Electronic Cigarettes Enhance Replication of Mycobacterium abscessus in Airway Epithelial Cells

• Published in: American journal of respiratory cell and molecular biology Vol. 60; no. 6; pp. 717 - 719
• Main Authors: Korukonda, Anu, Zhang, Chongxu, Rodriguez, Leslie, Guerrero, Andrea, Campos, Michael, Holt, Gregory, Fregien, Nevis L, Conner, Greg, Mirsaeidi, Mehdi
• Format: Journal Article
• Language: English
• Published: United States American Thoracic Society 01.06.2019
• Subjects: Adolescents; Aged; Alcohol; Animals; Antibiotic resistance; Antibiotics; Bacteria; Cell walls; Chronic obstructive pulmonary disease; Cigarettes; Cytokines; Cytokines - metabolism; Electronic cigarettes; Electronic Nicotine Delivery Systems; Endothelial cells; Epithelial cells; Epithelial Cells - microbiology; Epithelial Cells - pathology; Epithelial Cells - ultrastructure; Gene expression; Glycopeptidolipids; Humans; Infections; Lung - microbiology; Lung - pathology; Lungs; Macrolide antibiotics; Macrophages; Male; Mice; Middle Aged; Mycobacterium abscessus; Mycobacterium abscessus - growth & development; Nicotine; Oxidative stress; Replication; Respiratory tract; Smoking; Teenagers; Transmission electron microscopy; Young adults; Florida; United States > US
• ISSN: 1044-1549; 1535-4989
• DOI: 10.1165/rcmb.2018-0339LE

[...]of this perception, ECs have become popular among children in middle school and high school (3). Mycobacterium abscessus (MAB) has been found to be the one of the most isolated species of nontuberculous mycobacteria in the southeastern region of the United States (Florida to Texas) (8). Because MAB carries the erm gene and has a high cell wall lipid content, it exhibits antibiotic resistance to commonly used macrolide antibiotics (9). The bacteria adopt the smooth (S) morphotype and can then conform to the more virulent rough (R) form that lacks glycopeptidolipids and is resistant to macrophages (10). Because few studies have elucidated the mechanisms of how MAB infects the respiratory epithelia, and there is a lack of knowledge about ECs’ interaction with pulmonary epithelial cells infected with MAB, we developed a bilayer lung model with human bronchial cells and human lung endothelial cells to evaluate the effect of ECs on MAB replication. Given these findings concerning CCL-2 and the growing popularity of ECs among adolescents, it is important to conduct further research with larger sample sizes to study the effect of ECs in airway epithelial cell–MAB interactions and immune cell responses to these interactions. 1.