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Updated: Aug 11, 2026
A Non-invasive and Technically Non-intensive Method for Induction and Phenotyping of Experimental Bacterial Pneumonia in Mice
Published on: September 28, 2016
Different susceptibilities of PECAM-deficient mouse strains to spontaneous idiopathic pneumonitis
Alan R Schenkel1, Tina W Chew, Elizabeth Chlipala
1Department of Microbiology, Immunology and Pathology Colorado State University 1682 Campus Delivery Fort Collins, CO 80523-1682, USA. alan.schenkel@colostate.edu
Abstract:
Platelet Endothelial Cell Adhesion Molecule (PECAM) is an adhesion and signaling molecule used for leukocyte extravasation. We have generated two strains of PECAM-deficient mouse, one in the original C57BL/6 and a second by backcrossing nice generations into the FVB/n strain. The FVB/n strain has reduced responses in models of acute inflammation. We show here that this strain is also susceptible to a chronic pneumonia which leads to pulmonary fibrosis. In contrast, PECAM-deficient C57BL/6 mice do not develop this lung disease and have normal responses in acute models of inflammation. This demonstrates that PECAM-dependent and -independent mechanisms are found in both acute and chronic inflammation. Further, the PECAM-deficient FVB/n strain has many pathologic similarities to the human disease Idiopathic Pulmonary Fibrosis, suggesting that similar molecular mechanisms may play a role in human disease.
Insights
Platelet Endothelial Cell Adhesion Molecule (PECAM) deficiency in FVB/n mice causes chronic pneumonia and pulmonary fibrosis, unlike in C57BL/6 mice. This highlights PECAM-independent roles in inflammation and models human idiopathic pulmonary fibrosis.
Area of Science:
- Immunology
- Pulmonary Medicine
- Cell Biology
Background:
- Platelet Endothelial Cell Adhesion Molecule (PECAM) is crucial for leukocyte extravasation.
- Genetic background influences inflammatory responses, as seen in FVB/n mice with reduced acute inflammation.
- Understanding PECAM's role in different genetic contexts is vital for inflammatory disease research.
Purpose of the Study:
- To investigate the role of PECAM in different mouse strains during acute and chronic inflammation.
- To characterize the phenotype of PECAM-deficient mice on C57BL/6 and FVB/n backgrounds.
- To explore the potential of PECAM-deficient FVB/n mice as a model for human pulmonary fibrosis.
Main Methods:
- Generation of two PECAM-deficient mouse strains: C57BL/6 and FVB/n.
- Assessment of inflammatory responses in acute inflammation models.
- Induction and analysis of chronic pneumonia and pulmonary fibrosis.
- Pathological comparison with human Idiopathic Pulmonary Fibrosis.
Main Results:
- PECAM-deficient FVB/n mice developed chronic pneumonia and pulmonary fibrosis, unlike PECAM-deficient C57BL/6 mice.
- PECAM-deficient C57BL/6 mice exhibited normal responses in acute inflammation models.
- The FVB/n strain's lung pathology showed similarities to human Idiopathic Pulmonary Fibrosis.
- Demonstrated both PECAM-dependent and -independent mechanisms in acute and chronic inflammation.
Conclusions:
- PECAM-dependent and -independent pathways contribute to both acute and chronic inflammation.
- The FVB/n genetic background is critical for the development of PECAM-deficiency-induced lung disease.
- PECAM-deficient FVB/n mice represent a valuable model for studying Idiopathic Pulmonary Fibrosis and related mechanisms.
