Does dust‐associated pulmonary alveolar proteinosis represent an autoimmune disorder?

The role of autoantibodies against granulocyte‐macrophage colony‐stimulating factor (GM‐CSF) in the development of secondary pulmonary alveolar proteinosis (PAP) in patients exposed to occupational and environmental dust remains unclear. Herein, we describe two cases of secondary PAP who had GM‐CSF...

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Bibliographic Details
Published in:American journal of industrial medicine 2017-06, Vol.60 (6), p.591-597
Main Authors: Uzmezoglu, Bilge, Simsek, Cebrail, Gulgosteren, Sevtap, Gebesoglu, Berna E.
Format: Article
Language:English
Subjects:
Aged
Alveoli
Antibodies
Autoantibodies
Autoantibodies - blood
Colony-stimulating factor
Dust
dust exposure
Exposure
GM‐CSF autoantibodies
Granulocyte-macrophage colony-stimulating factor
Granulocyte-Macrophage Colony-Stimulating Factor - immunology
Humans
Immunoglobulins
Macrophages
Male
Middle Aged
Occupational Diseases - etiology
Occupational Diseases - immunology
Occupational Exposure - adverse effects
Phosphorylation
pulmonary alveolar proteinosis
Pulmonary Alveolar Proteinosis - etiology
Pulmonary Alveolar Proteinosis - immunology
STAT5 phosphorylation index
Stat5 protein
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Summary:The role of autoantibodies against granulocyte‐macrophage colony‐stimulating factor (GM‐CSF) in the development of secondary pulmonary alveolar proteinosis (PAP) in patients exposed to occupational and environmental dust remains unclear. Herein, we describe two cases of secondary PAP who had GM‐CSF antibodies and absence of STAT5 phosphorylation index, suggestive of a potential relationship between the appearance of GM‐CSF antibodies and environmental dust exposure. However, whether the presence of GM‐CSF antibodies is a part of the pathological process or represents an epiphenomenon is currently unknown. In this report, we would like to present two cases supporting these new data and briefly discuss the possible role of autoimmune mechanisms in the development of secondary PAP. Am. J. Ind. Med. 60:591–597, 2017. © 2017 Wiley Periodicals, Inc.
ISSN:0271-3586
1097-0274
DOI:10.1002/ajim.22702