Abstract
Background: Fibrosing lung diseases are a serious problem to health and are ranked high among chronic degenerative diseases due to its morbidity. Type V collagen [col (V)] is a minor collagen normally sequestered within the lung interstitium and therefore, hidden from the immune system. This collagen regulates heterotypic fiber diameter, and the maintenance of its properties is important for maintaining normal tissue architecture and function. Previously, we discovered an experimental model of systemic sclerosis by immunizing healthy New Zealand rabbits with human col (V). This resulted in intense inflammation of the lung and progressive ECM remodeling of the septal and bronchovascular axis.Objective: To evaluate the pulmonary parenchyma after immunization healthy C57Bl/6 mice. Methods: For induction of pulmonary fibrosis, groups of male mice C57Bl/6 (n=6), aged 4 to 6 weeks-old with 20-25g, were immunized with 150µg/200µl of Col(V) in complete Freund's adjuvant, followed by more two boosters in incomplete Freund's adjuvant. Sterile saline was used as control. For analysis, mice were sacrificed 75 days after induction. Lungs were removed for routine histology, immunohistochemistry and histomorphometry. Results: The immunized group presented intense inflammation of the lung and progressive ECM remodeling with significant higher amount of CD4 (p=0.002). The higher amounts of type I collagen, TGF and CTGF expression were observed in immunized groups respectively, (p<0.005, p<0.0025 and p<0.0001) when compared with control group. Conclusions: We concluded that human col (V)induced pulmonary fibrosis in healthy C57Bl/6 mice, suggesting a new pulmonary fibrosis model important for pulmonary fibrosis pathogenesis.
- © 2014 ERS