Aspergillosis pathophysiology: Difference between revisions
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==Allergic Bronchopulmonary Aspergillosis (ABPA)== | |||
For an unknown reason, patients with allergic bronchopulmonary aspergillosis develop a hypersensitivity response, both a type I response (atopic, with formation of immunoglobulin E or IgE) and a type III hypersensitivity response (with formation of immunoglobulin G or IgG). The reaction of immunoglobulin E with Aspergillus antigens results in mast cell degranulation with bronchoconstriction and increased capillary permeability. Immune complexes (a type III reaction) and inflammatory cells are then deposited within the mucous membranes of the airways, leading to necrosis (tissue death) and an eosinophilic infiltrate. Type 2 T helper cells secreting interleukin 4 and interleukin 5, and attraction of neutrophils by interleukin 8 seem to play an important role.[citation needed] | |||
In spite of this pronounced immune reaction, the fungus is not cleared from the airways. Proteolytic enzymes are released by the immune cells, and toxins are released by the fungi. Together these result in bronchiectasis, most pronounced in the central parts of the airways. Repeated acute episodes left untreated can result in progressive pulmonary fibrosis that is often seen in the upper zones and can give rise to a similar radiological appearance to that produced by tuberculosis. | |||
==Invasive Aspergillosis== | |||
==Aspergilloma== | |||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
Revision as of 01:43, 9 December 2013
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Aspergillosis Microchapters |
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Diagnosis |
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Treatment |
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Case Studies |
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Aspergillosis pathophysiology On the Web |
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American Roentgen Ray Society Images of Aspergillosis pathophysiology |
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Risk calculators and risk factors for Aspergillosis pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Christeen Henen, M.D. [2]
Allergic Bronchopulmonary Aspergillosis (ABPA)
For an unknown reason, patients with allergic bronchopulmonary aspergillosis develop a hypersensitivity response, both a type I response (atopic, with formation of immunoglobulin E or IgE) and a type III hypersensitivity response (with formation of immunoglobulin G or IgG). The reaction of immunoglobulin E with Aspergillus antigens results in mast cell degranulation with bronchoconstriction and increased capillary permeability. Immune complexes (a type III reaction) and inflammatory cells are then deposited within the mucous membranes of the airways, leading to necrosis (tissue death) and an eosinophilic infiltrate. Type 2 T helper cells secreting interleukin 4 and interleukin 5, and attraction of neutrophils by interleukin 8 seem to play an important role.[citation needed]
In spite of this pronounced immune reaction, the fungus is not cleared from the airways. Proteolytic enzymes are released by the immune cells, and toxins are released by the fungi. Together these result in bronchiectasis, most pronounced in the central parts of the airways. Repeated acute episodes left untreated can result in progressive pulmonary fibrosis that is often seen in the upper zones and can give rise to a similar radiological appearance to that produced by tuberculosis.