Biomedical subjects
J G Vinke
Publications and source records attributed to J G Vinke.
[Trigeminal trophic syndrome: 2 patients with a non-healing ulcer on the ala nasi].
Two female patients, aged 74 and 91 years respectively, had a skin ulcer on a nostril and ipsilateral sensory paralysis in the area covered by the N. trigeminus. This is known as trigeminal trophic syndrome. It may be caused by (iatrogenic) damage to the trigeminal nerve by chronic manipulation of the senseless skin. Only in case of doubt, histological examination of a tissue sample is advised to exclude malignancy. The main treatment consists of instructing the patient not to manipulate the skin. In some patients surgical reconstruction is necessary.
Local production and detection of (specific) IgE in nasal B-cells and plasma cells of allergic rhinitis patients.
Allergic diseases are characterized by allergic complaints in the shock organ and specific immunoglobulin (Ig)E in serum. Literature data indicate that the nasal mucosa itself could produce at least a large part of the specific IgE in allergic rhinitis patients. In order to investigate this hypothesis, nasal mucosal biopsies from the inferior turbinate were taken from symptomatic grass pollen allergic rhinitis patients, symptomatic house dust mite allergic rhinitis patients and nonallergic healthy controls, confirmed by radioallergosorbent test and skin-prick test. Immunohistochemical double-staining was performed for B-cells (CD19) with IgE, plasma cells (CD138) with IgE and plasma cells with biotinylated allergens. Significantly more IgE-positive B-cells and IgE-positive plasma cells were found in the nasal mucosa of allergic patients than in that of nonallergic controls. Double staining with biotinylated allergens and plasma cells showed allergen-positive plasma cells in the nasal mucosa of allergic patients and no allergen-positive plasma cells in the nasal mucosa of nonallergic patients. Blocking experiments using polyclonal antibodies directed against IgE showed a significant reduction in the number of allergen-positive cells in contrast to experiments using polyclonal antibodies directed against IgG, IgA or IgM. This study describes new evidence that specific immunoglobulin E is produced locally in the nasal mucosa in patients with seasonal allergic rhinitis and perennial allergic rhinitis, but not in nonallergic controls.
Passive smoking causes an 'allergic' cell infiltrate in the nasal mucosa of non-atopic children.
Environmental tobacco smoke (ETS) is one of the most common indoor pollutants to which many children are exposed. This study was set up to determine possible effects on cellular infiltrates in the nasal mucosa of children exposed to ETS. The research population consisted of a group of ten children exposed to more then 15 cigarettes/day and a control group of ten children without exposure. The groups were matched for age and gender. None of the children had an atopic constitution. Immunohistochemical staining techniques were used to determine the number of Langerhans cells, T cells, B cells, granulocytes, macrophages, mast cells and eosinophils in the nasal mucosa. IgE+ cells and eosinophils were seen in significantly higher cell numbers in the nasal mucosa of children exposed to ETS (Mann-Whitney U-test). IgE+ mast cells were not found to be more numerous in the ETS-exposed group. We can conclude that exposure to ETS causes changes in cellular infiltrates which partly resemble those seen in the nasal mucosa of allergic children. However, no sign of allergic sensitisation can be found in the nasal mucosa. Children with a genetic predisposition to allergic disease will probably suffer most from the 'unstable' nasal mucosa due to ETS.
The role of the adenoid in allergic sensitisation.
Allergic sensitisation of the airways occurs in the mucosa of the shock organ, or in the lymphatic stations draining these structures. The lymphatic structure closest to the nasal mucosa in humans is the adenoid and in mice the nasal mucosa associated lymphoid tissue (NALT). In this study we tried to find evidence for our hypothesis that allergic sensitisation can occur in the adenoid (NALT). The first part of the investigation was set up to determine possible cellular changes in the adenoid of allergic children compared to non-allergic controls using immunohistochemical staining techniques. We found CD1a (Langerhans cells) and eosinophils to be more numerous in the adenoid of allergic children. In the second part of this study we used a murine model to determine if an intranasally applied 'allergen' is processed in the NALT and/or cervical lymph nodes (CLN). An auto fluorescent dye (Di I) was applied into the nasal cavity of mice. At subsequent time intervals mice were terminated. NALT and CLN tissue sections were placed under fluorescent microscopy. We found that Di I transported to both the NALT and CLN. However, the dye remained in the NALT at least 2 days longer than in the CLN. In these studies we found evidence that the lymphoid compartment in the upper respiratory tract (adenoid and NALT) are involved in the processes of allergic diseases.
Differences in nasal cellular infiltrates between allergic children and age-matched controls.
Little is known about the cellular infiltrates in the nasal mucosa of children. This study was set up to compare the nasal cellular infiltrates in biopsy specimens from allergic children and controls. Atopic children were distinguished from controls on the basis of symptoms of allergic rhinitis and/or asthma, total serum immunoglobulin (Ig)E, family history and specific serum IgE to food and aeroallergens. Fifteen allergic patients (median age 4.3 yrs) and 15 age-matched nonallergic control subjects were evaluated. The number of cells positive for CD1a, CD4, CD8, CD19, CD68, chymase, tryptase, IgE and major basic protein was determined in the mucosa of the inferior turbinate. A significantly higher number of IgE-positive cells and mast cells was found in the epithelia of the allergic group. In the lamina propria, higher numbers of IgE-positive cells and eosinophils were found. Langerhans' cells positive for IgE were only seen in allergic children with specific serum IgE against aeroallergens. These children also had a higher number of IgE-positive mast cells compared to controls and atopic children without specific serum IgE. These results show that the nasal cellular infiltrates of allergic children differ from nonallergic control subjects. Prior to the detection of specific serum immunoglobulin E, cellular changes can be found in the nasal mucosa of atopic children.
Differences in cellular infiltrates in the adenoid of allergic children compared with age- and gender-matched controls.
BACKGROUND: Allergic sensitization of the airways occurs in the mucosa of the shock organ, or in the lymphatic stations draining these structures. The lymphatic structure closest to the nasal mucosa is the adenoid. OBJECTIVES: The objective of this study was to find evidence for our hypothesis that allergic sensitization can occur in the adenoid. Of special interest, in this context are cell types involved in antigen-allergen presentation (e.g. Langerhans cells) and effector cells of allergic disease. METHODS: In this study cellular infiltrates in adenoids of 16 allergic patients and 16 age- and gender-matched controls were evaluated. The number of cells positive for CD1a, CD4, CD8, CD-68, chymase, tryptase, IgE, MBP and cells positive for interleukin (IL)-4 were determined using immunohistochemical staining techniques. The epithelium, follicles and the interfollicular spaces were evaluated separately. RESULTS: When comparing the two groups a significant increase in cells positive for CD1a was found in interfollicular spaces of the allergic group (P = 0.008). CD1a+ cells in the follicular space and eosinophils in the interfollicular space showed a trend to be more numerous in the allergic group (P = 0.02 and P = 0.05, respectively). The other cell types investigated did not show significant differences between the groups. CONCLUSIONS: The results of this study show for the first time that cells involved in allergic sensitization and allergic disease differ in the adenoid of allergic children compared with controls. These findings support our hypothesis that allergic sensitization takes place in the adenoid. Furthermore, this study confirms that CD1a+ (Langerhans) cells are involved in allergic disease.
Local IgE production in the nasal mucosa: a review.
IgE is one of the most important markers for allergy. The presence of specific IgE on skin mast cells (skin test) and/or the existence of specific IgE in serum (RAST) indicates sensitization, but not necessarily clinical allergy, in the target organ. Discrepancies between sensitization and disease could be explained by local IgE production. The nasal mucosa contains all the cell types necessary for a local IgE immune response. Moreover, it has been shown that this local IgE is specific for the specific allergen to which the patient is allergic. The availability of IL-4 and IL-13 produced in the nasal mucosa creates the possibility for isotype switching of B cells to IgE-positive B cells, and proliferation and maturation of B cells to IgE-producing plasma cells. The IgE positivity of B cells and plasma cells implies that IgE production occurs in the nasal mucosa. The observation of the presence of allergen-positive plasma cells and the finding that all allergen-positive cells were also IgE-positive indicates that this local IgE production is allergen-specific. Data discussed in this review provide strong evidence for the local production of specific IgE in the nasal mucosa.