These results point to an important correlation between occupational dust exposure and NP occurrence.

The immune pathogenesis of chronic rhinosinusitis with nasal polyps (CRSwNP) remains obscure. Our aim was to compare humoral immunity and white blood cell counts in patients with CRSwNP and controls. A prospective case–control study was carried out in 37 patients with CRSwNP and 34 controls without CRS. Clinical data were gathered through a systematic interview. Computed tomography scan, skin prick test, spirometry, and immunological parameters (leukocyte differential count, immunoglobulin classes, and immunoglobulin [Ig] G subclasses) in serum specimens were obtained. Statistical analysis was performed using SPSS v.23. The prevalence of chronic lower respiratory diseases was greater in the CRSwNP group ( P < .001), but atopic disease had no significant difference. A significantly higher eosinophil ( P < .001) and basophil relative count ( P = .022) and a lower relative neutrophil count ( P = .013) were found among CRSwNP group. Patients with CRSwNP had higher IgG1 ( P = .022), but lower IgG2 ( P = .014) and IgG3 ( P = .018) serum levels compared to controls; IgG4, total IgG, IgA, IgM, and IgE serum levels did not differ between groups, as well as the prevalence of immunoglobulin classes or IgG subclasses deficiency. The variation observed in peripheral relative leukocyte count and the systemic IgG1 subclass shift are similar to what is known to happen in nasal polyp tissue. A unique systemic immune profile seems to be present in patients with CRSwNP.

EPOS 2012 states that investigation is needed to study a possible role for food allergy in the initiation and perpetuation of chronic rhinosinusitis with nasal polyps (CRSwNP). Our main goal was to compare serum levels of food-specific immunoglobulin G (IgG) and IgE antibodies in patients with CRSwNP and controls. A prospective case–control study with 33 patients with CRSwNP and 31 controls without CRS was carried out. Clinical data were gathered through a systematic interview and blood sample was collected. Enzyme-linked immunosorbent assay tests using OmegaDiagnostics kit with 40 food allergens for detection of specific IgG antibodies were performed and food-specific IgE antibodies were determined by immunoassay using ImmunoCAP. Immunoglobulin classes and IgG subclasses levels were also evaluated. Statistical analysis was performed using SPSS v.23. The overall sum of food IgG antibodies was significantly lower in CRSwNP compared to control group, and this difference was also observed for different specific IgG antibodies (corn, soya, grain legumes, pear and apple, berries, citric fruit). In controls, a positive correlation between IgG1 and the sum of food IgG antibodies was seen, but in CRSwNP group a negative correlation was found. In addition, a significant higher level of IgG1 and lower IgG2 and IgG3 was found among patients with CRSwNP. Levels of serum-specific IgE antibodies against multiallergen food mix (fx5) and against shrimp, strawberry, orange, rye, or egg yolk, as well as the sum of food IgE antibodies, did not differ significantly between the groups. These findings suggest that food allergy does not have an important role in CRSwNP etiopathogenesis, whether it is IgG or IgE mediated. Moreover, the observed suppression of specific IgG antibodies against food allergens, its negative correlation with IgG1 and the IgG1 switching in CRSwNP, can be related to deviated IgG responses against other targets (eg, airborne particles) and warrants future investigation.