects on AHR are mediated independently of IL-5 and eotaxin and may involve a direct effect on ASM to augment its responsiveness.
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PMID:IL-13 may mediate allergen-induced hyperresponsiveness independently of IL-5 or eotaxin by effects on airway smooth muscle. 1556 87

Recently we have shown that sound stress enhances allergic airway inflammation in a combined murine model. In the current study we investigated mediating factors and early kinetics of stress exacerbated allergic airway inflammation. Stress significantly increased allergen induced airway inflammation as identified by leukocyte numbers in BAL fluids. Eotaxin levels from stressed mice were significantly higher 24 h after stress. No differences were found for vascular or cellular adhesion molecule expression or cytokine levels. Our data indicate that the effect of stress on allergic airway inflammation might be mediated by the chemoattractant eotaxin, while Th2 cytokines and expression of adhesion molecules seem not to be differently regulated in stressed and non-stressed mice.
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PMID:Effect of stress on eotaxin and expression of adhesion molecules in a murine model of allergic airway inflammation. 1709 99

The B7-family molecule CD86, expressed on the surface of pulmonary and thoracic lymph node antigen-presenting cells, delivers essential costimulatory signals for T-cell activation in response to inhaled allergens. CD86-CD28 signaling is involved in priming allergen-specific T cells, but it is unclear whether these interactions play a role in coordinating memory T-helper 2 cell responses. In the ovalbumin (OVA)-induced mouse model of asthma, administration of CD86-specific antibody before systemic sensitization suppresses inhaled OVA-induced pulmonary inflammation and airway hyper-responsiveness (AHR). In previously OVA-sensitized mice, systemic and intranasal coadministration of CD86 antibody is required to produce these effects. To directly assess the importance of pulmonary CD86 expression in secondary immune responses to inhaled allergens, mice were sensitized and locally challenged with nebulized OVA before treatment with an inhaled aerosolized CD86 antisense oligonucleotide (ASO). CD86 ASO treatment suppressed OVA-induced up-regulation of CD86 protein expression on pulmonary dendritic cells and macrophages as well as on recruited eosinophils. Suppression of CD86 protein expression correlated with decreased methacholine-induced AHR, airway inflammation, and mucus production following rechallenge with inhaled OVA. CD86 ASO treatment reduced BAL eotaxin levels, but it did not reduce CD86 protein on cells in the draining lymph nodes of the lung, and it had no effect on serum IgE levels, suggesting a local and not a systemic effect. These results demonstrate that CD86 expression on pulmonary antigen-presenting cells plays a vital role in regulating pulmonary secondary immune responses and suggest that treatment with an inhaled CD86 ASO may have utility in asthma and other chronic inflammatory lung conditions.
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PMID:Inhaled CD86 antisense oligonucleotide suppresses pulmonary inflammation and airway hyper-responsiveness in allergic mice. 1738 43

Bronchiolitis obliterans syndrome (BOS) is one of the most important factors limiting the long-term survival of lung transplant recipients (LTR), however its pathogenesis still remains unclear. We hypothesized that an increased production of certain specific proinflammatory mediators in the first post-transplant year would predispose to BOS. We retrospectively evaluated temporal kinetics of some CC chemokines that have not yet been evaluated, including CCL3/MIP1-alpha, CCL4/MIP1-beta, CCL17/TARC, CCL19/MIP3-beta, CCL20/MIP3-alpha, CCL22/MDC and CCL26/eotaxin, in broncho-alveolar lavage fluid (BAL-f) in the first post-transplant year in a cohort of 8 LTR before the development of BOS (pre-BOS LTR) and 8 LTR with long-term stable clinical conditions (stable LTR). Chemokine levels were assayed by means of a multiplex sandwich ELISA. Furthermore, for those ligands which resulted significantly predictive of BOS onset, we analyzed the expression of specific receptors (CCR) on BAL cells. The proportion of CCR-expressing BAL cells was assessed by flow cytometry. We demonstrated that MIP3-beta/CCL19, MIP3-alpha/CCL20, MDC/CCL22 levels at 6 months post-transplant significantly predicted BOS onset. In addition, the temporal behavior of these factors resulted significantly different in pre-BOS patients as compared to stable LTR. Finally the expression of CCR was documented on BAL lymphocytes and macrophages, and, in some cases, their expression was found to vary between the two groups. Within the complexity of the chemokine network, these three CCL factors could play an additive role in the pathogenesis of the inflammatory process leading to bronchiolar fibro-obliteration.
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PMID:Chemokine redundancy in BOS pathogenesis. A possible role also for the CC chemokines: MIP3-beta, MIP3-alpha, MDC and their specific receptors. 1804 37

Helminths and their products have a profound immunomodulatory effect upon the inductive and effector phases of inflammatory responses, including allergy. We have demonstrated that PAS-1, a protein isolated from Ascaris suum worms, has an inhibitory effect on lung allergic inflammation due to its ability to down-regulate eosinophilic inflammation, Th2 cytokine release and IgE antibody production. Here, we investigated the role of IL-12, IFN-gamma and IL-10 in the PAS-1-induced inhibitory mechanism using a murine model of asthma. Wild type C57BL/6, IL-12(-/-), IFN-gamma(-/-) and IL-10(-/-) mice were immunized with PAS-1 and/or OVA and challenged with the same antigens intranasally. The suppressive effect of PAS-1 was demonstrated on the cellular influx into airways, with reduction of eosinophil number and eosinophil peroxidase activity in OVA+PAS-1-immunized wild type mice. This effect well correlated with a significant reduction in the levels of IL-4, IL-5, IL-13 and eotaxin in BAL fluid. Levels of IgE and IgG1 antibodies were also impaired in serum from these mice. The inhibitory activity of PAS-1 was also observed in IL-12(-/-) mice, but not in IFN-gamma(-/-) and IL-10(-/-) animals. These data show that IFN-gamma and IL-10, but not IL-12, play an important role in the PAS-1 modulatory effect.
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PMID:PAS-1, a protein from Ascaris suum, modulates allergic inflammation via IL-10 and IFN-gamma, but not IL-12. 1900 20

Interleukin-13 (IL-13) plays a central role in chronic airway diseases, including asthma. These studies were conducted to evaluate the safety of administration of a human anti-IL-13 monoclonal antibody (mAb) to normal macaques and in macaques with allergic asthma. In addition, serum and bronchioalveolar lavage fluid were collected from allergic cynomolgus macaques in order to identify potential surrogate markers of IL-13 pharmacology that could be useful for subsequent clinical trials. In vitro studies demonstrated that the anti-IL-13 mAb inhibited the pharmacological actions of both human and cynomolgus macaque IL-13. Allergic macaques were treated systemically with 10 mg/kg anti-IL-13 mAb 1 day prior to inhaled Ascaris suum antigen challenge. Normal macaques were dosed intravenously with anti-IL-13 once per week for 3 weeks at doses of 10 or 50 mg/kg. Treatment of macaques with the anti-IL-13 mAb was not associated with any toxicologically significant findings. A slight treatment-related but nonadverse decrease in platelet counts was observed in both the normal and allergic macaques. In allergic macaques, the anti-IL-13 mAb treatment did not affect lung function, lung eosinophilia, or serum or BAL immunoglobulin E (IgE) concentrations but did produce a reduction in BAL and serum eotaxin concentrations (p < .05) at 6 h post antigen challenge. This study shows that administration of an anti-IL-13 mAb was well tolerated in both normal and allergic asthmatic macaques and that serum eotaxin concentrations may be a useful early in vivo marker for evaluating IL-13 inhibition in patients with asthma.
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PMID:Preclinical safety and pharmacology of an anti-human interleukin-13 monoclonal antibody in normal macaques and in macaques with allergic asthma. 1903 5

ortho-Phthalaldehyde (OPA) is commonly used as a safer and more effective chemical disinfectant for use with medical devices in hospitals. However, the cases of patients with occupational bronchial asthma or contact dermatitis are recently reported among workers in the medical professions who were exposed to OPA disinfectant. Mechanism of allergic reaction associated with OPA is poorly understood. The purpose of this study is that OPA may act as an immunological adjuvant in the allergic reaction accompanied by enhanced specific-IgE production in response to allergen challenge in OVA-sensitized mice. OPA induced increase of total cell numbers, and reflected infiltration of neutrophils in BAL fluid after allergen challenge in sensitized mice, dose-dependently. However, total protein concentration in BAL fluid did not change in the all of groups. The OPA induced up-regulation of eotaxin and monocyte chemotactic protein-1 mRNAs in the lung as well as the increase in OVA-specific IgE in sensitized mice compared with non-sensitized controlled mice without increase in the level of OVA-specific IgG. Cytokines IL-4 and IL-5 mRNA were expressed by allergen (OVA) challenge in both lungs collected from OPA-administrated-sensitized and OPA-administrated-nonsensitized mice. From these data, we concluded that low concentration of OPA that enhanced the OVA-induced recruitment of neutrophils to the lung and the production of allergen-specific IgE, suggesting that OPA acts as an immunological adjuvant.
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PMID:ortho-Phthalaldehyde enhances allergen-specific IgE production without allergen-specific IgG in ovalbumin-sensitized mice. 1911 43


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