scholarly journals Transcriptome Differences in Pig Tracheal Epithelial Cells in Response to Pasteurella Multocida Infection

2021 ◽  
Vol 8 ◽  
Author(s):  
Xueying Wang ◽  
Fei Wang ◽  
Lin Lin ◽  
Wan Liang ◽  
Songtao Liu ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epithelial Cells ◽  
Signaling Pathway ◽  
Pasteurella Multocida ◽  
Transforming Growth Factor ◽  
Mapk Signaling ◽  
Barrier Functions ◽  
Tracheal Epithelial ◽  
Epithelial Barriers ◽  
Respiratory Epithelial

Pasteurella multocida generally colonizes mammalian/bird respiratory tracts and mainly causes respiratory disorders in both humans and animals. To date, the effects of P. multocida infection on the respiratory epithelial barriers and molecules in host respiratory epithelial cells in their response to P. multocida infection are still not well-known. In this study, we used newborn pig tracheal epithelial (NPTr) cells as an in vitro model to investigate the effect of P. multocida infection on host respiratory epithelial barriers. By detecting the transepithelial electrical resistance (TEER) values of NPTr cells and the expression of several known molecules associated with cell adherens and junctions, we found that P. multocida infection disrupted the barrier functions of NPTr cells. By performing RNA sequencing (RNA-Seq), we determined 30 differentially expressed genes (DEGs), including the vascular endothelial growth factor A (VEGFA) encoding gene VEGFA, which participated in biological processes (GO:0034330, GO:0045216, and GO:0098609) closely related to epithelial adhesion and barrier functions. These 30 DEGs participated in 22 significant signaling pathways with a p-value < 0.05, including the transforming growth factor (TGF)-beta signaling pathway (KEGG ID: ssc04350), hypoxia-inducible factor 1 (HIF-1) signaling pathway (KEGG ID: ssc04066), epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor resistance (KEGG ID: ssc01521), tumor necrosis factor (TNF) signaling pathway (KEGG ID: ssc04668), and mitogen-activated protein kinase (MAPK) signaling pathway (KEGG ID: ssc04010), which are reported to have roles in contributing to the production of inflammatory factors as well as the regulation of epithelial adhesion and barrier function in other tissues and organisms. The results presented in this study may help improve our understanding of the pathogenesis of P. multocida.

Immunolocalization of Transforming Growth Factor a and Epidermal Growth Factor Receptor in Lungs of Patients with Cystic Fibrosis

1999 ◽  
Vol 2 (5) ◽  
pp. 415-423 ◽  
Author(s):  
William D. Hardie ◽  
Pablo A. Bejarano ◽  
Mary Ann Miller ◽  
James R. Yankaskas ◽  
Jon H. Ritter ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Epithelial Cells ◽  
Lung Tissue ◽  
Transforming Growth Factor ◽  
Growth Factor Receptor ◽  
Epidermal Growth ◽  
Respiratory Epithelial

Transforming growth factor α (TGF-α) is expressed in respiratory epithelial cells and alveolar macrophages during development and following lung injury. In the present study the presence and sites of synthesis of TGF-α and its receptor, the epidermal growth factor receptor (EGF-R), were assessed in lung tissue from patients with severe lung disease caused by cystic fibrosis (CF). Lung sections from 24 individuals with CF, obtained at the time of lung transplantation, were compared to lung sections from five lung donors without CF. Cellular sites of TGF-α, EGF-R, and cellular sites of proliferation were assessed by immunohistochemistry All CF lung sections contained multiple cell types with detectable TGF-α. Compared to control sections, intensity of TGF-α immunostaining in macrophages, airway epithelial cells, and peribronchial submucosal cells was increased. EGF-R was detected in respiratory epithelial and peribronchial stromal cells but not in alveolar macrophages. The intensity of EGF-R staining in CF lung tissue did not differ from that of controls. An increased number of cells expressing Ki-67 nuclear antigen was detected in peribronchial submucosal cells but not bronchiolar epithelial cells in the CF lungs. The increased expression of TGF-α in CF lung tissue supports the concept that TGF-α plays a role in paracrine/autocrine regulation of lung remodeling associated with injury and repair in the lungs of individuals with cystic fibrosis.

Sign in / Sign up

Export Citation Format

Share Document