Breathe Well Live Well
Condition: Peripheral Arterial Diseases
Intervention: Drug: Active comparator (cilostazol) and Placebo comparator
Sponsors: National Cheng-Kung University Hospital; National Cheng-Kung University Hospital; Department of Health, Executive Yuan, R.O.C. (Taiwan)
Active, not recruiting – verified September 2013
View full post on ClinicalTrials.gov: asthma | received in the last 14 days
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Enzyme in airway lining cells could hold key for asthma sufferers
News-Medical.net An enzyme known for its role in heart disease may well be a promising target to treat asthma. Researchers from the University of Iowa have found that the enzyme, called CaMKII, is linked to the harmful effects of oxidation in the respiratory tract … |
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University of Iowa team finds enzyme in airway lining cells could hold key for …
Newswise (press release) Newswise — An enzyme known for its role in heart disease may well be a promising target to treat asthma. Researchers from the University of Iowa have found that the enzyme, called CaMKII, is linked to the harmful effects of oxidation in the … |
View full post on asthma – Google News
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Group 2 innate lymphoid cells in lung inflammation.
Immunology. 2013 Jul 19;
Authors: Li BW, Hendriks RW
Abstract
Although allergic asthma is a heterogeneous disease, allergen-specific T helper 2 (Th2) cells producing the key cytokines involved in type 2 inflammation, IL-4, IL-5 and IL-13, are thought to play a major role in asthma pathogenesis. This model is challenged by the recent discovery of group 2 innate lymphoid cells (ILC2) that represent a critical innate source of type 2 cytokines. These ILC2 are activated by epithelial cell-derived cytokines, including IL-25 and IL-33, which have been implicated in the initiation of asthma. In this review, we will discuss recent studies supporting a significant role for ILC2 in lung inflammation, with special attention to allergen-induced asthma. This article is protected by copyright. All rights reserved.
PMID: 23866009 [PubMed – as supplied by publisher]
View full post on pubmed: asthma
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[Effect of peroxisome proliferator-activated receptor-gamma on proliferation of airway smooth muscle cells in mice with asthma].
Zhongguo Dang Dai Er Ke Za Zhi. 2013 Jul;15(7):583-7
Authors: Gu MX, Liu XC, Jiang L
Abstract
OBJECTIVE: To investigate the effects of peroxisome proliferator-activated receptor-gamma (PPAR?) agonist rosiglitazone on the expression of cyclin D1 in lung tissue, and the proliferation of airway smooth muscle cells (ASMCs) in mice with bronchial asthma.
METHODS: Thirty clean BALB/c mice were randomly divided into control group (n=10), asthma group (n=10), and rosiglitazone treatment group (n=10). A mouse model of asthma was established by ovalbumin (OVA) sensitization and challenge. The treatment group received rosiglitazone (5 mg/kg) by gavage 1 hour before each challenge and the control group received saline instead of OVA sensitization and challenge. Leukocytes and eosinophils in bronchoalveolar lavage fluid (BALF) were counted under a microscope. Airway structural changes were observed by hematoxylin-eosin staining. Protein and mRNA expression levels of cyclin D1 were measured by immunohistochemical staining and RT-PCR. Perimeter of the basement membrane (Pbm), total bronchial wall area (WAt), airway smooth muscle area (WAm), and number of nuclei in ASMCs (N) were determined using image analysis software, and WAt/Pbm, WAm/Pbm, and N/Pbm were calculated.
RESULTS: Compared with the control group, the asthma group showed significant increases in the total number of leukocytes and percentage of eosinophils in BALF, as well as in the mRNA and protein expression of cyclin D1, but changes in these indices were significantly reduced in the rosiglitazone treatment group (P<0.05). In addition, compared with the control group, the asthma group had significantly increased WAt/Pbm, WAm/Pbm, and N/Pbm, but rosiglitazone significantly decreased these ratios (P<0.05).
CONCLISONS: Rosiglitazone may delay the process of airway remodeling by inhibiting the proliferation of ASMCs, so it can be used for preventing and treating chronic asthma.
PMID: 23866284 [PubMed – in process]
View full post on pubmed: asthma
Condition: Asthma
Intervention:
Sponsors: University of Wisconsin, Madison; University of Wisconsin, Madison; National Institutes of Health (NIH)
Not yet recruiting – verified July 2013
View full post on ClinicalTrials.gov: asthma | received in the last 14 days
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IL-13 exposure enhances vitamin D-mediated expression of the human cathelicidin antimicrobial peptide-hCAP18/LL-37 in bronchial epithelial cells.
Infect Immun. 2012 Oct 8;
Authors: Schrumpf JA, van Sterkenburg MA, Verhoosel RM, Zuyderduyn S, Hiemstra PS
Abstract
Vitamin D is an important regulator of the expression of antimicrobial peptides, and vitamin D deficiency is associated with respiratory infections. Regulating expression of antimicrobial peptides such as the human cathelicidin antimicrobial peptide (hCAP)18/LL-37 by vitamin D in bronchial epithelial cells requires local conversion of 25(OH)vitaminD(3) (25D(3)) into its bioactive metabolite 1,25(OH)(2)vitaminD(3) (1,25D(3)) by CYP27B1. Low circulating vitamin D-levels in childhood asthma are associated with more severe exacerbations, which are often associated with infections. Atopic asthma is accompanied by Th2 driven inflammation mediated by cytokines such as IL-4 and IL-13, and the effect of these cytokines on vitamin D metabolism and hCAP-18/LL-37 expression is unknown. Therefore we investigated this in well-differentiated bronchial epithelial cells. To this end, cells were treated with IL-13 with and without 25D(3) and expression of hCAP18/LL-37, CYP27B1, the 1,25D(3) inactivating enzyme CYP24A1, and vitamin D receptor was assessed by quantitative PCR. We show that IL-13 enhances the ability of 25D(3) to increase expression of hCAP18/LL-37 and CYP24A1. In addition, exposure to IL-13 resulted in increased CYP27B1 expression, whereas VDR expression was not significantly affected. The enhancing effect of IL-13 on 25D(3)-mediated expression of hCAP18/LL-37 was further confirmed using SDS-PAGE Western Blot and immunofluorescence staining. In conclusion, we demonstrate that IL-13 induces vitamin D(-)dependent hCAP18/LL-37 expression, most likely by increasing CYP27B1. These data suggest that Th2 cytokines regulate the vitamin D metabolic pathway in bronchial epithelial cells.
PMID: 23045480 [PubMed – as supplied by publisher]
View full post on pubmed: asthma
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When good cells go bad, allergic asthma can develop
Pittsburgh Post Gazette "We know that recurrent infections of RSV that require hospitalization in early life increase the risk for asthma in adult life," said Anuradha Ray, who along with Prabir Ray is a Pitt doctor of medicine and immunology. They are co-senior authors of … |
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A2B Adenosine Receptor Expression by Myeloid Cells Is Proinflammatory in Murine Allergic-Airway Inflammation.
J Immunol. 2012 Sep 5;
Authors: Belikoff BG, Vaickus LJ, Sitkovsky M, Remick DG
Abstract
Asthma is a chronic condition with high morbidity and healthcare costs, and cockroach allergens are an established cause of urban pediatric asthma. A better understanding of cell types involved in promoting lung inflammation could provide new targets for the treatment of chronic pulmonary disease. Because of its role in regulating myeloid cell-dependent inflammatory processes, we examined A(2B) R expression by myeloid cells in a cockroach allergen model of murine asthma-like pulmonary inflammation. Both systemic and myeloid tissue-specific A(2B) R deletion significantly decreased pulmonary inflammatory cell recruitment, airway mucin production, and proinflammatory cytokine secretion after final allergen challenge in sensitized mice. A(2B) R deficiency resulted in a dramatic reduction on Th2-type airways responses with decreased pulmonary eosinophilia without augmenting neutrophilia, and decreased lung IL-4, IL-5, and IL-13 production. Chemokine analysis demonstrated that eotaxin 1 and 2 secretion in response to repeated allergen challenge is myeloid cell A(2B) R dependent. In contrast, there were no differences in the levels of the CXC chemokines keratinocyte-derived chemokine and MIP-2 in the myeloid cell A(2B) R-deficient mice, strengthening A(2B) R involvement in the development of Th2-type airways inflammation. Proinflammatory TNF-?, IFN-?, and IL-17 secretion were also reduced in systemic and myeloid tissue-specific A(2B) R deletion mouse lines. Our results demonstrate Th2-type predominance for A(2B) R expression by myeloid cells as a mechanism of development of asthma-like pulmonary inflammation.
PMID: 22956582 [PubMed – as supplied by publisher]
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The effect of unilateral adrenalectomy on transformation of adrenal medullary chromaffin cells in vivo: a potential mechanism of asthma pathogenesis.
PLoS One. 2012;7(9):e44586
Authors: Hu CP, Zou YQ, Feng JT, Li XZ
Abstract
BACKGROUND: Decreased epinephrine (EPI) is an important underlying factor of bronchoconstriction in asthma. Exogenous ?(2)-adrenergic receptor agonist is one of the preferred options to treat asthma. We previously showed that this phenomenon involved adrenal medullary chromaffin cell (AMCC) transformation to a neuron phenotype. However, the underlying molecular mechanism is not fully understood. To further explore this, an asthmatic model with unilateral adrenalectomy was established in this study.
METHODOLOGY/PRINCIPAL FINDINGS: Thirty-two rats were randomly into four groups (n?=?8 each) control rats (controls), unilateral adrenalectomy rats (surgery-control, s-control), asthmatic rats (asthma), unilateral adrenalectomy asthmatic rats (surgery-induced asthma, s-asthma). Asthmatic rats and s-asthmatic rats were sensitized and challenged with ovalbumin (OVA). The pathological changes in adrenal medulla tissues were observed under microscopy. EPI and its rate-limiting enzyme, phenylethanolamine N-methyl transferase (PNMT), were measured. Peripherin, a type III intermediate filament protein, was also detected in each group. The asthmatic rats presented with decreased chromaffin granules and swollen mitochondria in AMCCs, and the s-asthmatic rats presented more serious pathological changes than those in asthmatic rats and s-control rats. The expressions of EPI and PNMT in asthmatic rats were significantly decreased, as compared with levels in controls (P<0.05), and a further decline was observed in s-asthmatic rats (P<0.05). The expression of peripherin was higher in the asthmatic rats than in the controls, and the highest level was found in the s-asthmatic rats (P<0.05).
CONCLUSION/SIGNIFICANCE: Compared with asthmatic rats and s-control rats, the transformation tendency of AMCCs to neurons is more obvious in the s-asthmatic rats. Moreover, this phenotype alteration in the asthmatic rats is accompanied by reduced EPI and PNMT, and increased peripherin expression. This result provides further evidence to support the notion that phenotype alteration of AMCCs contributes to asthma pathogenesis.
PMID: 22957086 [PubMed – in process]
View full post on pubmed: asthma