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Chapter 11 : Atopic and Anaphylactic Reactions (Allergy)

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Abstract:

The term allergy is now mostly used for atopic or anaphylactic reactions but is also used as a general term for reactions of discomfort of unknown origin. The effects produced by atopic or anaphylactic reactions are the result of a two-phase system initiated by mediators that are released by the reaction of antigen with effector cells passively sensitized by immunoglobulin E (IgE) antibody. The antigens that induce and elicit allergic reactions, allergens, have no unique features to distinguish them as a subset of antigenic molecules. Anaphylactic reactions to drugs are increasingly common and are discussed in this chapter. Reaginic antibody has a special ability to bind to skin or other tissues. The term atopic reagin was adopted to refer to the particular tissue-fixing antibody found in the serum of patients with hay fever and asthma. Anaphylaxis is edema and congestion due to vasodilation and increased vascular permeability that may occur locally (cutaneous anaphylaxis) or a systemic shock reaction (systemic anaphylactic shock) due to massive vasodilation and loss of blood pressure. Atopic eczema is morphologically more like a reaction of cellular or delayed-type hypersensitivity but is discussed in the chapter because of its association with atopic conditions. Therapeutic procedures to prevent or decrease atopic reactions may be applied at the various levels of the reaction: contact with antigen, IgE receptor, sensitivity of the mast cell to stimulation, degranulation of mast cell, mast cell mediator activity, sensitivity of end-organ cell, autonomic nervous system balance, and emotional state of the reactive individual.

Citation: Sell S. 2001. Atopic and Anaphylactic Reactions (Allergy), p 359-400. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch11
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Figure 11.1

Atopic or anaphylactic reactions. Reaction of antigen (allergen) with reaginic antibody (IgE) fixed to effector (mast) cells causes release of pharmacologically active agents stored in cytoplasmic granules (degranulation of mast cells). These released mediators, primarily histamine and serotonin, cause contraction of endothelial cells and bronchial smooth cells and produce edema and bronchoconstriction. Cell membrane-associated arachidonic acids also released from mast cells are converted to other inflammatory mediators—leukotrienes and prostaglandins— which are responsible for later stages of the reactions. The acute effects are termed anaphylactic; the more chronic effects, atopic.

Citation: Sell S. 2001. Atopic and Anaphylactic Reactions (Allergy), p 359-400. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch11
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Image of Figure 11.2
Figure 11.2

Immunotherapy of atopic allergies. Immunotherapy of atopic reactions by injection of the specific allergen is known to be effective, particularly for alleviation of the symptoms of hay fever. The mechanism of reduction of allergic symptoms is unclear. At least four possibilities are (1) hyposensitization, production of IgG blocking antibody; (2) desensitization, consumption of IgE antibody by repeated small doses of allergen; (3) tolerance, a loss or significant decrease in IgE antibody production to the allergen; and (4) production of suppressor T cells specific for IgE B cells. Another possible mechanism not yet identified as being due to specific immunotherapy is the production of nonspecific IgE that might block the effector cell receptors for IgE allergen-specific antibody.

Citation: Sell S. 2001. Atopic and Anaphylactic Reactions (Allergy), p 359-400. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch11
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Figure 11.3

Pharmacologic control of atopic-anaphylactic reactions. Effects of atopic or anaphylactic reactions are mediated by biologically active mediators released by mast cells that affect end-organ smooth muscle. The amount of mediators released and reactivity of end organ to mediators are controlled by cellular messenger systems. Mast cell sensitivity depends on the amount of reaginic antibody sensitizing the cell and on relative intracellular levels of cyclic AMP (cAMP) and cyclic GMP (cGMP). cAMP and cGMP levels are controlled by adrenergic receptors. Stimulation of α-receptors causes a decrease of cAMP, an increase of cGMP, and increased reactivity; stimulation of β-receptors activates adenyl cyclase and produces increased cAMP, decreased cGMP, and decreased reactivity. A similar mechanism is operative for end-organ smooth muscle. The degree of mast cell and end-organ excitability may be modified by pharmacologic agents that operate through adrenergic or autonomic systems. cAMP is broken down to 5ʹ-AMP by phosphodiesterase, so inhibition of phosphodiesterase activity by methylxanthines increases cAMP and decreases sensitivity of mast cell and end organs. Epinephrine stimulates both α- and β-receptors but generally has the pronounced ability to reverse acute allergic reactions at the usual therapeutic dose. Disodium cromoglycate and diethylcarbamazine inhibit histamine release from mast cells. Excitation of end organs is controlled by a balance of the autonomic nervous system. Parasympathetic effects are similar to anaphylactic effects (bronchial constriction, endothelial contraction, increased peristalsis, dilatation of the bladder sphincter, and so on), whereas sympathetic effects are the opposite. Certain situations may result in temporary imbalance of these systems and increase severity of reaction, as in patients with chronic asthma.

Citation: Sell S. 2001. Atopic and Anaphylactic Reactions (Allergy), p 359-400. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch11
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Image of Figure 11.4
Figure 11.4

Levels of possible therapeutic or preventive intervention in allergy. (1) Avoidance of contact with the allergen is the most effective means of preventing atopic allergic reactions, thus removing antigen activation of IgE receptors. Avoidance is not always feasible and other methods must be used. (2) The amount of IgE antibody may be reduced by hyposensitization, desensitization, or tolerance as the result of injection therapy (see above) or by treatment with humanized anti- IgE antibody. (3) The sensitivity of the mast cell upon reaction of IgE receptors with allergen may be controlled by the amount of cAMP available. This level may be affected by drugs as indicated in Fig. 11.3. If mast cell cAMP can be increased by the methods indicated above, the extent of mast cell mediator release upon reaction of sensitized cells with allergen may be decreased and atopic symptoms controlled. (4) Two drugs, diethylcarbamazine and disodium chromoglycate (cromines), significantly decrease the release of mediators from mast cells upon contact with allergen. (5) The effect of mast cell mediators may be partially controlled by drugs that interfere with histamine activity (antihistamines). The fact that antihistamines are only partially effective in decreasing atopic symptoms indicates that other mediators play an important role. (6) The rapidly increasing understanding of the role of arachidonic acid metabolites in allergic reactions could well lead to more effective therapy. In particular, nonsteroidal anti-inflammatory agents or agents that could control the balance of effects of prostaglandin E (bronchodilation) and prostaglandin F (bronchoconstriction) could have great potential beneficial effects. Steroids are used only as a last resort. (7) The sensitivity of the end organ (smooth muscle) to atopic mediators also depends upon β-adrenergic control of cellular cAMP levels. If end-organ cAMP can be increased, then atopic symptoms should be decreased. (8) Sympathetic stimulation or parasympathetic blockade may also have a significant beneficial effect upon atopic reactions through the effect of the autonomic nervous system upon organ excitability (Fig. 11.3). (9) It is well known that severity of atopic reactions (particularly asthma) depends upon the emotional state of the individual. Anxious or insecure patients have more severe symptoms than more secure or stable patients. Thus, the emotional state of the reactive individual should be evaluated and treated with psychotherapy, if necessary. Other experimental agents that block cytokines, chemokines, cell adhesion, signal transduction, or nuclear transcription may affect different stages of IgE production or IgE-mediated reactions.

Citation: Sell S. 2001. Atopic and Anaphylactic Reactions (Allergy), p 359-400. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch11
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Image of Figure 11.5
Figure 11.5

Allergic bronchopulmonary aspergillosis. Anaphylactic reaction to Aspergillus infection in the bronchi causes secondary pathologic effects leading to repeated asthmatic attacks and plugging of airways with thick mucus plugs.

Citation: Sell S. 2001. Atopic and Anaphylactic Reactions (Allergy), p 359-400. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch11
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Tables

Generic image for table
Table 11.1

Allergic symptoms and receptors: five organ systems

Citation: Sell S. 2001. Atopic and Anaphylactic Reactions (Allergy), p 359-400. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch11
Generic image for table
Table 11.2

Some properties of highly purified short ragweed (Ambrosia artemisifolia) antigens

Citation: Sell S. 2001. Atopic and Anaphylactic Reactions (Allergy), p 359-400. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch11
Generic image for table
Table 11.3

Passive transfer of antibody-mediated skin reactions

Citation: Sell S. 2001. Atopic and Anaphylactic Reactions (Allergy), p 359-400. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch11
Generic image for table
Table 11.4

Factors believed to predispose to development of allergic disease a

Citation: Sell S. 2001. Atopic and Anaphylactic Reactions (Allergy), p 359-400. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch11
Generic image for table
Table 11.5

Agents causing asthma in selected occupations a

Citation: Sell S. 2001. Atopic and Anaphylactic Reactions (Allergy), p 359-400. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch11
Generic image for table
Table 11.6

Calendar of some common airborne allergens in a temperate climate (England) a

Citation: Sell S. 2001. Atopic and Anaphylactic Reactions (Allergy), p 359-400. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch11
Generic image for table
Table 11.7

Mediators and symptoms of allergic rhinitis a

Citation: Sell S. 2001. Atopic and Anaphylactic Reactions (Allergy), p 359-400. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch11
Generic image for table
Table 11.8

Some purified water-soluble food antigens a

Citation: Sell S. 2001. Atopic and Anaphylactic Reactions (Allergy), p 359-400. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch11
Generic image for table
Table 11.9

Some arthropod allergens and common proteins of known sequence similarity or antigen cross-reactivity a

Citation: Sell S. 2001. Atopic and Anaphylactic Reactions (Allergy), p 359-400. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch11
Generic image for table
Table 11.10

Major urticarial and angioedematous reactions induced by physical stimuli

Citation: Sell S. 2001. Atopic and Anaphylactic Reactions (Allergy), p 359-400. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch11
Generic image for table
Table 11.11

Pharmacologic agents used in treatment of mast cell-mediated allergic reactions

Citation: Sell S. 2001. Atopic and Anaphylactic Reactions (Allergy), p 359-400. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch11
Generic image for table
Table 11.12

Current therapies for atopic diseases a

Citation: Sell S. 2001. Atopic and Anaphylactic Reactions (Allergy), p 359-400. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch11

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