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Fungal‐Specific Humoral Response in Eosinophilic Mucus Chronic Rhinosinusitis
Author(s) -
Pant Harshita,
Kette Frank E.,
Smith William B.,
Wormald Peter J.,
Macardle Peter J.
Publication year - 2005
Publication title -
the laryngoscope
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.181
H-Index - 148
eISSN - 1531-4995
pISSN - 0023-852X
DOI - 10.1097/01.mlg.0000161341.00258.54
Subject(s) - immunoglobulin e , immunology , alternaria alternata , aspergillus fumigatus , allergy , allergic bronchopulmonary aspergillosis , pathogenesis , fungal sinusitis , sinusitis , eosinophilic , aspergillus , immune system , biology , microbiology and biotechnology , mucus , medicine , antibody , pathology , botany , ecology
Objectives/Hypothesis: An immunoglobulin (Ig)E‐mediated allergic pathogenesis is presumed in allergic fungal sinusitis (AFS), yet extensive polyps and eosinophilic mucus (EM) in the paranasal sinuses may also occur in the absence of allergy. Although a noninvasive fungal pathogenesis is presumed in all chronic rhinosinusitis with EM (EMCRS), fungal‐specific nonallergic immune responses have not been thoroughly investigated. We tested the hypothesis that there is a fungal‐specific humoral response in EMCRS and that it is not confined to IgE. Study Design: EMCRS patients were prospectively stratified into subgroups based on the presence or absence of fungi within EM and of fungal‐specific systemic IgE. There were 12 AFS, 5 AFS‐like, 8 nonallergic fungal eosinophilic sinusitis (NAFES), and 5 nonallergic, nonfungal eosinophilic sinusitis (NANFES) patients. Methods: Alternaria alternata and Aspergillus fumigatus ‐specific serum IgE, IgG, IgM, and IgA was measured by enzyme‐linked immunosorbent assay and compared with strictly defined healthy and disease‐control groups. Results: Fungal‐specific IgG ( Alternaria alternata P = .0002; Aspergillus fumigatus P = .004), and IgA levels ( Alternaria alternata P = .0016; Aspergillus fumigatus P = .002) were higher in EMCRS compared with healthy volunteers but not with disease controls. Fungal‐specific IgG3 levels were significantly elevated in all the EMCRS subgroups compared with controls for either fungal antigen ( P < .0001). Importantly, fungal‐specific IgE levels were not significantly different between fungal‐allergic EMCRS and disease controls. Conclusions: Fungal‐specific immunity characterized by serum IgG3 and not IgE, distinguished the EMCRS subgroups from control groups regardless of the presence of fungus within EM or of systemic fungal allergy. Fungal‐specific IgE responses in fungal‐allergic EMCRS were no different to those in fungal‐allergic controls, thus challenging the presumption of a unique pathogenic role of fungal allergy in “allergic fungal sinusitis.”