tetano
Editor, Senior Moderator
Arch Toxicol
. 2022 Jun 7.
doi: 10.1007/s00204-022-03305-2. Online ahead of print.
Electronic cigarette vapor exposure exaggerates the pro-inflammatory response during influenza A viral infection in human distal airway epithelium
Niccolette Schaunaman[SUP] #[/SUP][SUP] 1 [/SUP], Taylor Crue[SUP] #[/SUP][SUP] 2 [/SUP], Diana Cervantes[SUP] 1 [/SUP], Kelly Schweitzer[SUP] 1 [/SUP], Harrison Robbins[SUP] 1 [/SUP], Brian J Day[SUP] 1 [/SUP], Mari Numata[SUP] 1 [/SUP], Irina Petrache[SUP] 3 [/SUP], Hong Wei Chu[SUP] 4 [/SUP]
Affiliations
Abstract
Electronic cigarettes or vaping products have been marketed as a safer alternative to smoking, but very little is known about the health effects in the human lung, particularly in the distal airways, a key site of airway obstruction and destruction in chronic obstructive pulmonary disease that is often exacerbated by viral infections. The aim of this study was to investigate the effects of electronic cigarette vapor (e-vapor) on human distal airway epithelial responses to influenza A virus (IAV) infection. We isolated primary small airway epithelial cells (SAECs) from donor lungs free of lung disease, and cultured them at air-liquid interface (ALI). To measure markers of epithelial injury such as integrity of epithelial barrier structure and function, we selected a regimen of non-toxic, barrier preserving e-vapor exposure of cultured cells to 15 puffs of e-vapor from a commercially available e-cigarette once per day for 3 days, prior to IAV infection. After 72 h of infection, media and cell lysates were collected to measure cytokines involved in inflammatory and antiviral responses. Pre-exposure to e-vapor with IAV infection, compared to IAV infection alone, significantly increased inflammatory and antiviral mediators including IL-8, CXCL10, IFN-beta, and MX1. Our results suggest that e-vapor exposure amplifies human distal airway pro-inflammatory response to IAV infection, independently of the severity of cell injury during viral infection.
Keywords: Inflammation; Influenza A virus; Small airway epithelium; e-vapor.
. 2022 Jun 7.
doi: 10.1007/s00204-022-03305-2. Online ahead of print.
Electronic cigarette vapor exposure exaggerates the pro-inflammatory response during influenza A viral infection in human distal airway epithelium
Niccolette Schaunaman[SUP] #[/SUP][SUP] 1 [/SUP], Taylor Crue[SUP] #[/SUP][SUP] 2 [/SUP], Diana Cervantes[SUP] 1 [/SUP], Kelly Schweitzer[SUP] 1 [/SUP], Harrison Robbins[SUP] 1 [/SUP], Brian J Day[SUP] 1 [/SUP], Mari Numata[SUP] 1 [/SUP], Irina Petrache[SUP] 3 [/SUP], Hong Wei Chu[SUP] 4 [/SUP]
Affiliations
- PMID: 35672461
- DOI: 10.1007/s00204-022-03305-2
Abstract
Electronic cigarettes or vaping products have been marketed as a safer alternative to smoking, but very little is known about the health effects in the human lung, particularly in the distal airways, a key site of airway obstruction and destruction in chronic obstructive pulmonary disease that is often exacerbated by viral infections. The aim of this study was to investigate the effects of electronic cigarette vapor (e-vapor) on human distal airway epithelial responses to influenza A virus (IAV) infection. We isolated primary small airway epithelial cells (SAECs) from donor lungs free of lung disease, and cultured them at air-liquid interface (ALI). To measure markers of epithelial injury such as integrity of epithelial barrier structure and function, we selected a regimen of non-toxic, barrier preserving e-vapor exposure of cultured cells to 15 puffs of e-vapor from a commercially available e-cigarette once per day for 3 days, prior to IAV infection. After 72 h of infection, media and cell lysates were collected to measure cytokines involved in inflammatory and antiviral responses. Pre-exposure to e-vapor with IAV infection, compared to IAV infection alone, significantly increased inflammatory and antiviral mediators including IL-8, CXCL10, IFN-beta, and MX1. Our results suggest that e-vapor exposure amplifies human distal airway pro-inflammatory response to IAV infection, independently of the severity of cell injury during viral infection.
Keywords: Inflammation; Influenza A virus; Small airway epithelium; e-vapor.