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- Title
IL-32 expression in the airway epithelial cells of patients with Mycobacterium avium complex lung disease.
- Authors
Bai, Xiyuan; Ovrutsky, Alida R.; Kartalija, Marinka; Chmura, Kathryn; Kamali, Amanda; Honda, Jennifer R.; Oberley-Deegan, Rebecca E.; Dinarello, Charles A.; Crapo, James D.; Chang, Ling-Yi; Chan, Edward D.
- Abstract
Lung disease due to Mycobacterium avium complex (MAC) organisms is increasing. A greater understanding of the host immune response to MAC organisms will provide a foundation to develop novel therapies for these recalcitrant infections. IL-32 is a newly described pro-inflammatory cytokine that enhances host immunity against various microbial pathogens. Cytokines that induce IL-32 such as interferon-gamma, IL-18, IL-12 and tumor necrosis factor-alpha are of considerable importance to mycobacterial immunity. We performed immunohistochemistry and morphometric analysis to quantify IL-32 expression in the lungs of 11 patients with MAC lung disease and 10 controls with normal lung tissues. After normalizing for basement membrane length, there was a profound increase in IL-32 expression in the airway epithelial cells of the MAC-infected lungs compared with controls. Following normalization for alveolar surface area, there was a trend toward increased IL-32 expression in type II alveolar cells and alveolar macrophages in the lungs of MAC patients. Human airway epithelial cells (BEAS-2B) infected with M. avium produced IL-32 by a nuclear factor-kappa B-dependent mechanism. In both BEAS-2B cells and human monocyte-derived macrophages, exogenous IL-32γ significantly reduced the growth of intracellular M. avium. This finding was corroborated by an increase in the number of intracellular M. avium recovered from THP-1 monocytes silenced for endogenous IL-32 expression. The anti-mycobacterial effect of IL-32 may be due, in part, to increased apoptosis of infected cells. These findings indicate that IL-32 facilitates host defense against MAC organisms but may also contribute to the airway inflammation associated with MAC pulmonary disease.
- Subjects
INTERLEUKINS; GENE expression; EPITHELIAL cells; MYCOBACTERIUM avium; LUNG diseases; IMMUNE response; IMMUNOHISTOCHEMISTRY
- Publication
International Immunology, 2011, Vol 23, Issue 11, p679
- ISSN
0953-8178
- Publication type
Article
- DOI
10.1093/intimm/dxr075