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Antigen inhaled

Holt PG, Britten D, Sedgwick JD Suppression of IgE responses by antigen inhalation Studies on the role of genetic and environmental factors. Immunology 1987 60 97-102. [Pg.43]

In short-term clinical trials, pretreatment with cromolyn or nedocromil blocks the bronchoconstriction caused by antigen inhalation, by exercise, by aspirin, and by a variety of causes of occupational asthma. This acute protective effect of a single treatment makes cromolyn useful for administration shortly before exercise or before unavoidable exposure to an allergen. [Pg.480]

Sedgwick, J.D. and Holt, P.G. (1985). Induction of IgE-secreting cells and IgE isotype-specific suppressor T cells in the respiratory lymph nodes of rats in response to antigen inhalation. Cell. Immunol. 94, 182-194. [Pg.51]

Two of the four patients showed inproved FEV,. Tracheal mucous velocity is decreased in asthmatics challenged with antigen. Inhalation of 0.5-1% FPL-55712 prevents the decrease in mucous velocity but does not inhibit the bronchospasm. Inhalation of LTC. or LTD. by normal subjects induces coughing which is blocked by aerosol FPL-55712. isi in Basenji-Greyhound dogs, the bronchospasm to inhaled citric acid is associated with increased plasma levels of SRS (but not histamine) and is partly blocked by FPL-55712. 1=2... [Pg.247]

Mouthon L, Khaled M, Cohen P, et al. Systemic small sized vessel vasculitis after massive antigen inhalation. Ann Rheum Dis 2001 60(9) 903-904. [Pg.653]

Cotton DJ, Bleeker-ER, Fisher SP, Graf PD, Gold WM, Nadel JA. Rapid shallow breathing after Ascaris suum antigen inhalation role of the vagus nerves. J Appl Physiol Respir Environ Exerc Physiol 1977 42 101-106. [Pg.623]

The first SRS-A antagonist, FPL-55712 (26) (149), was discovered before the stmctures of the leukotrienes were detemiined. Although this compound is relatively weak as an antagonist and suffers from a very short half-life in vivo, it played an important role both in leukotriene stmcture elucidation and as a model for later antagonists. In work stmcturaHy related to FPL-55712, LY-171883 was developed (27) (150). LY-171883 was evaluated in several clinical trials before development was stopped. Orally adrninistered, LY-171883 blocked slightly the response to aerosol LTD improved pulmonary function (FEV ) in mild asthmatics (151), decreased the sensitivity of asthmatics to cold air-induced bronchoconstriction (152), and significantly reduced the bronchoconstrictor response to inhaled antigen (153). However, in all these studies the beneficial effects were minimal. [Pg.445]

COPD is a chronic inflammatory disease that results from prolonged and repeated inhalation of particles and gases, chronic (or latent) infection or an interaction of these factors. In many cases, the inflammation persists even when the exposure (in most cases smoking) is stopped. Prominent among the infiltrating leukocytes are neutrophils, CD8+ lymphocytes (Co-receptor for the T-cell receptor. CD8+ is specific for the class IMHC protein. It is expressed on the surface of cytotoxic T-cells and natural killer cells.) and CD68+ monocytic cells (A lysosomal antigen. All cells that rich in... [Pg.363]

De Heer HJ. Hammad H. Soullie T. Hijdra D, Vos N, Willart MA. Hoogsteden HC. Lambrecht BN Essential role of lung plasmacytoid dendritic cells in preventing asthmatic reactions to harmless inhaled antigen. J Exp Med 2004 200 89-98. [Pg.39]

Asthma is characterized by inflammation, airway hyperresponsiveness (AHR), and airway obstruction. Inhaled antigens... [Pg.210]

The answer is d. (Katzung, pp 336-3373 The inhibitory effect of mediator release of cromolyn is cell specific In mast cells exposed to cromolyn, inhibition of the early response occurs to antigen challenge, while in eosinophils, it affects the late response, and in basophils it has almost no effect on mediator release. Cromolyn is effective in anti gen-induced asthma, occupation-exposure asthma, and in some cases of intrinsic asthma. Administration of cromolyn by inhalation is most effective in treating patients. [Pg.131]

Fujimaki, H., et al., Inhalation of diesel exhaust enhances antigen-specific IgE antibody production in mice, Toxicology. 116, 1-3, 227, 1997. [Pg.323]

Holt PG, Batty JE, Turner KJ Inhibition of specific IgE responses in mice by pre-exposure to inhaled antigen. Immunology 1981 42 409-417. [Pg.46]

Eisenbarth SC, Zhadkevich A, Ranney P, Herrick CA, Bottomly K IL-4-dependent Th2 collateral priming to inhaled antigens independent of Tolllike receptor 4 and myeloid differentiation factor 88. J Immunol 2004 172 4527-4534. [Pg.66]

Eisenbarth SC, Piggott DA, Huleatt JW, Visintin I, Herrick CA, Bottomly K Lipopolysaccharide-enhanced, toll-like receptor 4-dependent T-helper cell type 2 responses to inhaled antigen. J Exp Med 2002 196 1645-1651. [Pg.66]

He R, Oyoshi MK, Jin H, Geha RS Epicutaneous antigen exposure induces a Thl7 response that drives airway inflammation after inhalation challenge. Proc Natl Acad Sci USA 2007 104 15817-15822. [Pg.110]


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See also in sourсe #XX -- [ Pg.210 ]




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