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Notes: Langerhans cells (LC) are very potent antigen-presenting cells. In atopic disorders such as allergic rhinitis and atopic dermatitis LC are known to bear IgE surface molecules. IgE-positive LC can bind allergen and present it to T lymphocytes to induce an allergen-specific T-cell response and IgE synthesis. Therefore, IgE-bearing LC might play an important role in the triggering of the immune system to maintain ongoing IgE synthesis. The importance of the IgE-bearing LC in atopy has not been assessed but deserves further investigation to find out more about the part played by these cells, not only in the atopic disorders described here but also in others such as gastrointestinal allergy and allergic asthma.

Notes: Background Controversy still exists about the effect of 0.02% benzalkonium chloride (BKC). a preservative in many nasal sprays, on human nasal epithelium in vivo. Objective To determine the safety of BKC by assessing its effect on the function and morphology of cilia of human nasal epithelium.Methods A single-centre, double-blind nasal biopsy study in 22 patients with perennial allergic rhinitis, receiving fluticasone propionate aqueous nasal spray (FPANS) containing BKC. BKC plus placebo or placebo alone for 6 weeks. Before, at two weekly intervals during treatment and 2 weeks after treatment ceased an indigocarmine saccharine transport time (ICST) was performed. Results ICST results did not significantly vary between the groups. There was no statistical relationship between the number of ciliated cells present and the treatment the patients received. Scanning and transmission electron microscopy examination showed no effects of BKC.Conclusion Despite reports of its ciliostatic effects in vitro. BKC did not have such an effect when it was applied for 6 weeks (with/without fluticasone propionale) to the nasal mucosa of perennial allergic rhinitis patients in vivo.

Notes: Mast cell degranulation is thought to be an important component of the pathogenesis of allergic rhinitis. Quantitative studies on mast cells in nasal mucosa after allergen exposure have given widely divergent results, ranging from an overall decrease via redistribution to an overall increase. We investigated this problem by employing a combination of anti-IgE and toluidine blue staining of biopsy specimens. In allergic patients anti-IgE was found to identify all mast cells and toluidine blue to detect mast cells that were not (totally) degranulated.The study was composed of two parts done in different patient groups. In the first part of the study biopsies were performed in 23 patients with isolated grass-pollen allergy, once during natural provocation in the summer and once in the winter. Biopsies were also performed in 12 controls. Non-allergic controls were found to have the same number of mast cells in the lamina propria as asymptomatic allergic patients. The controls seldom have mast cells in the epithelium. The patients with isolated grass-pollen allergy showed an increase in the numbers of mast cells in the lamina propria during natural provocation and the same seemed to occur in the epithelium as well. During natural provocation almost all of the mast cells in the epithelium and half of those in the lamina propria were degranulated.In the second part of the study 17 patients with isolated grass-pollen allergy and four controls were challenged daily with allergen extract during a 2-week period in the winter. During this period biopsies were performed at eight different occasions, i.e. once before, six occasions during and once after the provocation period. The results of this part of the study showed that during provocation mast cells migrate to the surface of the nasal mucosa, where they become degranulated, and that the pool of mast cells in the lamina propria was apparently replenished by migration of mast cells from the vessels in the lamina propria. The total number of mast cells in the lamina propria remained approximately the same while the mast cells residing in an increasingly thick layer measured from the basal membrane into the lamina propria became degranulated. After 2 weeks, 82% of the mast cells in the lamina propria was degranulated and it was only in the deepest layers that some toluidine blue positive cells were found.This study can explain the seemingly conflicting reports in the literature on mast cell dynamics and degranulation and shows that the reported differences are due to differences in the techniques used and the time of evaluation.

Notes: Background Epidemiological studies in the past have focused on meteorological conditions, pollution and pollen and their relationship with symptoms of bronchial hyper-reactivity, however, there are no epidemiological studies which examine a wide range of such factors and determine their role in nasal hyper-reactivity.Objective To investigate whether environmental factors can influence symptomatology in non-allergic non-infectious perennial rhinitis (NANIPER) patients, who suffer primarily from nasal hyper-reactivity symptoms.Methods We studied 16 non-smoking NANIPER patients and seven non-smoking controls during a 218-day study period (March–October) by means of daily symptom scores and visual analogue scales for the subsets patency, secretions and sneezing, and compared them to seven primary factors which affected ‘symptoms’ and 10 secondary factors which affected primary factors only.Results The mean symptom scores in the NANIPER and control groups were 2.17 and 0.13, respectively. In NANIPER, the highest correlations of primary factors with symptomatology were found for symptom scores and sneezing with minimum daytime temperature (r = −0.62 and −0.45, respectively), ozone and NO concentrations. Patency and secretions were associated with minimum daytime temperature (r = −0.39 and 0.32, respectively). Time series analysis, however, correcting for several confounders such as autocorrelated symptomatology, showed that minimum daytime temperature and daytime relative humidity made an independent contribution to symptoms. In the control group, correlations were much lower, though present. Time series analysis was not possible.Conclusions We conclude that in a mild climate with relatively low levels of pollution, minor pollution and meteorological disturbances result in substantial changes in nasal reactivity symptoms in NANIPER patients, but not controls, irrespective of other factors such as allergy or infection.

Notes: In the skin, epidermal Langerhans cells (LC) constitute a major population of antigen-presenting cells. These cells are characterized by the expression of both CD-1 (T6) and HLA-DR on the cell membrane. We wanted to know whether similar CD-1/HLA-DR-positive cells occur in the nasal mucosa of patients with an isolated grass pollen allergy and in non-allergic controls. CD-1/HLA-DR-positive dendritic cells were found in columnar and cuboidal epithelium and the lamina propria of the nasal mucosa. These CD-1/HLA-DR-positive cells presumably correspond with LC in the skin. We also found significantly more CD-1-positive cells in nasal biopsy samples of allergic than in those of the non-allergic controls. In the allergic patients some of the CD-1-positive cells were found to be surface IgE-positive, possibly due to passive adherence of IgE to Fc receptors.

Notes: Mast cell degranulation, and the subsequent recruitment of infiltrating inflammatory cells, such as eosinophils, into the nasal mucosa has long been considered the most important model to explain allergic rhinitis. Several studies show a decrease in the number of eosinophils and possibly also mast cells during local corticosteroid treatment. Over the last decade, a new model to explain allergic inflammation has evolved. In this model, Langerhans’cells and T-cells play an important role. Langerhans’cells possess a high affinity receptor for IgE. In patients with allergic rhinitis, allergen provocation results in stimulation of T-cells by the IgE-positive Langerhans’cells. The T-cells produce a number of cytokines which stimulate IgE production as well as the inflammatory reaction. The number of T-cells is not usually influenced by corticosteroid treatment; however, the function of the T-cells, shown by the spectrum of cytokines produced, is clearly influenced. The cells that are most dramatically affected by local corticosteroid treatment are the Langerhans’cells, which completely disappear during treatment. This decrease suggests that there is a reduction in antigen presentation. The subsequent decrease in T-cell stimulation may result in a reduction of the reactions that are dependent on T-cell-derived mediators.

Notes: The effect of nasal corticosteroid therapy on allergic rhinitis is uncertain. In a double-blind, placebo-controlled study over 3 months, we investigated the influence of a new corticosteroid spray, fluticasone propionate aqueous nasal spray (FPANS), on Langerhans cells (CD1a+ cells), HLA-DR+ cells, and T cells in nasal mucosa. Efficacy was evaluated by nasal symptom score. This treatment significantly decreased the number of CDla+ cells and HLA-DR+ cells in the nasal mucosa. Furthermore, a clear trend of decreasing numbers of T cells in nasal epithelium was found. No change in nasal symptom score was found after the treatment period. These findings suggest that fluticasone propionate aqueous nasal spray decreases the antigen presentation in nasal allergy.