Nasal Mucosal Tissue Research Articles

Impaired Norepinephrine-Mediated Contraction of Isolated Nasal Mucosa in Guinea Pigs with Allergic Rhinitis

One of the causes of nasal obstruction associated with allergic rhinitis probably is caused by the dilatation of plexus cavernosum in nasal mucosa. In this study, the change in vascular responsiveness of nasal mucosa was investigated in the septal mucosae isolated from guinea pigs with allergic rhinitis. An allergic rhinitis model was prepared in guinea pigs by repeated challenge with aerosolized dinitrophenylated-ovalbumin antigen. Twenty-four hours after the last antigen challenge, the changes in the isometrical tension of isolated nasal septal mucosa were measured. In isolated nasal mucosal tissues, both norepinephrine (NE) and leukotriene D4 caused concentration-dependent contractile and relaxant responses, respectively. The NE-induced contractile response was significantly attenuated in nasal mucosae of the repeatedly antigen challenged guinea pigs. The mucosal relaxation induced by leukotriene D4 was slightly attenuated in this animal model of allergic rhinitis. This study shows an attenuation of NE-induced contraction of isolated nasal mucosa in the antigen-exposed guinea pigs. The impaired contractile response mediated by sympathetic alpha-adrenoceptors of nasal blood vessels might be involved in the development of nasal obstruction in allergic rhinitis.

Analysis of gene expression profiles of normal human nasal mucosa and nasal polyp tissues by SAGE

A systemic determination of gene expression profiles in nasal polyp compared with normal nasal mucosa would contribute considerably to the investigation of the disease marker in various rhinopathy and general knowledge on the formation of human nasal polyp. The aim of this study was to identify the transcriptome of the normal human nasal mucosa and nasal polyp by the serial analysis of gene expression. mRNA was extracted from normal inferior turbinate mucosa and nasal polyp. Short sequences (tags), each one usually corresponding to a distinct transcript, was isolated and concatemerized into long DNA molecules, which were cloned and sequenced. We detected 65,305 tags for normal nasal mucosa and 55,829 tags for nasal polyp, representing 20,629 and 17,636 potential transcripts species, respectively. Of the unique tags encountered more than once, 92% (normal nasal mucosa) and 90% (nasal polyp) matched known genes or expressed sequence tags, whereas the remainder did not match any GenBank sequences. Therefore, 504 and 539 novel transcripts were identified in normal nasal mucosa and nasal polyp, respectively. Although the expression levels of most transcripts in both libraries were similar, 114 transcripts were differentially expressed at a statistically significant level (P < .05)-that is, 65 and 49 transcripts among them were expressed at a higher level in normal nasal mucosa and nasal polyp, respectively. This information should be very useful for basic knowledge as well as for future studies on pathophysiological conditions of human nasal mucosa, providing some clues to evaluate the altered factors in a variety of rhinopathies. The results of this study might contribute to general knowledge on the formation of human nasal polyp.

Comparison of Norepinephrine Responsiveness of Mucosal Veins in Vivo with that of Isolated Mucosal Tissue in Vitro in Guinea Pig Nasal Mucosa

The vascular responsiveness of nasal mucosa has been determined frequently by using isolated mucosal tissues although it is not clear whether the response of the whole tissue truly reflects the response of the vasculature (especially veins) in mucosa. In this study, the in vivo responsiveness of mucosal veins was compared with in vitro responsiveness of isolated mucosal tissue in guinea pig nasal septa. The in vivo venous responsiveness to norepinephrine (NE) of guinea pig nasal septal mucosa was measured by changes in the diameters of mucosal veins, stereomicroscopically. The in vitro responsiveness to NE of isolated nasal septal mucosae from guinea pigs also was determined by standard organ-bath technique. Application of NE induced concentration-dependent contractile responses both in vivo and in vitro with the pD2 (negative logarithm for 50% effective concentration [M] of NE) values of 5.23 +/- 0.29 and 5.00 +/- 0.17, respectively. The equal potencies obtained by the in vivo and in vitro experiments suggest that an increase in tension of isolated nasal mucosal tissue might be caused by the contraction of mucosal veins. Both the in vivo and the in vitro methods used in this study might be useful for determining vasoreactivity of nasal mucosa in experimental animals.

Increased Expression of Inducible Nitric Oxide Synthase in Nasal Mucosae of Guinea Pigs with Induced Allergic Rhinitis

Nitric oxide (NO) is produced by the action of NO synthase (NOS) isoforms and is considered an important mediator of inflammatory response including airways. In this study, the changes in the expression levels of NOS isoforms in nasal mucosae were determined in a guinea pig model of allergic rhinitis. An allergic rhinitis model was prepared in guinea pigs by repeated challenge with aerosolized dinitrophenylated ovalbumin antigen. Twenty-four hours after the last antigen challenge, the expression levels of NOS isoforms in nasal mucosae were determined by immunoblottings. Changes in the isometrical tension of isolated mucosal tissues of nasal septa induced by histamine were measured also. Although the expression levels of endothelial NOS (eNOS) and neuronal NOS (nNOS) in nasal mucosae were not affected by the repeated antigen exposure, the inducible NOS (iNOS) level was markedly and significantly increased in the challenged animals. In isolated nasal mucosal tissues, histamine induced a concentration-dependent relaxation, which was sensitive to an H1-receptor antagonist, mepyramine, and an NOS inhibitor, L-NMMA. No significant change in the histamine responsiveness was observed between the sensitized control and repeatedly antigen-challenged groups. The expression of three isoforms of NOS, including eNOS, nNOS, and iNOS, was presented in guinea pig nasal mucosa. A marked increase in iNOS expression in the repeatedly antigen-challenged animals suggests an important role of iNOS in the pathogenesis of allergic rhinitis. However, the pathophysiological role(s) of NO generated by iNOS in nasal allergy is still unclear.

Effects of cryptoporus polysaccharide on rat allergic rhinitis associated with inhibiting eotaxin mRNA expression

Aqueous extract from the fruiting body of Cryptoporus volvatus has been reported to present anti-tumor, anti-allergy, anti-inflammation and immunomodulatory activities. However, the effect mechanisms of anti-allergy and anti-inflammation are poorly understood. The aim of study is to evaluate whether Cryptoporus polysaccharides (CP) extracted from fruiting body of Cryptoporus volvatus decrease the development of nasal symptoms, airway hyperresponsiveness (AHR) to methacholine (MCh) and the infiltration of eosinophils in nasal mucosa in rat model of allergic rhinitis, and investigate a possible action mechanism of CP by detecting the expression of eotaxin mRNA in nasal mucosa and lung tissues. Rats were immunized with ovalbumin and consecutive topical antigen instillation was performed. Repeated intranasal ovalbumin challenge caused rhinitis symptom, AHR to MCh, eosinophil infiltration and histological alterations into the nasal mucosa and increase of eotaxin mRNA expression in nasal mucosa and lung tissue were examined. Pretreatment with CP 3, 9 and 27 mg kg −1 (ig) decreased the numbers of sneezing 27.4%, 38.4% and 44.3% and nasal rubbing 27.5%, 34.9% and 47.7% comparison with model group, respectively. CP caused a dose-related inhibition of MCh-induced AHR. CP 27 mg kg −1 decreased the expression of eotaxin mRNA in the nasal mucosa by 35%. These results suggest CP can relieve the symptom, eosinophil infiltration and injury of tissue in nasal mucosa and lung tissue and AHR of allergic rhinitis in rats. Its action mechanism may be associated with the decrease of eotaxin mRNA expression.

Th2 Immunological Inflammation in Allergic Fungal Sinusitis, Nonallergic Eosinophilic Fungal Sinusitis, and Chronic Rhinosinusitis

Noninvasive fungal sinusitis is a heterogenous group of conditions including allergic fungal sinusitis (AFS) and nonallergic eosinophilic fungal sinusitis (NEFS). Th2-mediated cascades have been postulated to be the major inflammatory response in patients with AFS although other mechanisms also may be involved. The detailed mucosal Th2 cytological status of NEFS still has not been studied in great depth. Using a meticulous patient selection algorithm over a 2-year period, infundibular mucosal tissue from patients with AFS, NEFS, chronic rhinosinusitis (CRS), and normal controls was studied (n = 59). Immunohistochemistry for mast cells, eosinophils, and immunoglobulin E (IgE) cells was performed and cell counts per unit area were measured. Mast cell, eosinophil, and IgE+ cell numbers were significantly raised in patients with AFS, NEFS, and CRS when compared with controls. There was no significant difference between cell numbers in patients with AFS and NEFS. Patients with AFS exhibit a classic Th2 inflammatory response in nasal mucosal tissue with NEFS and CRS patients showing evidence of a similar Th2 cascade, including the presence of IgE+ cells.

Effects of 1400W, a potent selective inducible NOS inhibitor, on histamine- and leukotriene D4-induced relaxation of isolated guinea pig nasal mucosa

To clarify the role of inducible nitric oxide synthase (iNOS) in the relaxation of nasal vasculature, the effects of a potent selective iNOS inhibitor, N-[(3-aminomethyl)benzyl]acetamidine (1400W), on histamine- and leukotriene D4 (LTD4)-induced relaxations of isolated nasal septal mucosae were examined in naive guinea pigs. In addition to eNOS and nNOS, Western blots demonstrated a distinct expression of iNOS in nasal mucosal tissues of naive guinea pigs. In isolated nasal septal mucosae precontracted with norepinephrine (3 x 10(-5)M), both histamine (10(-7)-10(-3)M) and LTD4 (10(-10)-10(-7)M) exhibited relaxations, which were inhibited by a NOS inhibitor NG-monomethyl-L-arginine (L-NMMA; 10(-4)M). The inhibitory effect of L-NMMA was reversed by L-arginine (10(-3)M), indicating that the relaxations induced by histamine and LTD4 are mediated by NO. Furthermore, both the histamine- and LTD4-induced relaxations were also significantly attenuated by 1400W (10(-5)M). These findings suggest an involvement of NO generated by iNOS in agonist-induced relaxation of nasal mucosal vasculature in naive guinea pigs.

Malondialdehyde Level and Adenosine Deaminase Activity in Nasal Polyps

Although there are many reports on adenosine deaminase (ADA) activities in different tissues, no information is available about the enzyme activity in nasal mucosa and polyp tissues. Whereas ADA is related to the production of free radicals by neutrophils, malondialdehyde (MDA) is an indicator of lipid peroxidation that is a general mechanism of tissue damage by free radicals. This study is aimed at determining and comparing the ADA activity and MDA level in nasal polyps and normal mucosa. Twenty-three patients with nasal polyps and a control group consisting of 14 patients with septal deviation and lower turbinate hypertrophy were included in the study. Tissue MDA level was measured by the method of Okawa with modification and tissue ADA activity by the method of Giusti. In patients with nasal polyp, mean tissue MDA level and ADA activity were 2.43 +/- 0.38 nmol/mg protein (Pr) and 0.235 +/- 0.055 U/mg Pr, respectively, which were significantly higher than those of control nasal mucosa (1.03 +/- 0.41 nmol/mg protein and 0.056 +/- 0.011 U/mg Pr, respectively) (P < 0.05). In addition, tissue MDA level was positively correlated to ADA activity in nasal polyps (r = 0.701, P < 0.001). The present study showed the presence of detectable ADA activity in nasal mucosa, and also significant increases in both tissue MDA level and ADA activity in NP tissue when compared to normal turbinate tissue. B-2b.

Cutaneous Leishmaniasis? Check the Nose

Mucosal leishmaniasis (ML) — metastatic infection — is a well-known late complication of some forms of New World leishmaniasis. Because of its insidious onset and slow progression, this condition can cause extensive destruction of nasal mucosa, cartilage, and adjacent tissues before being recognized. Researchers in Brazil, an endemic area for Leishmania braziliensis (one …

Nasal Colonization with Streptococcus pneumoniae Includes Subpopulations of Surface and Invasive Pneumococci

We demonstrated that during colonization with Streptococcus pneumoniae the nasal mucosal tissues of mice support two populations of pneumococci. Transparent-phase pneumococci can be readily washed from the outer surface, while a second population composed of primarily opaque-phase pneumococci is released only by homogenization of the nasal tissue. The fact that the opaque phase has previously been associated with invasion and the fact that opaque-phase pneumococci were released by homogenization of previously washed nasal tissue suggest that the opaque-phase pneumococci may have invaded the nasal tissue. Consistent with this hypothesis was our observation that there was inflammation in portions of the nasal mucosa of the colonized mice but not in the mucosa of noncolonized mice, but this observation did not prove the hypothesis. If the opaque-phase pneumococci released from the nasal tissue were from within the tissue and/or if resistance of the opaque-phase subpopulation to antibody, complement, and phagocytes is essential for long-term carriage, it seems likely that the virulence factors of S. pneumoniae that are necessary for killing humans exist to facilitate carriage. Although this speculation is unproven, the observation that there are separate populations of pneumococci during colonization may help guide future attempts to understand the biology of nasal colonization by this pathogen.

In vitro IL-8 production by epithelial cells from nasal mucosa and polyp tissue: Modulation by IL-1B, TNF-a, and dexamethason

RATIONALE: Epithelial cells lining nasal mucosa are believed to contribute to the inflammatory response by the secretion of pro-inflammatory cytokines. We here studied the capacity of isolated epithelial cells to secrete IL-8 and its' modulation by IL-1B, TNF-a and dexamethason. METHODS: Biopsies were taken from inferior turbinates in non-polyp patients (n=20) and from nasal polyp tissue (n=14). A pure and viable epithelial cell population was obtained by the following procedure: incubation overnight with pronase, plating of upper cell layers on plastic plates for 1 hr and performing negative selections of the remaining cells using anti-CD45 and anti-CD15-labelled Dynabeads. 1x10E5 epithelial cells were incubated for 24 hr in medium with/without IL-1B (10 ng/ml), TNF-a (10 ng/ml) and dexamethason (10 mg/ml). RESULTS: IL-8 production by epithelial cells from concha and polyp tissue was similar (80.2 +/- 14.5 vs 102.5 +/- 24.1 pg/ml respectively). Addition of IL-1B to the medium increased (p<0.05) IL-8 production by cells from concha and polyp to 636 +/- 120.8 pg/ml and 344.8 +/- 46.2 pg/ml respectively. TNF-a has synergistic effects with IL-1B in stimulating IL-8 production by epithelial cells (1914 +/- 775 and 433 +/- 108 pg/ml for concha and polyp respectively). IL-8 production by epithelial cells in vitro is unresponsive to dexamethason, both in medium as well as after stimulation with IL-1 and/or TNF-a. CONCLUSIONS: An in vitro culture system for epithelial cells is presented, showing that IL-8 production by epithelial cells from concha and polyp is similar, can be stimulated by IL-1B and TNF-a and is unresponsive to dexamethason.

Suppressive activity of fexofenadine hydrochloride on metalloproteinase production from nasal fibroblasts in vitro

Allergic rhinitis (AR) is an inflammatory disease characterized by nasal wall remodelling with intense infiltration of eosinophils and mast cells/basophils. Matrix metalloproteinases (MMPs), MMP-2 and MMP-9, are the major proteolytic enzymes that induce airway remodelling. These enzymes are also important in the migration of inflammatory cells through basement membrane components. We evaluated whether fexofenadine hydrochloride (FEX), the carboxylic acid metabolite of terfenadine with selective H(1)-receptor antagonist activity, could inhibit MMP production from nasal fibroblasts (NFs) in response to TNF-alpha stimulation in vitro. NFs were established from nasal polyp-derived fibroblasts (PFs) taken from patients with AR. Nasal mucosal fibroblasts (MFs) were also induced from nasal mucosal tissues from septal deformity patients without allergy. PF and MF (2 x 10(5) cells/mL, each) were stimulated with TNF-alpha in the presence of various concentrations of FEX. After 24 h, culture supernatants were obtained and assayed for MMP-2, MMP-9, tissue inhibitor of metalloproteinase (TIMP)-1 and TIMP-2 levels by ELISA. The influence of FEX on mRNA expression of MMPs and TIMPs in 4 h-cultured cells was also evaluated by real-time RT-PCR. Furthermore, nuclear factor-kappa B (NF-kappa B) activation in fibroblasts treated with FEX for 4 h was examined by ELISA. FEX at more than 350 ng/mL inhibited the production of MMP-2 and MMP-9 from both PF and MF in response to TNF-alpha stimulation, whereas TIMP-1 and TIMP-2 production was scarcely affected by FEX. FEX also inhibited MMP mRNA expression and NF-kappa B activation in PF and MF after TNF-alpha stimulation. The present data suggest that the attenuating effect of FEX on MMP-2 and -9 production from NFs induced by inflammatory stimulation may underlie the therapeutic mode of action of the agent on allergic diseases, including AR.

Propylene oxide in blood and soluble nonprotein thiols in nasal mucosa and other tissues of male Fischer 344/N rats exposed to propylene oxide vapors--relevance of glutathione depletion for propylene oxide-induced rat nasal tumors.

High concentrations of propylene oxide (PO) induced inflammation in the respiratory nasal mucosa (RNM) of rodents. Concentrations > or =300 ppm caused nasal tumors. In order to investigate if glutathione depletion could be relevant for these effects, we determined in PO exposed male Fischer 344/N rats PO in blood and soluble nonprotein SH-groups (NPSH) in RNM and other tissues. Rats were exposed once (6 h) to PO concentrations between 0 and 750 ppm, and repeatedly for up to 20 days (6 h, 5 days/week) to concentrations between 0 and 500 ppm. At the end of the exposures, PO in blood and NPSH in tissues were determined. PO in blood was dependent on concentration and duration of exposure. After the 1-day exposures, NPSH depletion was most distinctive (RNM > liver > lung). Compared to controls, NPSH levels were 43% at 50 ppm PO in RNM and 16% at > or =300 ppm in both RNM and liver. Lung NPSH fell linearly to 20% at 750 ppm. After repeated exposures over 3 and 20 days to 5, 25, 50, 300, and 500 ppm, NPSH losses were less pronounced. At both time points, NPSH were 90%, 70%, 50%, 30%, and 30% of the control values in RNM. Liver NPSH decreased to 80% and 50% at 300 and 500 ppm, respectively. After 20 days, lung NPSH declined to 70% (300 ppm) and 50% (500 ppm). We conclude that continuous, severe perturbation of GSH in RNM following repeated high PO exposures may lead to inflammatory lesions and cell proliferation, critical steps on the path towards tumorigenicity.

The correlation between upper and lower respiratory inflammation

Rationale To evaluate the correlation between upper and lower respiratory inflammation. Methods 30 rats were randomly divided into allergic rhinitis group (AR), asthma group (AS), and control group (Con). The pulmonary function was measured by animal pulmonary function instrument, eosinophils and mast cells were detected by hematotoxylin-eosin staining (HE staining) and toluidine blue staining respectively, the expression of VCAM-I and IL-13 in nasal mucosa and lung tissue were examined by immunohistochemistry. ELISA was used to measure the concentration of IL-5 in the peripheral serum. Results The numbers of eosinophils and mast cells in nasal mucosa and lung tissue of AR were both significantly higher than those of Con, and similar results were observed between AS and Con. The forced expiratory volume in 0.3 second (FEV0.3)/forced vital capacity (FVC) of AR and AS was both significantly lower than that of Con. Thenumbers of VCAM-I and IL-13 positive vessels in lung tissue of AR were both significantly higher than those of Con, and similar results were observed between AS and Con. The concentration of IL-5 in the serum of AR and AS was both significantly higher than that of Con. The concentration of IL-5 in serum was positively correlated with the number of eosinophils in peripheral blood of AR and AS. Conclusions The inflammation is similar between AR and AS. Repeated challenging upper respiratory in allergic rhinitis models can result in the expression of VCAM-I and IL-13 in nasal mucosa and lung tissue, which may induce infiltration of eosinophils into lung tissue and result in reduction of FEV0.3/FVC.

Systemic aspects of chronic rhinosinusitis.

Atopic and atopy-related diseases such as asthma, allergic rhinitis, chronic rhinosinusitis, and atopic dermatitis until now have been conceived primarily as occurring in specific local tissues (eg, lung, nose, and skin, respectively). The notion of the systemic nature of allergy has been proposed, based on numerous clinical [1,2], neurophysiologic [3], and epidemiologic [4,5] findings. Although the exact nature of these relationships is not understood fully, an important mechanism to consider is the active participation of the bone marrow (BM) in these local processes, contributing to the ongoing systemic nature of allergic inflammation [6,7]. In response to allergen provocation, a systemic response is activated in patients with allergic diseases, including chronic rhinosinusitis, which involves the initiation of BM production of inflammatory cells (eosinophils, basophils, mast cells) by way of the release and differentiation of progenitors and their progeny; these cells then typically are recruited to nasal mucosa and other tissues in atopic individuals. Understanding the signaling that leads to these systemic responses between the tissue (especially the airways) and the BM at the molecular level may open up new avenues of therapy for allergic inflammation. This article examines how the BM supplies hemopoietic progenitors to sites of allergic inflammation and what modulates these progenitors physiologically and, potentially, therapeutically. Evidence that current and experimental therapies have a systemic effect also is examined.

Botulinum toxin type A induces apoptosis in nasal glands of guinea pigs.

Nasal hypersecretion is predominantly caused by overaction of nasal glands, which are mainly under cholinergic control. In this work, we investigated the influence of botulinum toxin A (BTA) on the nasal mucosal tissue of the maxillary sinus turbinates of guinea pigs (n = 10) that were painlessly sacrificed 10 days (short-term group) or 3 months (long-term group) after local treatment with 20 units of BTA (Botox) or 0.2 mL of 0.9% sodium chloride (control). Histologic investigation of the nasal mucosal tissue of the BTA-treated animals (short-term group) showed degeneration of glands and ducts and apoptotic nuclei on TUNEL staining of these structures. The control animals revealed normal glandular tissue and no apoptosis. The animals of the long-term group showed almost normal glandular tissue and only a few apoptotic nuclei. In conclusion, BTA induces temporary apoptosis in the nasal glandular compartment of guinea pigs.

The basal level of influenza specific antibody-secreting cells in healthy subjects

Background: In the absence of true efficacy markers, the serum haemagglutination inhibition titre has been correlated with protection against influenza infection. Serum antibody does not, however, play a direct role in protection against infection. Two important factors that may be involved in protection against influenza infection are the number of influenza specific activated B-cells and the specificity of the secreted antibodies in the epithelial mucosa of the respiratory tract. Methods: Nineteen patients scheduled for tonsillectomy were enrolled in this study. Tonsils, blood, saliva and a biopsy from the inferior turbinate in the nasal cavity were collected from the patients. None of the patients had been infected or vaccinated with influenza in the previous year. ELISPOT and ELISA assays were used to examine the basal level of antibody-secreting cell (ASC) levels and antibodies in the collected samples, respectively. Results: We found low numbers of influenza specific ASC in the blood and tonsils, but there were much higher numbers of specific ASC in the nasal tissue despite no recent influenza exposure or vaccination. Conclusion: We found antibody-secreting B-cells in the nasal mucosa tissue, which probably results in secretion of specific antibody at the surfaces and protection from influenza infection.

High prevalence of influenza specific antibody secreting cells in nasal mucosa.

Secretory immunoglobulin A (SIgA) provides the first line of defence against pathogens initiating infection via the mucosal route, e.g. the influenza virus. The aim of this study was to examine the basal level of influenza-specific antibody-secreting cell (ASC) in the local mucosa of the upper respiratory tract. Nineteen patients scheduled for tonsillectomy were enrolled for the study, and they had not experienced influenza during the previous year. Tonsils, blood, oral fluid and a nasal biopsy were sampled, and the basal levels of ASC and antibodies (Abs) were determined. We found low numbers of influenza-specific ASC in the blood and tonsils, but there were about 10-100 times higher numbers of specific ASC in the nasal mucosa tissue despite no recent influenza exposure. Thus, the basal level of influenza-specific ASC in the mucosa of the respiratory tract may be important in the protection against influenza infection.

Development of an ex vivo model to study adherence of Mannheimia haemolytica serovar 1 to mucosal tissues of the respiratory tract of cattle.

To develop and validate an ex vivo model for study of adherence of Mannheimia haemolytica (formerly Pasteurella haemolytica) to respiratory tract mucosa of cattle and to use this model to confirm adherence of M haemolytica serovar 1 (Mh1) to several relevant respiratory mucosal surfaces. Excised nasal, nasopharyngeal, turbinate, and tonsillar mucosal tissue from the bovine upper respiratory tract. Mh1 was radiolabeled by use of tritiated leucine. Various concentrations of labeled bacteria were incubated with bovine upper respiratory tract tissues for various times. Tissue was washed to remove nonadherent bacteria, and percentage of bacteria adhered (percentage of adherence) was estimated using radioactivity. Using an optimal inoculum concentration and incubation time, percentage of Mh1 adherence was compared on nasal, nasopharyngeal, turbinate, and tonsillar mucosal tissue, and adherence to nasopharyngeal tissue was confirmed by scanning and transmission electron microscopy. The optimal Mh1 inoculum concentration was 1 X 10(7) colony forming units/ml and incubation time was 3 hours. Percentage of adherence of Mh1 to nasopharyngeal tissue was greater than adherence to other tissue types. The ex vivo model maintained the functional and structural integrity of bovine upper respiratory tract mucosa, as confirmed by light and electron microscopy. Electron microscopy revealed participation of epithelial cell cilia and surface mucus in adherence of Mh1 to nasopharyngeal tissue. Adherence of Mh1 was confirmed in repeated assays, indicating that this organism adheres to upper respiratory tract mucosa of cattle.

Differences in mast cell-bound IgE in the nasal epithelial layer and lamina propria

Mast cells in the allergic nasal mucosa are reported to have higher concentrations of high affinity type I Fce receptors (FcεRI) than mast cells in the non-allergic mucosa. IgE binds to FcεRI on mast cells. However, it is not clear whether different zones within the nasal mucosa harbor different quantities of IgE-bound mast cells. We stained IgE and mast cells from the nasal mucosa of patients with allergic and non-allergic rhinitis using a double-labeling technique with anti-IgE and antitryptase antibodies and compared the intensities of IgE staining of mast cells. In the allergic nasal mucosa, mast cells displayed more IgE staining in the lamina propria than in the epithelial layer. Mast cells displayed more IgE-staining in the allergic nasal mucosa than in the non-allergic mucosa. We speculate that the quantity of IgE that binds to mast cells depends on the quantity of IgE in nasal mucosal tissue.