Human Airway Epithelial Cells Direct Significant Rhinovirus Replication in Monocytic Cells by Enhancing ICAM1 Expression
Autor: | Lingxiang Zhu, Yin Chen, Xu Zhou, Rosa Lizarraga |
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Jazyk: | angličtina |
Rok vydání: | 2017 |
Předmět: |
0301 basic medicine
Pulmonary and Respiratory Medicine DNA Complementary Rhinovirus Clinical Biochemistry Cell Primary Cell Culture Bronchi Biology Virus Replication Monocytes Proinflammatory cytokine Cell Line 03 medical and health sciences Downregulation and upregulation medicine Humans RNA Messenger RNA Small Interfering Receptor Molecular Biology Original Research Cell Biology Intercellular Adhesion Molecule-1 Epithelium Coculture Techniques Cell biology Up-Regulation 030104 developmental biology medicine.anatomical_structure Viral replication Cell culture Alveolar Epithelial Cells Culture Media Conditioned Gene Knockdown Techniques Immunology Respiratory epithelium Cytokines Receptors Virus RNA Interference |
Zdroj: | American Journal of Respiratory Cell and Molecular Biology |
Popis: | 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 be mediated 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 RV production, 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-dependent mechanism. This finding will open a new avenue for the study of RV infection in airway disease and its exacerbation. |
Databáze: | OpenAIRE |
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