Mucosal thickening in allergic and idiopathic rhinitis mucosa and its probable mechanism.
BACKGROUND
Rhinitis is a prevalent condition characterized by nasal mucosal irritation. Conflicting studies suggest that the mucosa of patients with allergic and nonallergic rhinitis undergoes thickening.


OBJECTIVE
To investigate mucosal epithelial thickening in allergic and idiopathic rhinitis and to determine if the mechanism is a consequence of altered proliferation or apoptosis.


METHODS
Interactive image analysis was performed on histologic sections of inferior nasal turbinate tissue to measure epithelial thickness in 3 patient groups. Patients with allergic rhinitis (n = 15), patients with idiopathic rhinitis (n = 15), and a healthy control group (n = 10) were compared. Immunohistochemical and morphometric analyses were used to quantify cell proliferation (Mib-1), apoptosis (terminal uridine nick end labeling technique), and the antiapoptotic factor Bcl-2.


RESULTS
Idiopathic epithelium was found to be significantly thickened compared with healthy epithelium (P = .04). Epithelial thickening occurred in some allergic patients, but the findings did not reach statistical significance (P = .22). No statistically significant difference in proliferation as evidenced by Mib-1 staining was seen among the 3 patient groups. Allergic mucosa differed statistically significantly to that of patients with idiopathic rhinitis (P = .01) and healthy controls (P = .005) in showing increased Bcl-2 staining, suggesting reduced apoptosis.


CONCLUSIONS
Allergic epithelium shows significantly decreased apoptosis, which might explain the increased epithelial thickening seen in some study participants. This mechanism does not, however, appear to explain the significantly increased thickening seen in the idiopathic epithelium. Furthermore, both allergic and nonallergic epithelium showed regional thinning and thickening possibly involving an inflammatory infiltrate.
Powe
Desmond G
DG
Department of Histopathology and Surgical Science, Queen's Medical Centre, Nottingham University Hospitals Trust, Nottingham, England. des.powe@nottingham.ac.uk
Keightley
Amy
A
Chester
Mark
M
Sisson
Melanie
M
Jones
Nicholas S
NS
D017209:Apoptosis / Q000276:immunology; D002452:Cell Count; D047093:Eosinophil Major Basic Protein / Q000378:metabolism; D004804:Eosinophils / Q000378:metabolism / Q000473:pathology; D004847:Epithelial Cells / Q000378:metabolism / Q000473:pathology; D006801:Humans; D020287:In Situ Nick-End Labeling; D008407:Mast Cells / Q000378:metabolism / Q000473:pathology; D009297:Nasal Mucosa / Q000378:metabolism / Q000473:pathology*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D012220:Rhinitis / Q000378:metabolism / Q000473:pathology*; D012221:Rhinitis, Allergic, Perennial / Q000378:metabolism / Q000473:pathology*; D053802:Tryptases / Q000378:metabolism; D044767:Ubiquitin-Protein Ligases / Q000378:metabolism
D019253:Proto-Oncogene Proteins c-bcl-2; C513496:MIB1 ligase, human; D044767:Ubiquitin-Protein Ligases; D047093:Eosinophil Major Basic Protein; D053802:Tryptases