Page 973 - Veterinary Immunology, 10th Edition
P. 973

chemokines from many different cell types. It stimulates the
  VetBooks.ir                It is probably therefore a major contributor to the development of
                           production of eosinophils. It acts on sensory neurons to induce itch.

                                                 type I hypersensitivity.


                  IL-33 promotes mast cell adherence to blood vessel walls,
               increases their IgE-mediated degranulation, and enhances their
               cytokine production. Additionally, it induces the release of

               leukotrienes and cytokines, and as a result, can trigger acute allergic
               attacks in the absence of antigen. Similarly, it stimulates basophils
               to produce their Th2 cytokines. As a result of this enhanced

               cytokine release, IL-33 recruits and activates eosinophils resulting
               in eosinophil infiltration (see also Chapter 28). IL-33 binds to
               sensory neurons triggering intense pruritus and enhancing
               scratching behavior. Levels of IL-33 are elevated in the blood of
               humans suffering anaphylactic shock, in helminth infections, in

               atopic human tissues, and in the lungs of those with severe asthma.



               Regulation of Mast Cell Degranulation


               Mast cells express two catecholamine receptors called the α- and β-
               adrenoceptors. These receptors have opposing effects. Molecules
               that stimulate the α-adrenoceptors (such as norepinephrine and
               phenylephrine) or block the β-adrenoceptors (such as propranolol)
               enhance mast cell degranulation (Table 29.2). Conversely,

               molecules that stimulate the β receptors or block the α receptors
               inhibit mast cell degranulation. β-stimulators include isoproterenol,
               epinephrine, and salbutamol and are widely used in the treatment

               of allergies. β-receptor blockers enhance mast cell degranulation
               and promote allergies. Some respiratory pathogens such as
               Bordetella pertussis and Haemophilus influenzae can cause β-blockade.
               As a result, the airways of infected animals are more likely to
               become inflamed because of mast cell degranulation. These

               infections may also predispose animals to the development of
               respiratory allergies.



               TABLE 29.2
               Effects of Stimulating α- and β-Adrenoceptors



                System      α Receptor Stimulation or β Blockade β Receptor Stimulation or α Blockade



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