Basophils mediator release

Schroeder JT, MacGlashan DW Jr. Lichtenstein LM Human basophils mediator release and cytokine production. Adv Immunol 2001 77 93-122. 

Hj antihistamines are the most commonly prescribed medications for AR. Hj antihistamines bind to and stabilize the Hj histamine receptor, thereby inhibiting mast cell and basophil mediator release and resulting in reduction of sneezing, itching, rhinorrhea, and ocular irritation. Antihistamines do not prevent histamine release, nor do they bind to already-released histamine. For this reason, maintenance therapy is considered optimal. However, antihistamines are also effective when taken on an as-needed basis.4,11,12 Antihistamines only minimally... 

Schleimer RP, Derse CP, Friedman B, Gillis S, Plant M, Lichtenstein LM, et al Regulation of human basophil mediator release by cytokines. I. Interaction with anti-inflammatory steroids. J Immunol 1989 143 1310-1327. 

Weber, M Uguccioni, M., Baggiolini, M Clark-Lewis, I., andDahinden, C. A. (1996) Deletion of the NH2-terminal residue converts monocyte chemotactic protein 1 from an activator of basophil mediator release to an eosinophil chemoattractant. J. Exp. Med. 183, 681-685. 

The pharmacologic effect of Hi antihistamines is to prevent histamine-Hi receptor interaction. Additionally, other receptors may be affected (Figure 13-3), antiinflammatory effects may occur, and mast cell and basophil mediator release is prevented. An increased luiderstanding of the pharmacologic mechanism has resulted in Hi antihistamines being reclassified as inverse agonists. 

A recent study by Brunner a al. (1993) has confirmed that mature human basophUs synthesize and release IL-4. For optimal secretion, priming with IL-3 for 18-48 h before activation with anti-IgE was required, although low amounts of IL-4 were occasionally detected following incubation with either IL-3 or anti-IgE alone. No spontaneous IL-4 production was detected, and other cytokines known to enhance basophil mediator release, namely IL-5, GM-CSF and nerve growth factor (NGF),... 

Shim JY, Kim BS, Cho SH, Min KU, Hong SJ Allergen-specific conventional immunotherapy decreases immunoglobulin E-mediated basophil histamine releasability. Clin Exp Allergy 2003 33 52-57. 

DW Jr, Bochner BS. Gillis S. Zsebo KM. Galli SJ, Lichtenstein LM The human recombinant c-kit 49 receptor ligand, rhSCF, induces mediator release from human cutaneous mast cells and enhances IgE-dependent mediator release from both skin mast cells and peripheral blood basophils. J Immunol 1992 149 599. sO... 

Stellato C, de Crescenzo G, Patella V, Mastronardi P. Mazzarella B, Marone G Human basophil/mast cell releasability. XL Heterogeneity of the effects of contrast media on mediator release. J Allergy Clin Immunol 1996 97 838. 

The detection of reactions mediated by specific IgE to agents triggering anaphylaxis may be achieved by means of serological methods serum-specific IgE, or by means of cellular tests which determine the release of basophil mediators (leukotrienes and histamine) or by means of the analysis of basophil expression markers, a technique known as the basophil activation test (BAT). 

No increase of plasma leukotrienes after RCM administration Mast cell mediator release correlates with severity of reaction, positive basophil activation test to RCM in patients... 

Omalizumab is a recombinant humanized monoclonal anti-IgE antibody that inhibits binding of IgE to receptors on mast cells and basophils, resulting in the inhibition of mediator release and attenuation of the early- and late-phase allergic response. It may be a treatment option for moderate to severe persistent asthmatics 12 years of age or older whose asthma is not controlled by inhaled corticosteroids and who have a positive skin test or in vitro reactivity to perennial allergens.37 Omalizumab significantly decreases inhaled corticosteroid use, number and length of exacerbations, and increases asthma-related quality of life.37... 

Clinical trials have indicated that omalizumab, a recombinant humanized monoclonal IgE antibody approved for use in moderate to severe persistent asthma in patients with reactivity to a perennial allergen, is effective in the treatment of SAR.25-27 Omalizumab inhibits the binding of IgE to mast cell and basophil receptors, resulting in a reduction of allergic mediator release.25 Additionally, serum free IgE levels are decreased.2 27 In SAR patients, omalizumab improves quality of life and nasal symptoms and reduces antihistamine needs. The most effective dose in SAR appears to be omalizumab 300 mg administered subcutaneously every 3 to 4 weeks depending on baseline IgE levels.26,27... 

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. 

Antigen (hapten or complete) via IgE mediated release of histsimine from basophils and tissue mast cells (complement independent). ... 

Omalizumab is an anti-IgE recombinant humanized monoclonal antibody that is approved for the treatment of allergic asthma in adult and adolescent patients whose symptoms are refractory to inhaled corticosteroids (see Chapter 20). The antibody blocks the binding of IgE to the high-affinity Fes receptor on basophils and mast cells, which suppresses IgE-mediated release of type I allergy mediators such as histamine and leukotrienes. Total serum IgE levels may remain elevated in patients for up to 1 year after administration of this antibody. 

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