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PubMedDate not supplied

Distribution of antileukoprotease in upper respiratory mucosa.

Human respiratory tract secretions contain enzyme inhibitors derived from plasma and a low molecular weight, acid-stable protease inhibitor, antileukoprotease. The distribution of antileukoprotease in normal upper respiratory tract mucosa has been studied using an immunohistologic technique. The inhibitor was localized to the serous parts of the submucosal glands of the maxillary sinus and the trachea but was not demonstrable in mucous glands and goblet cells. It is concluded that the antileukoprotease found in respiratory tract secretions is produced locally in the submucosal serous glands.

Humans↗
PubMed2003

Clinicopathologic differences in malignant melanoma arising in oral squamous and sinonasal respiratory mucosa of the upper aerodigestive tract.

OBJECTIVE: Primary mucosal melanomas are rare tumors. We compare melanomas arising in 2 histologically different mucosa, the stratified oral squamous mucosa and pseudostratified sinonasal respiratory mucosa, to investigate the clinicopathologic influence of native mucosal histology on the tumor. METHODS: Clinicopathologic features of 36 melanomas arising in the squamous mucosa of the oral cavity were compared with 59 melanomas arising in the sinonasal respiratory mucosa. RESULTS: The median age of patients was 61 and 63 years for oral and sinonasal melanomas, respectively, with the squamous and respiratory mucosa covering the maxilla being most frequently involved (68.7% and 66%, respectively). The former had a remarkable male predilection (28 men, 8 women), while the latter affected both sexes equally (29 men, 30 women). The oral melanomas were more likely to be detected in the early in situ or microinvasive stage (4 cases vs none, P =.008) and were more frequently amelanotic (14 vs 12, P =.049) than sinonasal melanomas. The sinonasal melanomas were frequently thicker (median thickness, 9 vs 2.6 mm), polypoid (29 vs none), ulcerated (57 vs 20), and necrotic (57 vs 14) than oral melanoma (P <.001). Pseudopapillary architecture was more frequent in sinonasal melanomas (16 tumors vs none, P <.001), and desmoplastic melanomas were more frequent in the oral mucosa (6 vs 1, P =.005). Sinonasal melanoma showed vascular and deep tissue invasion more frequently than oral melanoma; however, no significant difference in disease-specific survival was noted (median survival, 2.8 years vs 3.0 years; 5-year survival, 37% vs 35%, respectively). CONCLUSION: Sinonasal melanomas demonstrated aggressive morphologic features significantly more frequently than oral melanomas; however, prognosis remained similar in both groups.

Adult↗
PubMed2000

Interaction of Bordetella pertussis with human respiratory mucosa in vitro.

The human respiratory tract pathogen Bordetella pertussis is the major cause of whooping cough in infants and young children, and also causes chronic cough in adults. B. pertussis infection damages ciliated epithelium in the respiratory tract. However, the interaction of the bacterium with the respiratory mucosa is poorly understood, and previous studies have either utilized animal tissue which may not be appropriate, or isolated cell systems which lack the complexity of the respiratory mucosa. We have studied the interaction of B. pertussis strain BP536 with human nasal turbinate tissue in an air-interface organ culture over 5 days. We have also compared infection by BP536 with two other strains, Tohama I and CN2992, to determine whether the interactions observed with BP536 are consistent, and, in both nasal turbinate and adenoid organ cultures at 24 h, to determine whether there were differences between tissue from different parts of the respiratory tract. BP536 adhered to cilia, most commonly at their base, and disorganized their spatial arrangement, they also adhered to damaged tissue and mucus, but very rarely to unciliated cells. Within the first 24 h there was a five-fold increase in bacterial density on ciliated cells, and the total number of adherent bacteria increased up to 96 h. Infection caused increased mucus at 24h and an increase in damaged epithelium from 72 h which involved both ciliated and unciliated cells. The number of residual ciliated cells did not decrease after 72 h. The three different strains of B. pertussis exhibited similar interactions with the mucosa, and there was no tissue specificity for adenoid or turbinate tissue. We conclude that B. pertussis adhered to multiple sites on the mucosa and caused hypersecretion and epithelial damage which are the pathological changes described in vivo.

Adenoids↗
PubMed1983

Scanning electron microscopy of arteriovenous anastomosis in nasal respiratory mucosa.

Arteriovenous anastomosis (AVA) in nasal respiratory mucosa of humans and guinea pigs were studied with scanning electron microscopy (SEM) after removal of extracellular connective tissues by tryptic digestion and HCl hydrolysis. The shape of AVA in humans is different from that in guinea pigs. In guinea pigs, it is simple with no specific structure observed on the vessels. In humans, it is characterized by a spherical swelling at the intermediate segment. The Tunica media of the spherical body is formed by the aggregation of spindle-shaped cells and receives a rich nerve supply. These findings suggest powerful contractility of human AVA compared with guinea pigs. Arteriovenous anastomosis in human nasal respiratory mucosa may strongly influence arterial blood flow into the cavernosus sinusoid and determine the characteristic microcirculatory pattern in human nasal mucosa.

Adult↗
PubMed2005

Localization and differential activity of P-glycoprotein in the bovine olfactory and nasal respiratory mucosae.

PURPOSE: The purpose of this study was to demonstrate that P-glycoprotein (P-gp) is localized in the olfactory mucosa and is capable of limiting the nose-to-brain transport of substrates. Bovine olfactory and nasal respiratory mucosae were compared to both localize P-gp and to measure its activity within the epithelia. METHODS: Immunolocalization was performed on the bovine olfactory and nasal respiratory mucosa using the C219 monoclonal antibody. Flux of etoposide, a substrate reported to be primarily effluxed by P-gp, across bovine olfactory and nasal respiratory mucosae was measured using Sweetana-Grass (Navicyte) vertical diffusion cells. Experiments were performed to evaluate the effect of directionality, donor concentration, and the presence of inhibitors. RESULTS: Dense staining was observed on the apical surface of the ciliated epithelial cells and within the submucosal lymphatics/vasculature and mucosal glands of the bovine olfactory and nasal respiratory mucosae. Staining in the nasal respiratory epithelium was weak and patchy when compared to that observed in the olfactory mucosa. The secretory transport (Js-m) kinetics of etoposide in the olfactory (Km = 260.5 microM, Vmax = 0.179 microM/cm(2) min) and nasal respiratory (Km = 46.9 microM, Vmax = 0.034 microM/cm(2) min) mucosae were observed to be saturable and concentration-dependent. The flux of etoposide in the submucosal-mucosal (Js-m) direction was significantly greater than the flux in the mucosal-submucosal (Jm-s) direction in both the olfactory and nasal respiratory mucosa. The efflux ratios (Js-m/Jm-s) of etoposide across the olfactory and the nasal respiratory mucosae were 2.02 and 2.10, respectively. In the presence of inhibitors such as 2,4-dinitrophenol (1 mM) and quinidine (1 mM), etoposide showed an increase in Jm-s and a decrease in Js-m. The etoposide efflux was unaffected in the presence of a specific multiresistance associated protein 1 (MRP1) inhibitor (MK571) and methotrexate, a substrate for BCRP and MRP1-4. CONCLUSIONS: P-gp was localized in the epithelial cells, nasal glands, and the vascular endothelium of both the bovine olfactory and nasal respiratory mucosae, and the expressed P-gp was capable of effluxing a substrate such as etoposide. The Km and Vmax of etoposide efflux were higher in the olfactory mucosa compared to the nasal respiratory mucosa, and the expression of P-gp seems to be greater in the olfactory epithelium compared to the nasal respiratory epithelium based on the staining density observed using immunohistochemistry.

2,4-Dinitrophenol↗
PubMed1996

Effects of topical nasal steroids on human respiratory mucosa and human granulocytes in vitro.

Human respiratory mucosa and human granulocytes were exposed to topical nasal steroids in vitro. The preparations containing benzalkonium chloride and benzalkonium chloride alone destroyed the mucosa within 10 days. The same preparations also inhibited human neutrophil actin polymerization, degranulation and oxidative burst in vitro in a time and concentration dependent manner. Preparations without benzalkonium chloride, as well as the steroid compounds themselves, did not have these effects. It is concluded that benzalkonium chloride has toxic effects on human respiratory mucosa and human neutrophils in vitro.

Adenoids↗
PubMed2004

Inhibition of adherence of Mycobacterium avium complex and Mycobacterium tuberculosis to fibronectin on the respiratory mucosa.

Mycobacterium species adhere to the respiratory mucosa via mucus and fibronectin of extracellular matrix exposed by damaged epithelium. We have investigated whether inhibiting adherence to fibronectin influences subsequent infection of human respiratory tissue by Mycobacterium avium complex and Mycobacterium tuberculosis. Human respiratory tissue was pretreated with mycobacterial fibronectin attachment proteins prior to infection with M. avium complex and M. tuberculosis and the number of recoverable bacteria over time was compared to untreated controls. Inhibition significantly reduced recovery of M. avium complex at 15min (P= 0.02), 7days (P = 0.04), and 14 days (P= 0.03); whereas recovery of M. tuberculosis was only reduced at 15 min (P = 0.01) and not at later timepoints. We conclude that M. avium complex and M. tuberculosis infection of the mucosa proceeds by different mechanisms, since M. tuberculosis infection is independent of fibronectin adherence.

Adhesins, Bacterial↗
PubMed2003

[In vitro culture of cells from respiratory mucosa on foils of collagen, poly-L-lactide (PLLA) and poly-3-hydroxy-butyrate (PHB)].

BACKGROUND: The replacement of respiratory mucosa after surgical resections at different locations in the ENT-field (trachea, nasal septum, sinus maxillaris) seems to be essential or at least of great benefit for patients. Presently a satisfying solution for this challenge does not exist. Therefore we have analysed the growth of cells from respiratory mucosa on different matrices. METHODS: Cell cultures are initiated mainly by growing out cells from tissue pieces but also by seeding of cells after enzymatic dissociation (sequential trypsinization) of mucosa. Cells were cultured with serum-containing and serum-free media on 3 different foils: made of collagen, of Poly-L-lactic acid (PLLA) and Poly-hydroxybutyric acid (PHB). Culturing time was on average about 4 - 5 weeks. RESULTS: On all tested materials fibroblasts and epithelial cells have grown in principle. PLLA was the material with best properties concerning the aim of this study whereas culturing of cells on PHB only happens after surface modification by amino-functionalisation with plasma treatment. Visualisation of cells on materials of collagen could not realised by light-microscopy due to the 3-dimensional structure and the optical properties of this material. Here the cultures were analysed by cell membrane staining and by REM. We could not find a differentiation of epithelial cells with beating cilia 6 weeks after starting the culture. However 20 days after starting the culture on PLLA (good conditions for observation with light-microscope) cells with beating cilia could be observed, in our opinion resulting from dissociated cells from tissue pieces and not from proliferated cells. CONCLUSIONS: In principle the analysed materials are useful for the culturing of cells from respiratory mucosa. However, for obtaining differentiated epithelial cells the culture conditions have to be modified.

Cell Adhesion↗
PubMed1997

[Eosinophil activation by epithelial cells of the respiratory mucosa. Comparative study of normal mucosa and inflammatory mucosa].

BACKGROUND: To investigate the effect of epithelial cells from respiratory mucosa on eosinophil activation. PATIENTS AND METHODS: Epithelial cell cultures were obtained from healthy nasal mucosa and nasal polyps. Eosinophils were isolated from peripheral blood and incubated with epithelial cell conditioned media (HECM) in the presence or absence of dexamethasone (10 microM). Eosinophil survival, expression of EG2 and CD69, and production of eosinophil cationic protein (ECP) and leukotriene C4 (LTC4) were evaluated. Cytokine levels in HECM were assessed by ELISA. RESULTS: HECM induced eosinophil survival (78.6 +/- 9.9% for nasal mucosa, and 92.6 +/- 15% for nasal polyps) compared to controls (1 +/- 0.8%; p < 0.05). Dexamethasone blocked HECM induced eosinophil survival, this effect being greater when eosinophils were primed with nasal mucosa HECM. HECM promoted EG2 expression in eosinophils (47.9 +/- 9.1% for nasal mucosa, and 58.5 +/- 11.8% for nasal polyp) compared to controls (8.1 +/- 3.7%; p < 0.01). HECM had no effect on both CD69 expression and LTC4 release but decreased ECP secretion. Levels of interleukin (IL)-8 (35,700 +/- 7,300 pg/ml), IL-1 beta (11.3 +/- 1.8 pg/ml) and TNF-alpha (38.2 +/- 11 pg/ml) on nasal polyps HECM were significantly higher than on nasal mucosa HECM (17,600 +/- 2,700, 5.4 +/- 0.7 and 16.8 +/- 1.4 pg/ml, respectively; p < 0.05). CONCLUSIONS: Epithelial cells from respiratory mucosa proved to have potential to increase eosinophil survival and activation. The lower inhibitory effect of dexamethasone on nasal polyps induced eosinophil survival and activation may be caused by a higher release of eosinophil activating factors from nasal polyp epithelial cells (inflammed tissue) compared to nasal mucosa.

Antigens, CD↗
PubMed1998

Morphology of intraepithelial corpuscular nerve endings in the nasal respiratory mucosa of the dog.

Corpuscular nerve endings in the nasal respiratory mucosa of the dog were investigated by immunohistochemical staining specific for protein gene product 9.5 by light and electron microscopy. In the nasal respiratory mucosa, complex corpuscular endings, which displayed bulbous, laminar and varicose expansions, were distributed on the dorsal elevated part of the nasal septum and on the dorsal nasal concha. The endings were 300-500 microm long and 100-250 microm wide. Some axons gave rise to a single ending while others branched into 2 endings. Cryostat sections revealed that the corpuscular endings were located within the nasal respiratory epithelium. On electron microscopy, immunoreactive nerve terminals that contained organelles, including mitochondria and neurofilaments, were observed within the epithelial layer near the lumen of the nasal cavity. Some terminals contacted the goblet cell. Such terminal regions were covered by the cytoplasmic process of ciliated cells and were never exposed to the lumen of the nasal cavity. These nerve endings are probably activated by pressure changes.

Animals↗
PubMedDate not supplied

Penetration of doxycycline in respiratory mucosa.

In order to study the penetration of doxycycline (Idocyklin) in respiratory mucosa 100 mg tablets were given in standard dosage to 58 patients with longstanding secretory otitis media, the "secretion-in-cavity" model, and to 37 patients with nasal polyposis, the tissue model. Myringotomy with aspiration of the middle ear secretion or polypectomy was performed at different intervals during the course of medication. Blood samples were drawn simultaneously. The concentration in secretion, tissue and serum was assessed by means of a microbiological agar well method. The mean concentration of doxycycline in respiratory mucosa and secretion was found to exceed the MICs of the common respiratory pathogens as soon as 3 hours after the first dose, and remained on a therapeutical level until 24 hours after the last dose. The results are in full agreement with those obtained from penetration studies in other parts of the respiratory tract, thereby lending support to the validity of the models used.

Adolescent↗
PubMed1997

The effect of rolipram, a type IV phosphodiesterase inhibitor, on Pseudomonas aeruginosa infection of respiratory mucosa.

We have investigated the effect of rolipram, a type IV phosphodiesterase inhibitor, on Pseudomonas aeruginosa infection of the respiratory mucosa of an organ culture model and on the reduction in intracellular cAMP levels seen in human nasal epithelial cells incubated with P. aeruginosa culture filtrate. We have compared rolipram with salmeterol, a long-acting beta-2 agonist, and have also studied the effect of the two agents together. Infected organ cultures had significantly (P < or = .05) increased epithelial damage. Rolipram significantly (P < or = .05) reduced P. aeruginosa-induced epithelial damage and reduced the total number of bacteria adhering to the respiratory mucosa (P < or = .04) in a concentration-dependent manner, although neither rolipram nor salmeterol affected P. aeruginosa growth in broth cultures. Rolipram reduced P. aeruginosa-induced mucosal damage more than salmeterol (P < or = .03). The effect of the two agents was neither additive nor synergistic. Rolipram, salmeterol and both agents together significantly (P < or = .01) increased intracellular cAMP levels in epithelial cells treated with P. aeruginosa culture filtrate. Rolipram alone increased cAMP more than salmeterol or both agents together (P < or = .01), probably because of an interaction between the two agents. These results suggest that agents that elevate intracellular cAMP protect the epithelium during bacterial infection. Rolipram is more effective than salmeterol in preventing P. aeruginosa-induced epithelial damage.

Bacterial Adhesion↗
PubMed1987

Chromogranin in bronchopulmonary neuroendocrine cells. Immunocytochemical detection in human, monkey, and pig respiratory mucosa.

Immunoreactive chromogranin A was demonstrated by immunocytochemistry in the cytoplasm of neuroendocrine cells (NEC) and neuroepithelial bodies (NEB) in human, monkey, and pig respiratory mucosa. Three different antisera (one monoclonal and one polyclonal to human chromogranin A, and one polyclonal to bovine chromogranin A) were applied in this study. Chromogranin immunopositivity varied in extent and intensity according to the antiserum applied and the tissue investigated. The monoclonal antibody revealed the strongest immunoreaction. Good correlation between chromogranin immunoreactivity and Grimelius silver staining was observed by comparing adjacent sections, although more cells seemed to reveal chromogranin immunoreactivity than argyrophylia. Chromogranin appears to be a useful histological marker for APUD cells in the respiratory mucosa of several species.

Animals↗
PubMed1999

Effect of fluticasone propionate and salmeterol on Pseudomonas aeruginosa infection of the respiratory mucosa in vitro.

The purpose of this study was to investigate the effect of the corticosteroid, fluticasone propionate (FP), on Pseudomonas aeruginosa infection of the respiratory mucosa of an organ culture model in vitro. Organ cultures infected with P. aeruginosa had significantly (p< or =0.05) elevated levels of mucosal damage and significantly (p< or =0.05) less ciliated cells compared to controls. Preincubation of tissue with FP (10(-6) or 10(-5) but not 10(-7) M) prior to P. aeruginosa infection significantly (p< or =0.05) reduced the bacterially induced mucosal damage in a concentration-dependent manner. FP (10(-5) M) also significantly (p< or =0.05) prevented loss of ciliated cells. FP did not alter the density of bacteria adherent to the different mucosal features of the organ cultures, but did reduce total bacterial numbers due to the reduced amount of damaged tissue, which is a preferred site of P. aeruginosa adherence. It has previously been shown that the long-acting beta2-agonist salmeterol (4 x 10(-7)M) also reduces the mucosal damage caused by P. aeruginosa infection, probably via elevation of intracellular cyclic adenosine monophosphate concentrations. Preincubation of tissue with both 10(-7)M FP and 10(-7)M salmeterol, concentrations at which they did not by themselves influence the effect of P. aeruginosa infection, significantly (p< or =0.05) reduced P. aeruginosa-induced loss of cilia. However, there was no additional benefit from adding 4 x 10(-7)M salmeterol to 10(-6)M FP. In conclusion fluticasone propionate reduced mucosal damage caused by P. aeruginosa infection in vitro and preserved ciliated cells. There was a synergistic action with salmeterol in the preservation of ciliated cells.

Albuterol↗
PubMed2006

Up-regulation of MUC5AC and MUC5B mucin genes in nasopharyngeal respiratory mucosa and selective up-regulation of MUC5B in middle ear in pediatric otitis media with effusion.

OBJECTIVES: Mucins are the major component responsible for the gel-like properties of mucus secretion. Currently, little is known about the regulation of mucins in otitis media with effusion (OME). We investigated the expression of MUC5AC and MUC5B mucin gene messenger (m)RNAs in middle ear effusions as well as in tissue biopsies of the respiratory mucosa of the nasopharynx by means of reverse-transcription polymerase chain reaction (RT-PCR). STUDY DESIGN: A prospective, controlled, clinical trial. METHODS: The study group consisted of 25 children with a diagnosis of OME who were to undergo bilateral ventilation tube insertion with adenoidectomy. A sample of middle ear effusion (n = 50) as well as tissue biopsy from nasopharyngeal respiratory mucosa (n = 25) were obtained from each patient. For the nasopharyngeal mucosal biopsies, two control groups were made up from 30 children with healthy ears who underwent tonsillectomy +/- adenoidectomy operation; control A, 15 children with adenoid hypertrophy, and control B, 15 children with healthy nasopharynx. RNAs were extracted from effusion and tissue samples, and semiquantitative RT-PCR was performed for MUC5AC and MUC5B to investigate their expression. RESULTS: In the middle ear effusions, MUC5B mRNA expression was detected in 48 (96%), whereas MUC5AC mRNA was detected in 8 (16%). On semiquantitative analysis, MUC5AC/glyceraldehyde 3-phosphate dehydrogenase (GAPDH) and MUC5B/GAPDH mRNA ratios in the study group were significantly increased compared with those in both control groups (P < .05). CONCLUSIONS: The results suggest that the middle ear has a unique mucin gene expression pattern when compared with that of the nasopharynx. Up-regulation of MUC5B in the ear may play an important role in the pathogenesis of middle ear effusions.

Biopsy↗