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At least 55 records · Page 3Linked to original sources
PubMed1999

Increase in IL-8, IL-10, IL-13, and RANTES mRNA levels (in situ hybridization) in the nasal mucosa after nasal allergen provocation.

BACKGROUND: Allergic inflammation is regulated by the local production and release of several cytokines. OBJECTIVES: This study was designed to assess the changes in mRNA cytokine-positive cells after allergen provocation and to compare these cytokines with tissue eosinophilia as a marker of allergic inflammation. METHODS: A grass pollen allergen provocation study was conducted in autumn, out of the hay fever season. Nasal mucosal biopsy specimens were taken before provocation and 1 hour, 24 hours, and 1 week after allergen provocation. Eosinophils and mRNA-positive cells (in situ hybridization for IL-2, IL-3, IL-4, IL-5, IL-6, IL-8, IL-10, IL-13, IFN-gamma, RANTES, and TNF-alpha) were assessed in the biopsy specimens. RESULTS: After allergen provocation, an increase in cell number was found for eosinophils and cells expressing mRNA for the chemokines IL-8 and RANTES and for the TH2 cytokines IL-10 and IL-13. Significant correlations were found between eosinophils and RANTES and eosinophils and IFN-gamma in the early phase and between eosinophils and IL-5 and eosinophils and RANTES in the late phase. The increase in eosinophils and IL-10 and IL-13 mRNA-positive cells could still be observed 1 week after allergen provocation. CONCLUSIONS: Nasal allergen provocation induced significant tissue eosinophilia and a significant increase in IL-8, IL-13, and RANTES mRNA-positive cells. A significant increase in eosinophils and IL-10 and IL-13 mRNA-positive cells compared with baseline can still be observed 1 week after a single allergen provocation.

Adult↗
PubMed2001

Complement activation in the nasal mucosa following nasal ragweed-allergen challenge.

The aim of this study was to explore complement activation in the nasal lavage following a nasal ragweed-allergen challenge. The study was carried out with 15 adolescents who were allergic to ragweed and with six non-allergic healthy volunteers. Following the baseline measurement after the symptoms were registered, subjects were given increasing doses of ragweed allergen. Lavage fluid was collected and tested for a complement-activation product (C3bBbP). The allergic patients responded to allergen provocation with an increase in C3bBbP formation compared to the initial lavage (p = 0.001). The C3bBbP level remained low in the lavage fluids of the non-allergic controls. We found a strong correlation between the threshold dose that induced symptoms and the dose where the maximum complement activation was detected (r = 0.78, p = 0.001). Our findings indicate that in allergic patients nasal challenge with ragweed allergen induces a rise in complement activation in the nasal lavage fluid. These results highlight the role of the complement system in the allergic inflammation on the nasal mucosal surface.

Allergens↗
PubMedDate not supplied

Sympathetic neurogenic control of blood flow in human nasal mucosa.

Nasal mucosal blood flow was investigated in patients undergoing a stellate ganglion blockade. Elimination of the sympathetic neurogenic control did not affect the resting blood flow in the mucosa, as registered with the 133Xe washout technique. This indicates that the basal sympathetic vasoconstrictor activity is low in the mucosal vessels that regulate blood flow. With laser doppler flowmetry, the normal pattern of spontaneous oscillations in blood flow was seen to be altered following stellate ganglion blockade. This suggests that vasomotion in the mucosa is partly dependent on sympathetic neurogenic activity. Furthermore, the decrease in blood flow normally induced by a peripheral cold provocation could not be elicited after the ganglion blockade, which means that the decrease is mediated by sympathetic vasoconstrictor fibres.

Adult↗
PubMed1987

The clinical condition of IgA-deficient patients is related to the proportion of IgD- and IgM-producing cells in their nasal mucosa.

Nasal biopsy specimens from 15 adult patients with selective IgA deficiency but normal IgG-subclass levels were examined by immunohistochemistry for the presence of immunocytes producing various Ig isotypes. The mucosal samples were completely IgA-deficient except in two cases where 0.9% and 8.4% IgA cells were found, respectively (normal, 69.8%). Numerous IgG- (mainly IgG1-) producing cells were present in 10 samples; in five of these there were additional IgM- but virtually no IgD-producing cells, whereas in the other five a marked dominance of the IgD over the IgM isotype was seen. The latter category of patients had more upper airways infections (recurrent acute rhinosinusitis, otitis media, and tonsillitis) than the former, who had no recurrent upper respiratory tract infections except one patient with recurrent acute rhinosinusitis. The five remaining samples, which contained very few Ig-producing cells, were derived from patients with even more frequent infections than those showing IgD predominance. Our results indicate that IgM acts as a compensatory secretory Ig in the upper respiratory tract of some IgA-deficient subjects. However, immunoregulatory events favouring local IgD responses apparently do not support mucosal defence satisfactorily, either because local production of IgM is hampered or because IgD (which is not a secretory Ig) blocks complement-dependent reactions mediated by IgG and IgM antibodies within the mucosa.

Adolescent↗
PubMed1993

[Immunohistologic study of the nasal mucosa with reference to Langerhans cells].

The distribution of Langerhans cells in human oral mucosa, nasal mucosa and nasal polyps was studied by means of immunohistochemistry. Our study involved 35 participants. The specimens were frozen to -70 degrees C and sliced at 4 microns with a cryostat. Monoclonal antibodies CD1 (OKT6) and the peroxidase-antiperoxidase staining method were used to detect Langerhans cells. In the oral mucosa and the nasal vestibule lined with stratified squamous epithelium, CD1 positive cells were observed and these cells were dendric in form. The cells were found mainly from the intermediate layer to the deep layer of the epithelium. In the inferior turbinate lined with ciliated epithelium, we could not find any CD1 positive cells at all. The nasal polyps in some cases had a normal ciliated columnar epithelium while others had metaplastic stratified squamous epithelium. Both types of epithelium in the same polyp were noted on some occasions. In nasal polyps, CD1 positive cells which showed dendric form were found in the metaplastic squamous epithelium only, and could not be observed in the ciliated columnar epithelium at all. Based on the above results, the presence of Langerhans cells is confirmed not by the anatomical location but by the type of epithelium. Langerhans cells could be detected only in the squamous epithelium. Keratinocytes, which constitute the squamous epithelium, are known to release cytokines. IL-1 (interleukin-1) and GM-CSF (granulocyte-macrophage colony stimulating factor) released from keratinocytes are thought to influence the viability and function of Langerhans cells. The migration of Langerhans cells into squamous epithelium may be regulated by cytokines released from keratinocytes.

Adolescent↗
PubMed1993

The distribution of eosinophil cationic protein positive eosinophils in the nasal mucosa of the nasal allergy patients.

The relationship between the distribution of eosinophils and epithelial damage of the nasal mucosa in nasal allergy was investigated by means of hematoxylin and eosin staining and a technique of immunohistochemistry using the anti-human EG2 mouse monoclonal antibody that reacts with the secreted form of eosinophil cationic protein (ECP). Nasal mucosa tissue of 26 adult nasal allergy patients and of 24 adult non-allergic rhinitis patients was removed surgically. Eosinophilia in the nasal mucosa of the allergy group was greater than that in the non-allergy group. A great number of ECP positive eosinophils accumulating in the nasal mucosa of the allergy group were mostly degranulated at the superficial layer of the lamina propria. Desquamation of the epithelium was observed mainly in the area of eosinophilia with degranulation of the secreted form of ECP in the nasal allergy group.

Adult↗
PubMed1989

[Electron microscopic study of intercellular junction in nasal mucosa of nasal allergy by lectin histochemistry].

To explain of the mechanism of the enhanced nasal epithelial permeability to HRP in patients with nasal allergy, the inferior turbinate mucosa was removed from 6 normal adults and 7 adults with nasal allergy. Difference of the fine structure of the intercellular junction was compared between normal mucosa and mucosa of nasal allergy by electron microscope. Staining pattern of four kinds of HRP-conjugated lectin (HRP-WGA, PNA, UEA-I and RCA-I) was also studied by electron microscope. There was no significant difference in the intercellular space of the mucosa between the normal mucosa and mucosa of nasal allergy. In the epithelial cell membrane, pattern of HRP-lectin staining was almost similar in both groups. In normal nasal epithelium, the intercellular junction consisted of junctional complex; adherent junction, desmosome and gap junction. The intercellular space was approximately 150-250 A in width. The tight junction was located beneath the luminal surface of the epithelium, and belt-like continuation connecting the adjacent cells. It was concluded that enhanced permeability to HRP in nasal allergy was not morphologic changes of the intercellular junction and component and distribution of the glycoconjugates in epithelial cellular membrane, but this may be based on functional changes.

Glycoconjugates↗
PubMed1996

Role of substance P in the vascular response of nasal mucosa in nasal allergy.

The effects of topically administered substance P (SP) on nasal blood flow and nasal airway resistance (NAR) were evaluated in 11 subjects with perennial nasal allergy. The change in NAR induced by SP was compared with those induced by nasal challenge with histamine, leukotriene D4 (LTD4), and antigen. In doses > or = 16 nmol, SP caused a significant increase of nasal blood flow within 5 minutes that lasted for less than 20 minutes. In doses > or = 16 nmol, SP caused a dose-dependent, short-lasting, significant increase in NAR. The magnitude of the increase in NAR was LTD4 > SP > histamine when compared on a molar basis. Our results may suggest that SP released from C fiber terminals is partially involved in an early nasal vascular response after antigen challenge by acting on adjacent vascular smooth muscle to cause a transient vasodilatation of both resistance and capacitance vessels only while sensory stimulation persists in subjects with nasal allergy.

Adolescent↗
PubMed1999

[Microcirculation in the nasal mucosa].

The nasal mucosa has important physiological roles, including the removal of foreign bodies and the warming and humidification of inspired air. The microcirculation in the nasal mucosa facilitates the above processes and plays a role in the periodic swelling and shrinking of the nasal mucosa. In the present article, we reviewed the unique vascular architecture of the nasal mucosa, the complicated feature of innervations by the sympathetic, parasympathetic and sensory nerves, the actions of some chemical mediators released under some pathologic conditions, and the state of microcirculation in the nasal mucosa in cases of nasal allergy and cold exposure. Although it is likely that the sympathetic neurotransmitter norepinephrine has a major role in controlling the microcirculation in the nasal mucosa, the physiological or pathophysiological roles of other transmitters such as neuropeptide Y, ATP, acetylcholine, and vasoactive intestinal polypeptide seem to be minor and vary between species. Nevertheless, nitric oxide, which is shown to be released from parasympathetic neurons, is believed to have some physiological and/or pathophysiological role. Unfortunately, we have yet to describe the mechanism of nasal congestion. Further study of the function of nasal congestion in various illnesses could result in the alleviation of unpleasant symptoms.

Animals↗
PubMed1995

Morphologic examination of rabbit nasal mucosa after the nasal administration of insulin peanut oil suspension and a powder dosage form with soybean-derived sterylglucoside.

Soybean-derived sterylglucoside mixture (SG) is a potentially effective absorption enhancer for the nasal absorption of insulin. Insulin is a peanut oil suspension dosage form and in a powder dosage form with SG were administered into the rabbit nasal cavity. After 0.5 or 1 h, nasal mucosa was taken from the nasal cavity and side effects were examined by an optiphoto light microscope. The insulin in the peanut oil suspension produced a histological change in the nasal epithelium mucosae, as well as mucodermal phlogistic cellular infiltration. The peanut oil suspension with SG showed side effects slightly stronger than without SG. SG alone and the insulin powder dosage form with SG produced no signs of inflammation, erosion or squamous metaplasia. The results from this study indicate that SG can be considered safe.

Administration, Intranasal↗
PubMedDate not supplied

[Eosinophils in nasal mucosa of patients with nasal polyps: preliminary histochemical study].

Glycoproteins and glycolipids play an important role in cellular biological specificity. The use of lectins as histochemical probes may be useful in studying the nasal mucosa. Eosinophils are a common finding in the nasal mucosa of patients with nasal polyposis. Histocytochemistry of eosinophils in the nasal mucosa of such patients revealed reactivity to all lectins used in this study except LTA. This suggests that alpha-L-fucose was not present in the eosinophils of the nasal mucosa of patients with nasal polyposis and asthma.

Asthma↗
PubMed2000

[An electron microscopic study of the relation between epithelial cell damage and eosinophilia in the nasal mucosa of patients with nasal allergy].

To determine the relationship between epithelial damage and eosinophilia in the nasal mucosa of patients with nasal allergy, we examined the nasal mucosa (obtained by surgery) from 74 patients with allergic rhinitis, using light and electron microscopy. The extent of eosinophilia correlated significantly to grades of epithelial damage and torn tight junctions of the epithelial cells. No significant relationships were found between the severity of nasal symptoms and the extents of eosinophilia or grades of torn tight junctions of the epithelial cells. More than 50% specific granules in eosinophils in the allergic nasal mucosa showed normal findings. There were no significant relationships between the extent of eosinophil degranulation and grades of epithelial damage. Based on our results, the release of tubular vesicular structures from the eosinophil granule may be one form of eosinophil degranulation in the nasal mucosa of patients with nasal allergy.

Adult↗