Expression of apoptosis mediators p53 and caspase 3, 7, and 9 in chronic rhinosinusitis with nasal polyposis.

Background: The causal factor for the perpetuation of the inflammatory process in chronic rhinosinusitis with nasal polyps (CRSwNPs) has been extensively studied. However, little is known about the influence of cell death in this disease. Thus, the molecular assessment of mechanisms involved in apoptosis might shed light on the pathogenesis of CRSwNPs.

Matrix metalloproteinases and their impact on sinusal extension in chronic rhinosinusitis with nasal polyps.

Unlabelled: MMPs (metalloproteinases) and their inhibitor TIMP (tissue inhibitor of metalloproteinases) are important in tissue remodeling and have been implicated in nasal polyp pathophysiology. The objective of the present study was to evaluate gene expression of MMP-1, MMP-2, MMP-9 and TIMP-1 gene expression in nasal polyps and compare them with normal nasal mucosa. Since MMPs could induce a more prominent tissue edema, we also assessed if these gene expressions could be related to a more extensive disease.

Expression of RANTES, eotaxin-2, ICAM-1, LFA-1 and CCR-3 in chronic rhinosinusitis patients with nasal polyposis.

Purpose: To compare gene expression of the chemokines RANTES and eotaxin-2, its receptor, CCR-3, adhesion molecule ICAM-1 and its receptor LFA-1 in eosinophilic polyps and in control normal nasal mucosa.

Methods: Gene expression was quantified by Real Time PCR in polyps (n=35) and in healthy nasal mucosa (n=15).

Results: Eosinophilic polyps showed a higher expression of eotaxin-2 and RANTES, but not of CCR-3, ICAM-1 or LFA-1 compared to control nasal mucosa.