Iannuzo, N.; Dy, A.B.C.; Guerra, S.; Langlais, P.R.; Ledford, J.G. The Impact of CC16 on Pulmonary Epithelial-Driven Host Responses during Mycoplasma pneumoniae Infection in Mouse Tracheal Epithelial Cells. Cells2023, 12, 1984.
Iannuzo, N.; Dy, A.B.C.; Guerra, S.; Langlais, P.R.; Ledford, J.G. The Impact of CC16 on Pulmonary Epithelial-Driven Host Responses during Mycoplasma pneumoniae Infection in Mouse Tracheal Epithelial Cells. Cells 2023, 12, 1984.
Iannuzo, N.; Dy, A.B.C.; Guerra, S.; Langlais, P.R.; Ledford, J.G. The Impact of CC16 on Pulmonary Epithelial-Driven Host Responses during Mycoplasma pneumoniae Infection in Mouse Tracheal Epithelial Cells. Cells2023, 12, 1984.
Iannuzo, N.; Dy, A.B.C.; Guerra, S.; Langlais, P.R.; Ledford, J.G. The Impact of CC16 on Pulmonary Epithelial-Driven Host Responses during Mycoplasma pneumoniae Infection in Mouse Tracheal Epithelial Cells. Cells 2023, 12, 1984.
Abstract
CC16 plays many protective roles within the lung; however, the complete biological functions, es-pecially regarding the pulmonary epithelium during infection, remain undefined. We have previ-ously shown that CC16 deficient (CC16-/-) mouse tracheal epithelial cells (MTECs) have enhanced Mp burden, compared to CC16 sufficient (WT) MTECs; therefore, in this study, we wanted to fur-ther define how the pulmonary epithelium responds to infection in the context of CC16 deficiency. Using mass spectrometry and quantitative proteomics to analyze proteins secreted apically from MTECs grown at an air-liquid interface, we investigated the protective effects that CC16 elicits within the pulmonary epithelium during Mycoplasma pneumoniae (Mp) infection. When chal-lenged with Mp, WT MTECs have an overall reduction in apical protein secretion, whereas CC16-/- MTECs have increased apical protein secretion compared to their unchallenged controls. Fol-lowing Gene Ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) assessment, many of the proteins upregulated from CC16-/- MTECS (unchallenged and during Mp infection) were related to airway remodeling, which were not observed by WT MTECs. These findings sug-gest that CC16 is instrumental in providing protection within the pulmonary epithelium during respiratory infection with Mp, the major causative agent of community-acquired pneumoniae.
Keywords
Mycoplasma pneumoniae; CC16; CCSP; CC10; mass spectrometry; remodeling
Subject
Biology and Life Sciences, Immunology and Microbiology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
