title: Expression of Innate Immunity Genes in Epithelial Cells of Hypertrophic Adenoids with and without Pediatric Chronic Rhinosinusitis: A Preliminary Report.
abstract: BACKGROUND
  Adenoid hypertrophy (AH) is associated with pediatric chronic rhinosinusitis (pCRS), but its role in the inflammatory process of pCRS is unclear. It is thought that innate immunity gene expression is disrupted in the epithelium of patients with chronic rhinosinusitis (CRS), including antimicrobial peptides and pattern recognition receptors (PRRs). The aim of this preliminary study was to detect the expression of innate immunity genes in epithelial cells of hypertrophic adenoids with and without pCRS to better understand their role in pCRS.
  
  
  METHODS
  Nine pCRS patients and nine simple AH patients undergoing adenoidectomy were recruited for the study. Adenoidal epithelium was isolated, and real-time quantitative polymerase chain reaction (RT-qPCR) was employed to measure relative expression levels of the following messenger RNAs in hypertrophic adenoid epithelial cells of pediatric patients with and without CRS: Human β-defensin (HBD) 2 and 3, surfactant protein (SP)-A and D, toll-like receptors 1-10, nucleotide-binding oligomerization domain (NOD)-like receptors NOD 1, NOD 2, and NACHT, LRR and PYD domains-containing protein 3, retinoic acid-induced gene 1, melanoma differentiation-associated gene 5, and nuclear factor-κB (NF-κB). RT-qPCR data from two groups were analyzed by independent sample t-tests and Mann-Whitney U-tests.
  
  
  RESULTS
  The relative expression of SP-D in adenoidal epithelium of pCRS group was signiﬁcantly lower than that in AH group (pCRS 0.73 ± 0.10 vs. AH 1.21 ± 0.15; P = 0.0173, t = 2.654). The relative expression levels of all tested PRRs and NF-κB, as well as HBD-2, HBD-3, and SP-A, showed no statistically significant differences in isolated adenoidal epithelium between pCRS group and AH group.
  
  
  CONCLUSIONS
  Down-regulated SP-D levels in adenoidal epithelium may contribute to the development of pCRS. PRRs, however, are unlikely to play a significant role in the inflammatory process of pCRS.
authors.forename: Xiao-Peng
authors.initials: XP
authors.lastname: Qu
authors.forename: Zhen-Xiao
authors.initials: ZX
authors.lastname: Huang
authors.forename: Yan
authors.initials: Y
authors.lastname: Sun
authors.forename: Ting
authors.initials: T
authors.lastname: Ye
authors.forename: Shun-Jiu
authors.initials: SJ
authors.lastname: Cui
authors.forename: Qian
authors.initials: Q
authors.lastname: Huang
authors.forename: Li-Jing
authors.initials: LJ
authors.lastname: Ma
authors.forename: Qing-Wen
authors.initials: QW
authors.lastname: Yang
authors.forename: Hong
authors.initials: H
authors.lastname: Wang
authors.forename: Er-Zhong
authors.initials: EZ
authors.lastname: Fan
authors.forename: Ying
authors.initials: Y
authors.lastname: Li
authors.forename: Liang
authors.initials: L
authors.lastname: Zhang
authors.affiliation: Department of Otolaryngology-Head and Neck Surgery, Beijing Tongren Hospital, Capital Medical University, Beijing 100730, China.
authors.forename: Bing
authors.initials: B
authors.lastname: Zhou
mesh_terms: D000234:Adenoids / Q000166:cytology; D023181:Antimicrobial Cationic Peptides / Q000378:metabolism; D002648:Child; D004847:Epithelial Cells / Q000378:metabolism*; D005260:Female; D006801:Humans; D007113:Immunity, Innate / Q000235:genetics / Q000502:physiology*; D008297:Male; D051192:Receptors, Pattern Recognition / Q000378:metabolism; D012852:Sinusitis / Q000378:metabolism*; D051193:Toll-Like Receptors / Q000378:metabolism
chemical_list: D023181:Antimicrobial Cationic Peptides; D051192:Receptors, Pattern Recognition; D051193:Toll-Like Receptors