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Chapter 26 : Allergic Bronchopulmonary Aspergillosis

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Allergic Bronchopulmonary Aspergillosis, Page 1 of 2

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Abstract:

The chapter provides an overview on allergic bronchopulmonary aspergillosis (ABPA). Recombinant DNA technology has allowed for identification and production of many allergens that may play a role in pathogenesis and find use in diagnostic testing. A role for the anti-inflammatory cytokine IL-10 in protection against has been shown in experimental murine ABPA, and a broader role for IL-10 as an anti-inflammatory regulatory cytokine in lung inflammation in both asthma and cystic fibrosis (CF) is likely. A critical immunogenetic feature of ABPA is inheritance and expression of certain major histocompatibility complex (MHC) alleles that act to regulate CD4 Tcell responses to . Susceptibility to ABPA appears to be independently increased by mutations in the CF transmembrane conductance regulator (CFTR) gene. Oral glucocorticoids are an effective first-line treatment for ABPA and appear as effective in CF as they are in asthmatic APBA. Serum IgE levels are a useful way to follow a patient’s response to pharmacotherapy and guide steroid dosing. Reduction of fungal antigenic burden with antifungal agents is a logical addition to the ABPA treatment program. This approach has been validated by administering itraconazole to asthmatic patients with ABPA in double-blind, placebocontrolled, randomized multicenter studies. Measures which may contribute to remission and/or prevent exacerbation include avoidance of outdoor exposures, such as turned compost heaps or moldy hay piles, examination and cleaning of humid moldy indoor areas, and perhaps use of HEPA filters. Measurement of indoor fungal spore counts may be helpful in identifying occult exposure.

Citation: Moss R. 2009. Allergic Bronchopulmonary Aspergillosis, p 333-350. In Latgé J, Steinbach W (ed), and Aspergillosis. ASM Press, Washington, DC. doi: 10.1128/9781555815523.ch26

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Allergic Bronchopulmonary Aspergillosis
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Major Histocompatibility Complex
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Adaptive Immune System
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Tumor Necrosis Factor alpha
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Figure 1.

Immunopathogenesis of ABPA. In this schematized hypothesis, hyphal growth of in the airways triggers innate defenses via pattern recognition receptors, such as Toll-like receptors 2 and 4 (TLR2/4), on dendritic cells (DC) and/or pulmonary macrophages (AM). Penetration of antigens is enhanced by epithelial cell activation and shedding induced by proteases. Secretion of chemokines, particularly CCL17 (TARC), from DC stimulated by hyphal forms of results in attraction and activation of T-cell and macrophage subsets via their surface CCR4 receptors. Activated regulatory T cells and Th2 cells dampen Th1 responses, while activated Th2 cells secrete sentinel cytokines IL-4, IL-13, and IL-5, stimulating B cells, airway hyperreactivity and remodeling, and eosinophils, respectively. IL-4 receptors on B cells drive differentiation to IgE-secreting plasmacytes. IgE antibodies arm effector cells, such as mast cells and basophils, to activate and degranulate in the presence of allergens that cross-link their surface-bound IgE, releasing mediators such as histamine and sulfidoleukotrienes. Eosinophils release toxic exoproducts, such as major basic protein, that result in inflammatory tissue damage. Macrophage-mediated fungal killing may also be inhibited by TARC-mediated suppression of Th1 cytokines, such as tumor necrosis factor alpha (TNF-α) and IL-12. Lines with blunted ends indicate inhibition, and lines with arrowed ends indicate activation. From Hartl et al. (2006) with permission of the author and publisher.

Citation: Moss R. 2009. Allergic Bronchopulmonary Aspergillosis, p 333-350. In Latgé J, Steinbach W (ed), and Aspergillosis. ASM Press, Washington, DC. doi: 10.1128/9781555815523.ch26
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Tables

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Table 1.

Pulmonary diseases caused by species

Citation: Moss R. 2009. Allergic Bronchopulmonary Aspergillosis, p 333-350. In Latgé J, Steinbach W (ed), and Aspergillosis. ASM Press, Washington, DC. doi: 10.1128/9781555815523.ch26
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Table 2.

Fungi other than associated with allergic bronchopulmonary disease

Citation: Moss R. 2009. Allergic Bronchopulmonary Aspergillosis, p 333-350. In Latgé J, Steinbach W (ed), and Aspergillosis. ASM Press, Washington, DC. doi: 10.1128/9781555815523.ch26
Generic image for table
Table 3.

Allergens of

Citation: Moss R. 2009. Allergic Bronchopulmonary Aspergillosis, p 333-350. In Latgé J, Steinbach W (ed), and Aspergillosis. ASM Press, Washington, DC. doi: 10.1128/9781555815523.ch26
Generic image for table
Table 4.

Risk factors for ABPA

Citation: Moss R. 2009. Allergic Bronchopulmonary Aspergillosis, p 333-350. In Latgé J, Steinbach W (ed), and Aspergillosis. ASM Press, Washington, DC. doi: 10.1128/9781555815523.ch26
Generic image for table
Table 5.

Diagnosis of ABPA

Citation: Moss R. 2009. Allergic Bronchopulmonary Aspergillosis, p 333-350. In Latgé J, Steinbach W (ed), and Aspergillosis. ASM Press, Washington, DC. doi: 10.1128/9781555815523.ch26
Generic image for table
Table 6.

Stages of ABPA

Citation: Moss R. 2009. Allergic Bronchopulmonary Aspergillosis, p 333-350. In Latgé J, Steinbach W (ed), and Aspergillosis. ASM Press, Washington, DC. doi: 10.1128/9781555815523.ch26
Generic image for table
Table 7.

Minimal diagnostic criteria for ABPA in CF

Citation: Moss R. 2009. Allergic Bronchopulmonary Aspergillosis, p 333-350. In Latgé J, Steinbach W (ed), and Aspergillosis. ASM Press, Washington, DC. doi: 10.1128/9781555815523.ch26
Generic image for table
Table 8.

Pharmacotherapy of ABPA

Citation: Moss R. 2009. Allergic Bronchopulmonary Aspergillosis, p 333-350. In Latgé J, Steinbach W (ed), and Aspergillosis. ASM Press, Washington, DC. doi: 10.1128/9781555815523.ch26

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