Jm. Bernstein et al., NASAL POLYPOSIS - IMMUNOHISTOCHEMISTRY AND BIOELECTRICAL FINDINGS (A HYPOTHESIS FOR THE DEVELOPMENT OF NASAL POLYPS), Journal of allergy and clinical immunology, 99(2), 1997, pp. 165-175
Nasal polyps and turbinates were obtained from individuals undergoing
surgery for symptomatic nasal obstruction caused by nonatopic rhinosin
usitis or allergic rhinosinusitis. One part of the tissue from each pa
tient was fixed in neutral buffered formalin and prepared for study by
histochemical and immunohistochemical methods. Monoclonal antibodies
were used to identify macrophages, lymphocytes, and plasma cells. In m
ost cases (12 of 16, 75%) the remainder of the polyp and turbinate sam
ples was treated with protease to achieve disaggregation of the epithe
lial cells. Those cells were cultured on permeable collagen matrix sup
ports. Transepithelial potential difference and resistance were measur
ed daily. At the time of maximal transepithelial potential difference,
the epithelial cells were mounted in modified Ussing chambers and exp
osed to a sodium-positive channel blocker (amiloride hydrochloride) an
d to selected chloride-negative channel agonists (isoproterenol bitart
rate and adenosine triphosphate). Middle turbinates and polyps were fo
und to have more macrophages, lymphocytes, plasma cells, HLA-DR-positi
ve cells, and eosinophils than the inferior turbinates. Epithelial cel
ls obtained from polyps exhibited higher transepithelial potential dif
ferences and equivalent short-circuit currents than turbinate cell cul
tures. The responses to amiloride, isoproterenol, and adenosine tripho
sphate were also greater for polyp than for turbinate cultures. A theo
ry for the pathogenesis of nasal polyps is proposed. Local release of
inflammatory mediators could cause sodium absorption and chloride perm
eability to be higher in polyps than in turbinate epithelia. Increased
sodium absorption is consistent with the hypothesis that epithelial f
luid absorption contributes to the development of nasal polyps and is
a result of the increased recruitment of inflammatory cells, which are
present in nasal polyps.