Condition: Asthma
Intervention:
Sponsor: University of California, San Francisco
Not yet recruiting – verified June 2016
View full post on ClinicalTrials.gov: asthma | received in the last 14 days
Strategy for depleting immune cells implicated in asthma-associated inflammation – Science Daily
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Strategy for depleting immune cells implicated in asthma-associated inflammation
Science Daily Patients with asthma have chronic lung inflammation that results in sporadic narrowing of the airways and difficulty breathing. Symptoms and severity are variable among individuals; however, the cells and inflammatory factors that trigger asthmatic … |
View full post on asthma – Google News
Asthma Caused by Dust Mites May Damage Lung Cells – Healthline
Healthline |
Asthma Caused by Dust Mites May Damage Lung Cells
Healthline This ability, say researchers, may influence the severity of an asthma attack. “In addition to activation of immune responses, patients' DNA repair capacity may affect disease progression,” said Engelward. The results of the study were published May 1 … |
View full post on asthma – Google News
In Vitro Evaluation of a Novel Drug on Airway Epithelial Cells Obtained From Participants With Severe Asthma
Condition: Asthma
Intervention: Drug: VR588
Sponsors: Imperial College London; Vectura Limited
Recruiting – verified February 2016
View full post on ClinicalTrials.gov: asthma | received in the last 14 days
Epigenetic Dysfunction in Turner Syndrome Immune Cells.
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Related Articles |
Epigenetic Dysfunction in Turner Syndrome Immune Cells.
Curr Allergy Asthma Rep. 2016 May;16(5):36
Authors: Thrasher BJ, Hong LK, Whitmire JK, Su MA
Abstract
Turner syndrome (TS) is a chromosomal condition associated with partial or complete absence of the X chromosome that involves characteristic findings in multiple organ systems. In addition to well-known clinical characteristics such as short stature and gonadal failure, TS is also associated with T cell immune alterations and chronic otitis media, suggestive of a possible immune deficiency. Recently, ubiquitously transcribed tetratricopeptide repeat on the X chromosome (UTX), a histone H3 lysine 27 (H3K27) demethylase, has been identified as a downregulated gene in TS immune cells. Importantly, UTX is an X-linked gene that escapes X-chromosome inactivation and thus is haploinsufficient in TS. Mice with T cell-specific UTX deficiency have impaired clearance of chronic viral infection due to decreased frequencies of T follicular helper (Tfh) cells, which are critical for B cell antibody generation. In parallel, TS patients have decreased Tfh frequencies in peripheral blood. Together, these findings suggest that haploinsufficiency of the X-linked UTX gene in TS T cells underlies an immune deficit, which may manifest as increased predisposition to chronic otitis media.
PMID: 27039394 [PubMed – in process]
View full post on pubmed: asthma
Mesenchymal stem cells induce suppressive macrophages through phagocytosis in a mouse model of asthma.
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Mesenchymal stem cells induce suppressive macrophages through phagocytosis in a mouse model of asthma.
Stem Cells. 2016 Feb 17;
Authors: Braza F, Dirou S, Forest V, Sauzeau V, Hassoun D, Chesné J, Cheminant-Muller MA, Sagan C, Magnan A, Lemarchand P
Abstract
Mesenchymal stem cell (MSC) immunosuppressive functions make them attractive candidates for anti-inflammatory therapy in allergic asthma. However the mechanisms by which they ensure therapeutic effects remain to be elucidated. In an acute mouse model of house dust mite (Der f)-induced asthma, one i.v. MSC injection was sufficient to normalize and stabilize lung function in Der f-sensitized mice as compared to control mice. MSC injection decreased in vivo airway responsiveness and decreased ex vivo carbachol-induced bronchial contraction, maintaining bronchial expression of the inhibitory type 2 muscarinic receptor. To evaluate in vivo MSC survival, MSCs were labelled with PKH26 fluorescent marker prior to i.v. injection, and 1 to 10 days later total lungs were digested to obtain single-cell suspensions. 91.5?±?2.3% and 86.6?±?6.3% of the recovered PKH26(+) lung cells expressed specific macrophage markers in control and Der f mice respectively, suggesting that macrophages had phagocyted in vivo the injected MSCs. Interestingly, only PKH26(+) macrophages expressed M2 phenotype, while the innate PKH26(-) macrophages expressed M1 phenotype. Finally, the remaining 0.5% PKH26(+) MSCs expressed 10 to 100 fold more COX-2 than before injection, suggesting in vivo MSC phenotype modification. Together, the results of this study indicate that MSCs attenuate asthma by being phagocyted by lung macrophages, which in turn acquire a M2 suppressive phenotype. This article is protected by copyright. All rights reserved.
PMID: 26891455 [PubMed – as supplied by publisher]
View full post on pubmed: asthma
HB-EGF-Promoted Airway Smooth Muscle Cells and Their Progenitor Migration Contribute to Airway Smooth Muscle Remodeling in Asthmatic Mouse.
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HB-EGF-Promoted Airway Smooth Muscle Cells and Their Progenitor Migration Contribute to Airway Smooth Muscle Remodeling in Asthmatic Mouse.
J Immunol. 2016 Jan 29;
Authors: Wang Q, Li H, Yao Y, Lu G, Wang Y, Xia D, Zhou J
Abstract
The airway smooth muscle (ASM) cells’ proliferation, migration, and their progenitor’s migration are currently regarded as causative factors for ASM remodeling in asthma. Heparin-binding epidermal growth factor (HB-EGF), a potent mitogen and chemotactic factor, could promote ASM cell proliferation through MAPK pathways. In this study, we obtained primary ASM cells and their progenitors from C57BL/6 mice and went on to explore the role of HB-EGF in these cells migration and the underlying mechanisms. We found that recombinant HB-EGF (rHB-EGF) intratracheal instillation accelerated ASM layer thickening in an OVA-induced asthmatic mouse. Modified Boyden chamber assay revealed that rHB-EGF facilitate ASM cell migration in a dose-dependent manner and ASM cells from asthmatic mice had a greater migration ability than that from normal counterparts. rHB-EGF could stimulate the phosphorylation of ERK1/2 and p38 in ASM cells but further migration assay showed that only epidermal growth factor receptor inhibitor (AG1478) or p38 inhibitor (SB203580), but not ERK1/2 inhibitor (PD98059), could inhibit rHB-EGF-mediated ASM cells migration. Actin cytoskeleton experiments exhibited that rHB-EGF could cause actin stress fibers disassembly and focal adhesions formation of ASM cells through the activation of p38. Finally, airway instillation of rHB-EGF promoted the recruitment of bone marrow-derived smooth muscle progenitor cells, which were transferred via caudal vein, migrating into the airway from the circulation. These observations demonstrated that ASM remodeling in asthma might have resulted from HB-EGF-mediated ASM cells and their progenitor cells migration, via p38 MAPK-dependent actin cytoskeleton remodeling.
PMID: 26826248 [PubMed – as supplied by publisher]
View full post on pubmed: asthma
Nuclear factor-?B mediates the phenotype switching of airway smooth muscle cells in a murine asthma model.
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Nuclear factor-?B mediates the phenotype switching of airway smooth muscle cells in a murine asthma model.
Int J Clin Exp Pathol. 2015;8(10):12115-28
Authors: Qiu C, Zhang J, Su M, Fan X
Abstract
Airway smooth muscle cells (ASMCs) phenotype modulation, characterized by reversible switching between contractile and proliferative phenotypes, is considered to contribute to airway proliferative diseases such as allergic asthma. Nuclear Factor-?B (NF-?B) has been reported as a key regulator for the occurrence and development of asthma. However, little is known regarding its role in ASM cell phenotypic modulation. To elucidate the role of NF-?B in regulating ASM cells phenotypic modulation, we investigated the effects of NF-?B on ASM cells contractile marker protein expression, and its impact on proliferation and apoptosis. We found that chronic asthma increased the activation of NF-?B in the primary murine ASM cells with a concomitant marked decrease in the expression of contractile phenotypic marker protein including smooth muscle alpha-actin (?-SMA). Additionally, we used the normal ASM cells under different processing to build the phenotype switching when we found the activation of NF-?B. Meanwhile, the expression of ?-SMA in asthma was significantly increased by the NF-?B blocker. NF-?B blocker also suppressed asthma mouse ASM cell proliferation and promoted apoptosis. These findings highlight a novel role for the NF-?B in murine ASM cell phenotypic modulation and provide a potential target for therapeutic intervention for asthma.
PMID: 26722396 [PubMed – in process]
View full post on pubmed: asthma
Apigenin inhibits TGF-?1-induced proliferation and migration of airway smooth muscle cells.
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Apigenin inhibits TGF-?1-induced proliferation and migration of airway smooth muscle cells.
Int J Clin Exp Pathol. 2015;8(10):12557-63
Authors: Li LH, Lu B, Wu HK, Zhang H, Yao FF
Abstract
It is well known that the proliferation and migration of ASM cells (ASMCs) plays an important role in the pathogenesis of airway remodeling in asthma. Previous studies reported that apigenin can inhibit airway remodeling in a mouse asthma model. However, its effects on the proliferation and migration of ASMCs in asthma remain unknown. Therefore, the aim of our present study was to investigate the effects of apigenin on ASMC proliferation and migration, and explore the possible molecular mechanism. We found that apigenin inhibited transforming growth factor-?1 (TGF-?1)-induced ASMC proliferation. The cell cycle was blocked at G1/S-interphase by apigenin. It also suppressed TGF-?1-induced ASMCs migration. Furthermore, apigenin inhibited TGF-?1-induced Smad 2 and Smad 3 phosphorylation in ASMCs. Taken together, these results suggested that apigenin inhibited the proliferation and migration of TGF-?1-stimulated ASMCs by inhibiting Smad signaling pathway. These data might provide useful information for treating asthma and show that apigenin has potential for attenuating airway remodeling.
PMID: 26722444 [PubMed – in process]
View full post on pubmed: asthma
Carbon nanotubes found in lung cells of all asthma patients – Science Recorder
Science Recorder |
Carbon nanotubes found in lung cells of all asthma patients
Science Recorder The scientists studied lung cells from 69 randomly selected asthma patients aged two to 17 who receive routine fiber-optic bronchoscopy as part of their treatment. Particulate matter was found in the alveolar macrophage cells–the cells that prevent … Carbon nanotubes found in children's lungs for the first time Carbon Nanotubes Found for the First Time Ever in Human Lungs of Asthmatic … Carbon nanotubes found in children's lungs in Paris |
View full post on asthma – Google News