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Epithelial cells airway, cytokine production

B. The Role of Airway Epithelial Cells in Cytokine Production... [Pg.124]

Kato A, Favoreto S Jr, Avila PC, Schleimer RP TLR3- and Th2 cytokine-dependent production of thymic stromal lymphopoietin in human airway epithelial cells. J Immunol 2007 179 1080-1087. [Pg.41]

Until recently, epithelial cells were considered to function solely as the ciliated barrier lining in the airways and as conduits for gas exchange at the air/blood interphase. As techniques have improved to isolate and culture these cells and measure their gene products, it has become clear that they have a key role in lung defense and repair. Epithelial cells secrete a number of anti-microbial compounds and immunoregulatory cytokines [52], and are also capable of ingesting and killing bacteria [53],... [Pg.311]

Ritz SA, Wan J, Diaz-Sanchez D (2007) Sulforaphane-stimulated phase II enzyme induction inhibits cytokine production by airway epithelial cells stimulated with diesel extractAm J Physiol 292(1 ) L33-L39. [Pg.256]

Nearly all cells express kinin receptors that mediate the activities of both bradykinin and kallidin. The activation of these G-protein coupled receptors causes relaxation of venular smooth muscle and hypotension, increased vascular permeability, contraction of smooth muscle of the gut and airway leading to increased airway resistance, stimulation of sensory neurons, alteration of ion secretion of epithelial cells, production of nitric oxide, release of cytokines from leukocytes, and the production of eicosanoids from various cell types [11,12]. Because of this broad spectrum of activity, kinins have been implicated as an important mediator in many pathophysiologies including pain, sepsis, asthma, rheumatoid arthritis, pancreatitis, and a wide variety of other inflammatory diseases. Moreover, a recent report demonstrated that bradykinin B2 receptors on the surface of human fibroblasts were upregulated three-fold beyond normal in patients with Alzheimer s disease, implicating bradykinin as a participant in the peripheral inflammatory processes associated with that disease [13]. [Pg.121]

Airway epithelia and alveolar macrophages constitutively express neurotrophins, and under normal conditions, low levels of neurotrophins are produced. However, in allergic inflammation, these levels rise considerably in atopic patients. After inhalation of an allergen by asthmatic patients, there are high concentrations of NGF, NT-3 and BDNF. The cellular sources of the increased neurotrophins include invading leukocytes and resident lung cells. Inflammatory cytokines, IL-1 and TNF-a stimulate epithelial neurotrophin expression. The increased production of neurotrophins... [Pg.139]

EM also has a motilin-like stimulating activity on gastrointestinal smooth muscles [39]. Therefore, the inhibitory effect on cytokine expression in human cells summarized here may be a third bioactivity of the macrolide antibiotic. We recently reported that some of these derivatives have inhibitory effect on IL-8 production by human airway epithelial cells [72], These analogues also showed inhibitory action on the activation of NFkB and AP-1 assessed by EMSA (M. Desaki etal., unpublished observations, January 2001). Characterization of the chemical structure responsible for its potential would be important to pursue and further investigation for the molecular mechanism would be necessary for a possible new type of anti-inflammatory agent. [Pg.552]

Boland S, Baeza-Squiban A, Fournier T et al (1999) Diesel exhaust particles are taken up by human airway epithelial cells in vitro and alter cytokine production. Am J Physiol 276 L604-L613... [Pg.445]

Canadian Medical Association (CMA) (2(X)8) No breathing room National illness costs of air pollution. http //www.cma.ca/multimedia/cma/content Images/Inside cma/Office Public Health/ICAP/CMA ICAP sum e.pdf. Accessed 29 August 2009 Carter JD, Ghio AJ, Saraet JM et al (1997) Cytokine production by human airway epithelial cells after exposure to an air pollution particle is metal-dependent. Toxicol Appl Pharmacol 146 180-188... [Pg.445]

Carter JD, Ghio AJ, Samet JM, Devlin RB (1997) Cytokine production by human airway epithelial cells after exposure to an air pollution particles is metal-dependent. Toxicol Appl Pharmacol 146 180-188... [Pg.568]

Given that most adolescents and adults are chronically colonized with P. aeruginosa, attention has logically been focused on determining the role of this bacterium and its products in the production of pro-inflammatory cytokines and chemokines in normal and cystic fibrosis airway epithelia, and in epithelial cell lines established from patients with cystic fibrosis, or all lines which model the mutation of the CFTR. [Pg.124]


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See also in sourсe #XX -- [ Pg.548 ]




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