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Published on: September 19, 2016
Immunoglobulin responses to experimental silicosis
S H Huang1, A F Hubbs, C F Stanley
1West Virginia University, Morgantown, West Virginia 26506, USA.
Summary
Silicosis causes immune dysfunction, increasing immunoglobulin G (IgG) and immunoglobulin M (IgM) in serum and bronchoalveolar lavage (BAL). Lung-associated lymph nodes are key sites for this increased antibody production in rats.
Area of Science:
- Immunology
- Pulmonary Medicine
- Toxicology
Background:
- Silicosis, a lung disease from silica inhalation, causes immune system dysfunction.
- Elevated serum and bronchoalveolar lavage (BAL) immunoglobulins (IgG, IgM) are hallmarks of human silicosis.
- An established rat model of silicosis exhibits pulmonary inflammation and fibrosis.
Purpose of the Study:
- To confirm increased serum and BAL IgG and IgM in a rat silicosis model.
- To identify the anatomical sites responsible for elevated immunoglobulin production.
- To compare immunoglobulin levels and production in silica-exposed rats versus controls.
Main Methods:
- Rats inhaled crystalline silica, titanium dioxide (TiO(2)), or air (sham).
- Serum and BAL IgG and IgM levels were measured.
- Ex vivo IgG and IgM production by mononuclear cells from lungs, lymph nodes, and spleens was assessed.
Main Results:
- Silicosis model rats showed elevated serum and BAL IgG and IgM compared to controls.
- Lung-associated lymph nodes (LALN) were the primary sites of increased IgG and IgM production.
- Lungs contributed to a lesser extent to the immunoglobulin response.
Conclusions:
- Experimental silicosis in rats mimics human disease with increased systemic and pulmonary immunoglobulins.
- Lung-associated lymph nodes are critical in driving the B lymphocyte response in silicosis.
- B lymphocyte expansion in LALN correlates with increased IgG and IgM production.
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