TY - JOUR
T1 - Human airway epithelial cells direct significant rhinovirus replication in monocytic cells by enhancing ICAM1 expression
AU - Zhou, Xu
AU - Zhu, Lingxiang
AU - Lizarraga, Rosa
AU - Chen, Yin
N1 - Funding Information:
This work was supported by National Institutes of Health grants AI061695 and AI113526, grant 123055-CIA from the Flight Attendant Medical Research Institute, and Biomedical Investigator Award BIG-3064 from the Arizona Biomedical Research Commission.
Publisher Copyright:
© 2017 by the American Thoracic Society.
PY - 2017/8
Y1 - 2017/8
N2 - Human rhinovirus (RV) is the major cause of common cold, and it also plays a significant role in asthma and asthma exacerbation. The airway epithelium is the primary site of RV infection and production. In contrast, monocytic cells (e.g., monocytes and macrophages) are believed to be nonpermissive for RV replication. Instead, RV has been shown to modulate inflammatory gene expressions in these cells via a replication-independent mechanism. In the study presented here, replication of RV16 (a major-group RV) was found to be significantly enhanced in monocytes when it was cocultivated with airway epithelial cells. This effect appeared to bemediated by secretory components from epithelial cells,which stimulated RV16 replication and significantly elevated the expression of a number of proinflammatory cytokines. The lack of such an effect on RV1A, a minor-group RV that enters the cell by a different receptor, suggests that intercellular adhesion molecule 1 (ICAM1), the receptor for major-group RVs, may be involved. Indeed, conditioned media from epithelial cells significantly increased ICAM1 expression in monocytes. Consistently, ICAM1 overexpression and ICAM1 knockdown enhanced and blocked RVproduction, respectively, confirming the role of ICAM1 in this process. Thus, this is the first report demonstrating that airway epithelial cells direct significant RV16 replication in monocytic cells via an ICAM1-dependentmechanism. This finding will open a new avenue for the study of RV infection in airway disease and its exacerbation.
AB - Human rhinovirus (RV) is the major cause of common cold, and it also plays a significant role in asthma and asthma exacerbation. The airway epithelium is the primary site of RV infection and production. In contrast, monocytic cells (e.g., monocytes and macrophages) are believed to be nonpermissive for RV replication. Instead, RV has been shown to modulate inflammatory gene expressions in these cells via a replication-independent mechanism. In the study presented here, replication of RV16 (a major-group RV) was found to be significantly enhanced in monocytes when it was cocultivated with airway epithelial cells. This effect appeared to bemediated by secretory components from epithelial cells,which stimulated RV16 replication and significantly elevated the expression of a number of proinflammatory cytokines. The lack of such an effect on RV1A, a minor-group RV that enters the cell by a different receptor, suggests that intercellular adhesion molecule 1 (ICAM1), the receptor for major-group RVs, may be involved. Indeed, conditioned media from epithelial cells significantly increased ICAM1 expression in monocytes. Consistently, ICAM1 overexpression and ICAM1 knockdown enhanced and blocked RVproduction, respectively, confirming the role of ICAM1 in this process. Thus, this is the first report demonstrating that airway epithelial cells direct significant RV16 replication in monocytic cells via an ICAM1-dependentmechanism. This finding will open a new avenue for the study of RV infection in airway disease and its exacerbation.
KW - Airway
KW - Epithelium
KW - ICAM1
KW - Rhinovirus
UR - http://www.scopus.com/inward/record.url?scp=85026869022&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85026869022&partnerID=8YFLogxK
U2 - 10.1165/rcmb.2016-0271OC
DO - 10.1165/rcmb.2016-0271OC
M3 - Article
C2 - 28328242
AN - SCOPUS:85026869022
SN - 1044-1549
VL - 57
SP - 216
EP - 225
JO - American journal of respiratory cell and molecular biology
JF - American journal of respiratory cell and molecular biology
IS - 2
ER -