title: Levocetirizine inhibits rhinovirus-induced bacterial adhesion to nasal epithelial cells through down-regulation of cell adhesion molecules.
abstract: BACKGROUND
  The first critical step for bacterial infection is attachment of bacteria to the cell adhesion molecules of epithelial cells. The rhinovirus (RV)-induced increased expression of cell adhesion molecules including fibronectin (Fn) and carcinoembryonic antigen-related cell adhesion molecules (CEACAMs) is closely related to the activation of nuclear factor-kappa B (NF-κB). Recent studies have demonstrated that Levocetirizine (LCT) has anti-inflammatory properties that are mediated by inhibitory effects on NF-κB in addition to classic antihistaminic effects.
  
  
  OBJECTIVE
  To investigate the inhibitory effects of LCT on the RV-induced expression of Fn and CEACAMs in human nasal epithelial cells (HNECs) and identified the effects of LCT on secondary Staphylococcus aureus and Haemophilus influenzae adhesion to RV-infected HNECs.
  
  
  METHODS
  Primary HNECs obtained from inferior turbinate mucosa were pretreated with 50 nM LCT 24 hours before RV-16 infection and for 48 hours thereafter. The expression levels of Fn and CEACAMs were assayed by real-time polymerase chain reaction (PCR) and Western blotting. Bacterial adhesion to cells was assessed by confocal microscopy.
  
  
  RESULTS
  Fibronectin and CEACAM messenger RNA (mRNA) and protein levels in HNECs were significantly increased by RV-16 infection. Levocetirizine significantly reduced these increases in mRNA levels and protein expression of Fn and CEACAMs. Confocal microscopy showed that treatment with LCT significantly reduced the adhesion levels of S aureus and H influenza in RV-infected HNECs compared with RV-infected, untreated HNECs.
  
  
  CONCLUSIONS
  These findings suggest that LCT inhibits the expression of Fn and CEACAMs and has the potential to prevent secondary bacterial infections in RV-infected HNECs by interfering with bacterial adhesion.
authors.affiliation: Department of Otolaryngology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea.
authors.forename: Jin-Young
authors.initials: JY
authors.lastname: Min
authors.affiliation: Department of Otolaryngology, Catholic University of Daegu, School of Medicine, Daegu, South Korea.
authors.forename: Seung-Heon
authors.initials: SH
authors.lastname: Shin
authors.affiliation: Department of Otolaryngology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea.
authors.forename: Hyun Ja
authors.initials: HJ
authors.lastname: Kwon
authors.affiliation: Department of Otolaryngology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea. Electronic address: jangyj@amc.seoul.kr.
authors.forename: Yong Ju
authors.initials: YJ
authors.lastname: Jang
mesh_terms: D015703:Antigens, CD / Q000187:drug effects / Q000235:genetics / Q000378:metabolism; D001422:Bacterial Adhesion / Q000187:drug effects* / Q000502:physiology; D015815:Cell Adhesion Molecules / Q000187:drug effects* / Q000235:genetics / Q000378:metabolism; D002478:Cells, Cultured; D017332:Cetirizine / Q000494:pharmacology*; D015536:Down-Regulation; D004847:Epithelial Cells / Q000382:microbiology* / Q000821:virology*; D005353:Fibronectins / Q000187:drug effects / Q000235:genetics / Q000378:metabolism; D006193:Haemophilus influenzae / Q000187:drug effects / Q000502:physiology; D006801:Humans; D009297:Nasal Mucosa / Q000166:cytology* / Q000382:microbiology / Q000821:virology; D012229:Rhinovirus / Q000187:drug effects* / Q000472:pathogenicity; D013211:Staphylococcus aureus / Q000187:drug effects / Q000502:physiology
chemical_list: D015703:Antigens, CD; C069847:CD66 antigens; D015815:Cell Adhesion Molecules; D005353:Fibronectins; C472067:levocetirizine; D017332:Cetirizine