期刊
MUCOSAL IMMUNOLOGY
卷 10, 期 6, 页码 1400-1411出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/mi.2017.3
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资金
- Concerted Research Action of the Ghent University (BOF/GOA) [01G02714]
- Fund for Scientific Research in Flanders (FWO Vlaanderen)
- Interuniversity Attraction Poles program (IUAP) [P7/30]
- COSTAction, Developmental Origins of Chronic Lung Disease [BM1201]
- Fund for Scientific Research-Flanders
- Group-ID Multidisciplinary Research Platform of Ghent University
- Interuniversity Attraction Poles Program [P7/07]
- Strategic Basic Research program of the Instituut voor Innovatie door Wetenschap en Technologie (IWT)
The molecular mechanisms underlying the pathogenesis of chronic obstructive pulmonary disease (COPD) are still unclear, however signaling pathways associated with lung development, such as the transforming growth factor (TGF)-beta superfamily, could be implicated in COPD. Growth differentiation factor (GDF)-15, a member of the TGF-beta superfamily, is involved in inflammation, mucus secretion, and cachexia. We analyzed the pulmonary expression of GDF-15 in smokers and patients with COPD, in cigarette smoke (CS)-exposed cultures of primary human bronchial epithelial cells (pHBECs), and in CS-exposed mice. Next, we exposed GDF-15 KO and control mice to air or CS and evaluated pulmonary inflammation. GDF-15 levels were higher in sputum supernatant and lung tissue of patients with COPD and smokers without COPD compared with never smokers. Immunohistochemistry revealed GDF-15 staining in the airway epithelium. Increased expression and secretion of GDF-15 was confirmed in vitro in CS-exposed pHBECs compared with air-exposed pHBECs. Similarly, GDF-15 levels were increased in lungs of CS-exposed mice. Importantly, GDF-15 deficiency attenuated the CS-induced pulmonary inflammation. These results suggest that increased GDF-15-as observed in lungs of smokers and patients with COPD-contributes to CS-induced pulmonary inflammation.
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