Complement factor 3 mediates particulate matter-induced airway hyperresponsiveness. - Wikidata - awgldk - TriplyDB

Complement factor 3 mediates particulate matter-induced airway hyperresponsiveness.

Complement factor 3 mediates particulate matter-induced airway hyperresponsiveness.

http://www.wikidata.org/entity/Q39632141

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Lessons learned for the National Children's Study from the National Institute of Environmental Health Sciences/U.S. Environmental Protection Agency Centers for Children's Environmental Health and Disease Prevention Research.Complement mediators: key regulators of airway tissue remodeling in asthma Perspective: ambient air pollution: inflammatory response and effects on the lung's vasculature Particulate matter disrupts human lung endothelial barrier integrity via ROS- and p38 MAPK-dependent pathways Traffic-related air pollution and incident type 2 diabetes: results from the SALIA cohort study Serum amyloid A, properdin, complement 3, and toll-like receptors are expressed locally in human sinonasal tissue Air Pollution and Climate Change Effects on Allergies in the Anthropocene: Abundance, Interaction, and Modification of Allergens and Adjuvants.Regulation of COX-2 expression and IL-6 release by particulate matter in airway epithelial cells Particulate matter induces cardiac arrhythmias via dysregulation of carotid body sensitivity and cardiac sodium channels.Induced sputum proteome in healthy subjects and asthmatic patients Particulate matter-induced airway hyperresponsiveness is lymphocyte dependent A regulatory role for the C5a anaphylatoxin in type 2 immunity in asthma.Factor B of the alternative complement pathway regulates development of airway hyperresponsiveness and inflammation Interleukin 13- and interleukin 17A-induced pulmonary hypertension phenotype due to inhalation of antigen and fine particles from air pollution Disruption of the transcription factor Nrf2 promotes pro-oxidative dendritic cells that stimulate Th2-like immunoresponsiveness upon activation by ambient particulate matter.Early neoplastic progression is complement independent.Allergens induce enhanced bronchoconstriction and leukotriene production in C5 deficient mice.Downregulation of glutathione S-transferase pi in asthma contributes to enhanced oxidative stress An overlapping syndrome of allergy and immune deficiency in children Activation of C3a receptor is required in cigarette smoke-mediated emphysema Time to draw breath: asthma-susceptibility genes are identified.Properdin Contributes to Allergic Airway Inflammation through Local C3a Generation New insights into the role of the complement pathway in allergy and asthma.Particulate matter air pollution disrupts endothelial cell barrier via calpain-mediated tight junction protein degradation.Complement component 3C3 and C3a receptor are required in chitin-dependent allergic sensitization to Aspergillus fumigatus but dispensable in chitin-induced innate allergic inflammation.Complement activation pathways: a bridge between innate and adaptive immune responses in asthma.Murine lung responses to ambient particulate matter: genomic analysis and influence on airway hyperresponsiveness.Matrix metalloproteinase 8 contributes to solubilization of IL-13 receptor alpha2 in vivo.IL-13 receptor α2 contributes to development of experimental allergic asthma.Resistance of Mycoplasma pulmonis to complement lysis is dependent on the number of Vsa tandem repeats: shield hypothesis.A complex role for complement in allergic asthma.The role of complement in the diagnosis and management of allergic rhinitis and allergic asthma.Complement components as potential therapeutic targets for asthma treatment.Th17 cytokines are critical for respiratory syncytial virus-associated airway hyperreponsiveness through regulation by complement C3a and tachykinins.Old dogs-new tricks: immunoregulatory properties of C3 and C5 cleavage fragments.Design and characterization of a sequential cyclone system for the collection of bulk particulate matter.PM2.5-induced airway inflammation and hyperresponsiveness in NC/Nga mice.Effects of nanoparticles on lung physiology in the presence or absence of antigen.Complement-mediated regulation of the IL-17A axis is a central genetic determinant of the severity of experimental allergic asthma.Complement activation is critical to airway hyperresponsiveness after acute ozone exposure.

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P2860

Complement factor 3 mediates particulate matter-induced airway hyperresponsiveness.

http://www.wikidata.org/entity/Q39632141

description

2002 nî lūn-bûn

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2002年の論文

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2002年論文

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2002年論文

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2002年論文

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2002年論文

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2002年論文

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2002年论文

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2002年论文

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2002年论文

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name

Complement factor 3 mediates particulate matter-induced airway hyperresponsiveness.

@en

Complement factor 3 mediates particulate matter-induced airway hyperresponsiveness.

@nl

type

label

Complement factor 3 mediates particulate matter-induced airway hyperresponsiveness.

@en

Complement factor 3 mediates particulate matter-induced airway hyperresponsiveness.

@nl

prefLabel

Complement factor 3 mediates particulate matter-induced airway hyperresponsiveness.

@en

Complement factor 3 mediates particulate matter-induced airway hyperresponsiveness.

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American Journal of Respiratory Cell and Molecular Biology

P1476

Complement factor 3 mediates particulate matter-induced airway hyperresponsiveness.

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P2093

Brian Schofield

http://www.w3.org/2001/XMLSchema#string

Dianne M Walters

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Marsha Wills-Karp

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Patrick N Breysse

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P2860

Acute respiratory effects of particulate air pollution

Diesel exhaust particulate induces airway hyperresponsiveness in a murine model: essential role of GM-CSF

Differential susceptibility to ozone-induced airways hyperreactivity in inbred strains of mice

Pulmonary alveolar type II epithelial cells synthesize and secrete proteins of the classical and alternative complement pathways

Particulate air pollution and chronic respiratory disease.

Serum complement levels in children in communities with different levels of air pollution in Japan.

Ambient urban Baltimore particulate-induced airway hyperresponsiveness and inflammation in mice.

Interleukin-4 augments production of the third complement component by the alveolar epithelial cell line A549.

Complement factors C3a and C5a are increased in bronchoalveolar lavage fluid after segmental allergen provocation in subjects with asthma.

Inhalation of diesel exhaust enhances allergen-related eosinophil recruitment and airway hyperresponsiveness in mice.

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413-418

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10.1165/RCMB.4844

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4

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27

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2002-10-01T00:00:00Z

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11100117

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12356574

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