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M. Inoue
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MINI 28 - Psychological Impact of Lung Cancer and its Treatment (ID 150)
- Event: WCLC 2015
- Type: Mini Oral
- Track: Palliative and Supportive Care
- Presentations: 1
- Moderators:A. Oton
- Coordinates: 9/09/2015, 16:45 - 18:15, 102+104+106
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MINI28.10 - C-Type Natriuretic Peptide Attenuates Bleomycin-Induced Fibrosis and Inflammation in Murine Lung (ID 471)
17:40 - 17:45 | Author(s): M. Inoue
- Abstract
- Presentation
Background:
Interstitial lung diseases (ILDs) are sometimes seen in patients with primary lung cancer. Therapeutic interventions for lung cancer patients with ILDs occasionally induce acute exacerbation (AE), which is a potentially fatal complication. However, no prophylactic treatments have been established. Although the etiology of ILD-related AE is unknown, management of the ILD disease process, including fibrotic changes and inflammatory reactions, is thought to lead to the prophylaxis of AE. C-type natriuretic peptide (CNP) is a member of the natriuretic peptide family, which includes atrial and brain natriuretic peptides. CNP has cardioprotective effects, such as anti-fibrotic and anti-inflammatory effects, in animal models of myocarditis and myocardial infarction. The objective of the present study was to investigate the anti-fibrotic and anti-inflammatory effects of CNP on bleomycin (BLM)-induced lung injury.
Methods:
C57BL/6 mice were divided into two groups, vehicle- and CNP-treated groups, for evaluation of pulmonary fibrosis and inflammation induced by BLM. CNP (2.5 µg/kg/min) or vehicle were subcutaneously infused using an osmotic mini-pump from 24 h before BLM administration until the mice were euthanized. On 14 days after intratracheal administration of BLM (1 mg/kg), histological changes, collagen content, and mRNA expression of inflammatory cytokines in lungs and bronchoalveolar lavage fluid (BALF) were assessed.
Results:
Continuous infusion of CNP attenuated BLM-induced fibrotic changes. Quantitative histological analysis showed that BLM-induced fibrotic lesions were significantly smaller in CNP treated mice compared to vehicle mice. The collagen content, determined with the hydroxyproline assay, increased in BLM-administered lung and CNP treatment reduced BLM-induced collagen production. CNP treatment tended to improve body weight loss after BLM administration. In BALF, BLM administration augmented the number of inflammatory cells in the vehicle group, which was significantly lower in CNP treated mice. The expression of IL-1β, IL-6, and bFGF mRNA were significantly elevated by BLM administration, and CNP treatment significantly attenuated these increases. Figure 1
Conclusion:
These results indicate that CNP attenuates fibrotic changes, namely the accumulation of inflammatory cells, and the increased expression of inflammatory cytokines in BLM-induced pulmonary fibrosis. CNP may have therapeutic potential in patients with ILD and lead to prophylaxis for AE.
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