HISTOLOGY AND HISTOPATHOLOGY

From Cell Biology to Tissue Engineering

 

The role of the non-ciliated bronchiolar cell in tolerance to inhaled vanadium of the bronchiolar epithelium

Nelly López-Valdez1,2, Gabriela Guerrero-Palomo1, Marcela Rojas-Lemus1, Patricia Bizarro-Nevares1, Adriana Gonzalez-Villalva1, Martha Ustarroz-Cano1, Norma Rivera-Fernández3 and Teresa I. Fortoul1

1Department of Cellular and Tissular Biology, School of Medicine, 2Posgrado en Ciencias Biológicas and 3Department of Microbiology and Parasitology, School of Medicine, UNAM, México City

Offprint requests to: Teresa I. Fortoul, Department of Cellular and Tissular Biology, School of Medicine, UNAM; Av. Ciudad Universitaria 3000, C.P. 04510, Coyoacán, México city. e-mail: fortoul@unam.mx


Summary. The Non-Ciliated Bronchiolar Cell (NCBC) is responsible for the defense and maintenance of the bronchiolar epithelium. Several cellular defense mechanisms have been associated with an increase in the secretion of CC16 and changes in the phenotype of the cell; these mechanisms could be linked to tolerance to the damage due to exposure to inhaled Particulate Matter (PM) of the epithelium. These defense mechanisms have not been sufficiently explored. In this article, we studied the response of the NCBC to inhaled vanadium, an element which adheres to PM. This response was measured by the changes in the phenotype of the NCBC and the secretion of CC16 in a mouse model. Mice were exposed in two phases to different vanadium concentrations; 1.56 mg/m3 in the first phase and 2.57 mg/m3 in the second phase. Mice were sacrificed on the 2nd, 4th, 5th, 6th and 8th weeks. In the second phase, we observed the following: sloughing of the NCBC, hyperplasia and small inflammatory foci remained without changes and that the expression of CC16 was higher in this phase than in phase I. We also observed a change in the phenotype with a slow decrease in both phases. The increase in the secretion of CC16 and the phenotype reversion could be due to the anti-inflammatory activity of CC16. The changes observed in the second phase could be attributed to the tolerance to inhaled vanadium. Histol Histopathol 35, 497-508 (2020)

Key words: NCBC, CC16, Vanadium, Tolerance, Phenotype

DOI: 10.14670/HH-18-165