Abstract:
:Nasal polyposis (NP) is characterized by chronic mucosal inflammation with infiltrating eosinophils. Eosinophil‑mediated tissue remodeling may be involved in NP pathogenesis; therefore, improved understanding of tissue remodeling may result the identification of novel pathways and therapeutic strategies. The present study aimed to investigate the pathological changes occurring during tissue remodeling in NP, in order to assess the role of intercellular adhesion molecule‑1 (ICAM‑1) in localized tissue remodeling and the potential association between ICAM‑1 expression and markers of eosinophil activation. A total of 28 eligible patients and 10 healthy controls participated in the current study. Nasal mucosal tissues of these subjects were retrospectively evaluated for mucosal remodeling using histopathological staining. ICAM‑1 and eosinophil cationic protein (ECP) expression levels were determined by immunohistochemical analysis. Compared with the healthy controls, all the specimens from NP patients presented substantial epithelial damage, skewed cellular distribution with a reduced density of goblet cells, an increased density of subepithelial gland and increased subepithelial collagen deposition. In addition, the NP specimens exhibited significantly higher eosinophil infiltration and ICAM‑1 expression compared with the controls. Positive correlations were observed between ICAM‑1 and ECP expression levels (P=0.010), as well as between extracellular collagen deposition and ICAM‑1 (P=0.010) and ECP (P=0.012) expression levels in the NP specimens, but not in the control specimens. Morphological evidence demonstrated eosinophil‑mediated tissue remodeling in NP tissues. ICAM‑1 expression in activated eosinophils was associated with NP remodeling, indicating the possibility that ICAM‑1 may regulate NP remodeling.
journal_name
Mol Med Repjournal_title
Molecular medicine reportsauthors
Xin J,Sun H,Kong H,Li L,Zheng J,Yin C,Cao Y,Jia Y,Li Cdoi
10.3892/mmr.2015.3174subject
Has Abstractpub_date
2015-05-01 00:00:00pages
3391-7issue
5eissn
1791-2997issn
1791-3004journal_volume
11pub_type
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