Title of article :
Immunohistochemical localization of cytokines and cell adhesion molecules in maxillary sinus mucosa in chronic sinusitis
Author/Authors :
Tsutomu Nonoyama، نويسنده , , Teruhiko Harada، نويسنده , , Jun Shinogi، نويسنده , , Eiji Yoshimura، نويسنده , , Yasuo Sakakura، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2000
Pages :
8
From page :
51
To page :
58
Abstract :
Objective: Chronic sinusitis is a common disease characterized by persistent inflammation of the nasal and paranasal sinus mucosa. Accumulating evidence supports the importance of proinflammatoty cytokines and endothelial cell adhesion molecule (CAM) expression as an initiating process in tissue inflammation. This study was conducted to investigate the localization of major cytokines and CAMs in the maxillary sinus mucosa from patients with chronic sinusitis and from normal subjects. Methods: Maxillary sinus mucosal specimens from patients with chronic sinusitis (n=10) and from normal subjects (n=6) were immunostained with specific antibodies directed against the cytokines (IL-1α, IL-1β, IL-6, IL-8 and TNF-α) and the CAMs (intercellular adhesion molecule-1, ICAM-1 and vascular CAM-1, VCAM-1). Results: The number of immunoreactive cells for IL-1α, IL-1β, IL-6, IL-8, and TNF-α was increased significantly in patients with chronic sinusitis compared with normal controls. Immunoreactivity for ICAM-1 was also increased significantly in patients with chronic sinusitis compared with normal controls, whereas VCAM-1 is only minimally expressed or is absent in both groups. Conclusion: These findings indicate that bacterial and/or viral infection may induce functional and morphologic changes in the maxillary sinus mucosa in chronic sinusitis through enhanced generation of specific cytokines in conjunction with CAMs.
Keywords :
cytokines , Cell adhesion molecules , immunohistochemistry , Maxillary sinus mucosa , Sinusitis
Journal title :
Auris Nasus Larynx
Serial Year :
2000
Journal title :
Auris Nasus Larynx
Record number :
567309
Link To Document :
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