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PubMed1983

Lectin binding to cell surfaces: comparisons between normal and migrating corneal epithelium.

Comparisons were made between cell surfaces of normal and migrating corneal epithelium of the rat by localizing and/or quantifying concanavalin A (Con A) and wheat germ agglutinin (WGA) binding. Our results indicate that apical cell surfaces of the leading edge of a migrating sheet of epithelium differ from those of normal epithelium and that the various cell layers within the stratified normal epithelium have different lectin-binding characteristics. Three methods of monitoring lectin binding to cell surfaces were employed. Based on ferritin-conjugated Con A, ferritin-conjugated WGA, and [3H]Con A binding, apical cell membranes of migrating epithelia bind more Con A and WGA than do apical membranes of superficial cells of normal stratified epithelia. With both fluorescein isothiocyanate (FITC)-Con A and -WGA, membranes of all the cells of the leading edge of the migrating sheet fluoresce intensely. FITC-Con A binding of normal stratified epithelium is relatively uniform through all cell layers with no discernible staining of the apical membrane of superficial cells. With FITC-WGA, however, fluorescence is present only on basal cell layers but not on superficial cells. These data demonstrate that apical cell surface sugars on a sheet of epithelium migrating to cover a wound differ from the apical cell surface sugars of normal epithelium. As indicated by FITC-WGA binding, cells of the migrating sheet have cell surface characteristics similar to basal cells of normal epithelia. Perhaps, upon wounding, the leading edge of the migrating sheet is derived from the basal cell population of the normal stratified epithelium, or perhaps there is an alteration in cell surface glycoproteins as the cells become migratory.

Animals↗

PubMed1992

Effect of epithelium removal and of enkephalin inhibition on the bronchoconstrictor response to three endothelins of the human isolated bronchus.

The three endothelins ET-1, ET-2 and ET-3 induced a potent contractile response in the human isolated bronchus with an intact epithelium, which proceeded on two different stages. The first stage was observed at low concentrations (high potency) (10(-12) to 10(-9) M) but corresponded to a low intrinsic activity (Emax maximal effect induced by ACh 10(-3) M), the second stage appeared at higher concentrations and corresponded to higher intrinsic activity. The rank order of potency for the two stages of contractile activity was ET-1 greater than ET-2 = ET-3. Removal of the epithelium significantly enhanced the two stages of the contractile responses to the three endothelins and abolished the differences in potency efficacy that were observed between ET-1, ET-2 and ET-3 when the epithelium was present. Phosphoramidon (10(-5) M), an enkephalinase inhibitor, was as potent as epithelium removal in enhancing the contractile responses to these agonists at low concentrations (first stage of contraction, 10(-16) to 10(-9) M). However, with high concentrations of endothelins (greater than 10(-9) M, second stage of contraction), phosphoramidon was less potent than epithelium removal in enhancing the contractile responses. In epithelium-denuded strips, preincubation with phosphoramidon did not further increase the maximal contractions induced by/or the potencies of ET-1, ET-2 or ET-3. After epithelium removal, responses to low doses of endothelins were attenuated by nicardipine (10(-6) M) whereas responses to high doses of the endothelins were not affected, as was also observed when the epithelium was present. (ABSTRACT TRUNCATED AT 250 WORDS)

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

PubMed1995

Epithelium-derived inhibitory prostaglandins modulate human bronchial smooth muscle responses to histamine.

The role of the bronchial epithelium and inhibitory prostaglandins in the induction of histamine tachyphylaxis in human isolated bronchial smooth muscle was investigated using bronchi obtained from 14 patients who had been treated with non-steroidal anti-inflammatory drugs (NSAID) for > 2 months and from 14 untreated patients. Epithelium-intact bronchial strips from untreated patients demonstrated tachyphylaxis to histamine with the maximum response (Emax) reduced by 30 +/- 5% (P < 0.02) and the EC50 increased 1.86-fold (P < 0.02). Tachyphylaxis was not observed in epithelium-denuded strips. In epithelium-intact bronchial preparations from NSAID treated patients, the mean initial maximum tension generated in response to histamine was significantly greater than that for bronchial preparations from untreated patients (P < 0.05). In NSAID-treated patients, both epithelium-intact and denuded preparations failed to demonstrate tachyphylaxis. The generation of prostaglandin E2 and prostacyclin was assessed by radio-immunoassay using bronchi from untreated patients (n = 8). In epithelium-intact bronchial preparations, the generation of both prostaglandin E2 and prostacyclin was significantly increased by histamine exposure (P < 0.05) and was completely inhibited by indomethacin. However, the selective histamine H2 receptor antagonist, ranitidine, selectively inhibited the synthesis of prostaglandin E2 alone. Production of both prostaglandins was not altered by exposure to acetylcholine. These results suggest that prostaglandin E2 and prostacyclin are released primarily from the epithelium in response to histamine and may be specifically involved in inhibiting human bronchial smooth muscle responsiveness to this mediator. Significantly, the release of prostaglandin E2 appears to be selectively controlled by histamine H2 receptors, resident on the epithelium.

Acetylcholine↗

PubMed1995

K+ channel openers produce epithelium-dependent relaxation of the guinea-pig trachea.

The relaxant effects of the K+ channel openers, NIP-121, (+)-7,8-dihydro-6,6-dimethyl-7-hydroxy-8-(2-oxo-piperidin-1-yl)-6H - pyrano[2,3-f]benz-2,1,3-oxadiazole, and cromakalim, were investigated in epithelium-intact and -denuded tracheal spirals isolated from guinea-pigs. In the presence of 5 microM indomethacin, NIP-121 (0.01-1 microM) and cromakalim (0.1-10 microM) relaxed, in a concentration-dependent manner, epithelium-intact and -denuded trachea precontracted with a thromboxane A2 mimetic, U46619, 9,11-dideoxy-9 alpha, 11 alpha-methanoepoxy-prostaglandin F2 alpha (30 nM). The relaxations of epithelium-denuded trachea were significantly decreased as compared with those of epithelium-intact trachea. The relaxations induced by salbutamol or aminophylline were not affected by epithelium removal. In epithelium-intact trachea, the NIP-121- and cromakalim-induced relaxations were not modulated by the neutral endopeptidase inhibitor, phosphoramidon (10 microM), or the nitric oxide synthesis inhibitor, N omega-nitro-L-arginine (100 microM). However, the guanylate cyclase inhibitor, methylene blue (100 microM), significantly reduced NIP-121- and cromakalim-induced relaxation of epithelium-intact trachea. Methylene blue also reduced sodium nitroprusside-induced relaxation but did not affect isoprenaline-induced relaxation. These findings suggest that the K+ channel openers, NIP-121 and cromakalim, may induce, at least in part, epithelium-dependent and methylene blue-sensitive relaxation of the guinea-pig isolated trachea.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMed1987

Calcium uptake into guinea-pig trachealis: the effect of epithelium removal.

Removal of the epithelium from preparations of guinea-pig airways in vitro increases the responsiveness of the smooth muscle of normal and ovalbumin-sensitized animals to a number of contractile agents. To determine if epithelium removal results in an increase in Ca2+ entry into the smooth muscle, the effect of removing the epithelium on Ca2+ uptake into the trachealis smooth muscle was studied using a modified La3+-technique. KCl increased Ca2+ uptake in the presence and absence of the epithelium in control and sensitized animals. Methacholine did not promote Ca2+ uptake, whether or not the epithelium was present, in either control or sensitized animals. Ovalbumin did not stimulate Ca2+ uptake into the trachealis of sensitized animals. These results indicate that the increase in responsiveness of airway smooth muscle seen on epithelium removal is not a consequence of a facilitation of Ca2+ entry into the muscle. The increased responsiveness to methacholine in control animals, and to ovalbumin in preparations in tension studies in epithelium-free tissues from sensitized animals, cannot be explained by an increased availability of extracellular Ca2+ into the muscle, but, rather may reflect some other effect of the epithelium-derived modulatory factor.

Animals↗

PubMed1990

The effect of epithelium removal on human bronchial smooth muscle responsiveness to acetylcholine and histamine.

The respiratory epithelium produces a variety of inflammatory mediators which may be influencing the bronchial hyperreactivity observed in patients with asthma. Animal studies have demonstrated that removal of the epithelium from tracheal and bronchial smooth muscle causes enhanced responses to cholinergic agonists and histamine (Hist). In this study the effect of epithelium removal on human bronchial smooth muscle response to acetylcholine (ACh) and Hist was assessed. Bronchial smooth muscle was obtained fresh from the operating theatre from 12 patients undergoing thoracotomy. Cumulative concentration effect curves (CCEC) for Hist and ACh were generated for epithelium intact and epithelium denuded muscle strips. All CCEC's were performed in duplicate and all denuded strips were obtained from the same airway immediately adjacent to the intact strip. The mean (+/- SEM) maximum response for Hist for the intact strip was 8.6 +/- 1.1 (grams/gram wet weight) and 12.0 +/- 1.4 (grams/gram wet weight) for the denuded strip (p less than 0.05). For ACh the values were 9.3 +/- 1.3 (g/g wet weight and 14.3 +/- 1.8 (g/g wet weight), respectively (p less than 0.05). The pD2 (-log EC50) for ACh was increased two-fold following epithelium removal (p less than 0.05). For Hist there was a similar increase in pD2 but this did not reach statistical significance. Thus removal of the epithelium from human isolated bronchial smooth muscle appears to modulate responsiveness to ACh and Hist. This enhanced responsiveness consequent to epithelium loss may prove important with respect to the development of worsening asthma.

Acetylcholine↗

PubMed2006

Influence of epithelium on beta-adrenoceptor desensitization of guinea pig tracheal smooth muscle.

The effect of tissue incubation with a beta2-agonist of denuded and intact epithelium trachea on the responsiveness to isoprenaline and beta-receptor blocked by propranolol (CR-1) was examined in this study. We examined the effect of epithelium removal on the beta-adrenoceptor desensitization resulting from incubation of guinea pig trachea in the beta-adrenergic agonist isoprenaline (10 microM). Desensitization was measured as the change in EC50, the concentration of beta-agonist that produced 50% relaxation of tracheal rings contracted with methacholine. As a second measure of desensitization, we measured the shift in EC50 resulting from incubation of tracheal rings with the beta-adrenoceptor antagonist propranolol (20 nM), expressed as CR-1 ([post-propranolol EC50/baseline EC50]-1). Initially, we measured desensitization immediately after incubation in isoprenaline; subsequently, we repeated the protocol and allowed a 30 min rest between the end of incubation and the measurement. The sensitivity of denuded epithelium trachea to isoprenaline and (CR-1) was significantly higher than that of intact epithelium only in non-incubated preparations (p<0.05 to p<0.001). Incubation to isoprenaline caused a significant reduction in the tracheal response to isoprenaline in both the denuded groups (p<0.005 for both cases) and intact epithelium groups (p<0.05 for both cases). Incubation to isoprenaline also caused a significant reduction in (CR-1) value in both the denuded groups (p<0.005 for group 2 and p<0.001 for group 4) and intact epithelium only in group 1 (p<0.05). However, the changes in EC50 due to tissue incubation with isoprenaline were significantly greater in denuded than intact epithelium trachea (p<0.05 for all cases) and for CR-1 value only in groups 1 and 2 (p<0.05). These results indicate decrease in both tracheal response to beta-agonist (tolerance) and CR-1 (due to incubation of tissues with isoprenaline), which were greater in denuded epithelium groups.

Adrenergic beta-Agonists↗

PubMed2006

Differential role of FGF9 on epithelium and mesenchyme in mouse embryonic lung.

Mesothelial Fibroblast Growth Factor 9 (Fgf9) has been demonstrated by inactivation studies in mouse to be critical for the proliferation of the mesenchyme. We now show that Fgf9 is also expressed at significant levels in the distal epithelium from the mid-pseudoglandular stages. Using mesenchymal-free lung endoderm culture, we show that FGF9 triggers the proliferation of the distal epithelium leading to the formation of a cyst-like structure. On embryonic Fgfr2b-/- lungs, FGF9 induces proliferation of the mesenchyme but fails to trigger a similar effect on the epithelium, therefore involving the FGFR2b receptor in the proliferative response of the epithelium to FGF9. While FGF9 inhibits the differentiation of the mesenchyme, the epithelium appears to differentiate normally. At the molecular level, FGF9 up-regulates Fgf10 expression in the mesenchyme likely via increased expression of Tbx4 and 5 and controls the transcription of Hedgehog targets Ptc and Gli-1 in a Hedgehog-independent manner. We also show that FGF9 inhibits the activation of the canonical Wnt pathway in the epithelium by increasing Dkk1 expression, a canonical Wnt antagonist. Our work shows for the first time that FGF9 acts on the epithelium involving FGFR2b to control its proliferation but not its differentiation and contributes to the regulation of canonical Wnt signaling in the epithelium.

Animals↗

PubMed1993

HLA expression by benign and malignant prostatic epithelium: augmentation by interferon-gamma.

Chronic prostatitis is a poorly understood entity that is characterized by lymphocytic infiltration of benign prostatic epithelium. Previously, we and others have shown that prostatic epithelium involved by prostatitis is phenotypically different from uninvolved epithelium. In addition, we have shown that malignant prostatic epithelium is rarely, if ever, infiltrated by lymphocytes. We now report that benign prostatic epithelium expresses HLA-DR only in the presence of lymphocytic inflammation, and that benign epithelium without chronic prostatitis and malignant prostatic epithelium do not express HLA-DR. In order to determine whether HLA-DR expression is inducible on malignant prostatic epithelium and therefore, at least theoretically, susceptible to immune regulation, we studied the DU-145 cell line in culture under various conditions. DU-145 cells did not express HLA-DR under routine culture conditions. However, the addition of interferon-gamma (100 to 6000 U/ml.) resulted in HLA-DR expression by DU-145 cells at 24 hours with maximal expression by 72 hours. In contrast, other cytokines (tumor necrosis factor, interleukin-1, interleukin-2) had no effect on HLA-DR expression. These investigations show that interferon-gamma induces HLA-DR expression on the DU-145 prostatic adenocarcinoma cell line, raising the theoretical possibility that malignant prostatic cells may be induced in vivo to express HLA-DR and thus become susceptible to immune regulation.

Adenocarcinoma↗

PubMed1983

The effect of donor cornea epithelium removal on the incidence of allograft rejection reactions.

The most frequent cause of human corneal transplant failure is immunologic rejection. Surface antigenic determinants on nucleated cells are thought to prime the host's immune system for rejection. Greater than 90% of the nucleated cells of the cornea reside in the epithelium; therefore, one might expect that host sensitization and subsequent graft rejection could be modified by epithelium removal prior to transplantation. The major objective of this two-institution combined prospective and retrospective clinical study was to determine the effect of epithelium removal on the incidence of human corneal allograft rejection reaction. A retrospective study of 152 patients showed an incidence of 24.7% rejection reactions in patients with epithelium transplanted compared to 7.2% in the epithelium-removed group (P = 0.008). In the prospective study of 55 patients, there was a rejection incidence of 30% in the epithelium-on group versus 8.0% with epithelium removed (P = 0.04). The decision to remove graft epithelium, however, must be tempered by anticipation of postoperative healing problems.

Cornea↗

PubMed1991

Corneal epithelium following intraepikeratophakia.

The corneal epithelium in eight patients was surveyed by biomicroscopy and specular microscopy before and after the intraepikeratophakia procedure. Autografting of the epithelium was also examined by electron microscopy. Although the superficial layer of the epithelium was damaged, the wing cell layer remained intact, contributing to the epithelialization of the cornea. Epithelialization of the cornea after surgery was completed in three days in all cases. The epithelium was stained with fluorescein, revealing abnormalities in the superficial layer. This stained superficial epithelium was replaced with new epithelium within seven days, but the new, unstained epithelium exhibited an abnormal pattern when observed under the specular microscope. Abnormally shaped cells, cells with nuclei, and white cells were observed, and normal maturation of the epithelial cells was disrupted. These abnormalities lasted more than eight months in three patients. Patient selection and careful follow-up is advised because of the abnormalities of the epithelium.

Adolescent↗

PubMedDate not supplied

Maintaining squamous epithelial architecture in a human cervical epithelium to SCID mouse xenograft model system.

OBJECTIVE: To establish a mouse model system of human cervical epithelium that maintains the stratified squamous architecture overlying a well-defined basement membrane. METHODS: Normal cervical tissue specimens were obtained from the transformation zone of hysterectomy specimens. Small (2 mm) cubes of tissue containing stroma and epithelium were placed subdermally into severe combined immunodeficient (SCID) mice and harvested between 7 and 45 days. Specimens were examined histologically for the presence of stroma, epithelium, and basement membrane. RESULTS: In 49 xenograft attempts in 24 mice, 35 (71%) were identified microscopically. Of these, 28 (80%) had identifiable epithelium and 20 (57%) formed cysts lined with stratified squamous epithelium. A cuboidal basal layer clearly defined the basement membrane. Proliferation within the cyst epithelium was demonstrated by expression of the Ki67 proliferation marker and the presence of mitotic figures. CONCLUSIONS: A human to mouse xenograft model system is described that maintains, in high yield, stratified squamous epithelium overlying a well-defined basement membrane. Advantages of this model system include the following: (1) The tissue originates from readily available human specimens; (2) A stratified squamous epithelial architecture is maintained for a sufficient time to study viral effects on proliferation; (3) The basement membrane of the epithelium is well defined, allowing for investigation of connective tissue factors in cervical intraepithelial neoplasia and cervical cancer.

Animals↗

PubMed2001

The ocular lens epithelium.

An adult lens contains two easily discernible, morphologically distinct compartments, the epithelium and the fiber-cell mass. The fiber-cell mass provides the lens with its functional phenotype, transparency. Metabolically, in comparison to the fiber cells the epithelium is the more active compartment of the ocular lens. For the purposes of this review we will only discuss the surface epithelium that covers the anterior face of the adult ocular lens. This single layer of cells, in addition to acting as a metabolic engine that sustains the physiological health of this tissue, also works as a source of stem cells, providing precursor cells, which through molecular and morphological differentiation give rise to fiber cells. Morphological simplicity, defined developmental history and easy access to the experimenter make this epithelium a choice starting material for investigations that seek to address universal questions of cell growth, development, epithelial function, cancer and aging. There are two important aspects of the lens epithelium that make it highly relevant to the modern biologist. Firstly, there are no known clinically recognizable cancers of the ocular lens. Considering that most of the known malignancies are epithelial in origin this observation is more than an academic curiosity. The lack of vasculature in the lens may explain the absence of tumors in this tissue, but this provides only a teleological basis to a very important question for which the answers must reside in the molecular make-up and physiology of the lens epithelial cells. Secondly, lens epithelium as a morphological entity in the human lens is first recognizable in the 5th-6th week of gestation. It stays in this morphological state as the anterior epithelium of the lens for the rest of the life, making it an attractive paradigm for the study of the effects of aging on epithelial function. What follows is a brief overview of the present status and lacunae in our understanding of the biology of the lens epithelium.

Adult↗

PubMed2002

A histopathological and lectin-histochemical study of the lining epithelium in postoperative maxillary cysts.

OBJECTIVE: Histopathological and lectin-histochemical characteristics were studied in the lining epithelium of postoperative maxillary cysts (POMC). MATERIALS AND METHODS: Histological (HE, PAS, AB), immunohistochemical (CD3 and L26) and lectin (wheat germ agglutinin, WGA; Ulex europaeus agglutinin I, UEA-I; concanavalin A, ConA) stainings were performed in the 360 POMC specimens. The number of goblet cells and inflammatory cells was counted and statistically analyzed. RESULTS: The lining epithelium was classified into three types based on histopathological characteristics; pseudostratified ciliated epithelium (pSCE), transitional epithelium (TE) and stratified squamous epithelium (SSE). Local infiltration of inflammatory cells into the cyst wall was associated with an increased number of goblet cells in the lining epithelium. The observed association between the infiltration of inflammatory cells and an increase in the number of goblet cells was statistically significant in groups with lining pSCE and TE. Glycoconjugate histochemical analysis revealed that the surfaces of the lining epithelium with squamous metaplasia showed an increased degree of staining reactivity with UEA-I, whereas the staining reactivity with ConA was reduced. Goblet cells were able to be stained with WGA and UEA-I, but showed extremely low reactivity with ConA. CONCLUSION: Changes in the glycoconjugate expression of the metaplastic lining epithelium and goblet cell development play an important role in the local defense mechanisms against inflammatory factors in POMC.

Adult↗

PubMed1999

Development of dysplastic mucinous epithelium from endometriosis of the appendix.

AIM: We report an unusual case of mucinous metaplasia and epithelial dysplasia occurring in endometriotic epithelium in the appendix. METHODS AND RESULTS: A 39-year-old woman developed an appendiceal endometriosis in which the endometrial glands displayed extensive areas consisting of mucinous epithelium and Paneth cells. Focally the mucinous epithelium showed low-grade epithelial dysplasia. These changes occurred in portions of the endometriotic tissue closest to the appendiceal lumen. Both the intestinal and endometrial epithelial components were surrounded by typical endometrial-type stroma showing positive reactivity for oestrogen receptor. CONCLUSIONS: Formation of the mucinous epithelium most likely represents a metaplastic process of the endometrial epithelium rather than a result of a simple 'collision' of the appendiceal and endometrial epithelium. Further support for this being a metaplastic process was the presence of glandular structures containing a mixture of mucinous cells, goblet cells, Paneth cells, ciliated and nonciliated endometrial cells, and ciliated and nonciliated mucinous cells, all showing the same positive reactivity for oestrogen receptor. The disposition of mucinous epithelium in the foci of endometriosis in this case suggests that the appendiceal mucosa or extracellular mucin may play a role as an inducer of mucinous cell metaplasia in endometriotic epithelium.

Adult↗

PubMed2005

[Repair and regeneration of the airway epithelium].

Despite an efficient defence system, the airway surface epithelium, in permanent contact with the external milieu, is frequently injured by inhaled pollutants, microorganisms and viruses. The response of the airway surface epithelium to an acute injury includes a succession of cellular events varying from the loss of the surface epithelium integrity to partial shedding of the epithelium or even to complete denudation of the basement membrane. The epithelium has then to repair and regenerate to restore its functions, through several mechanisms including basal cell spreading and migration, followed by proliferation and differentiation of epithelial cells. The cellular and molecular factors involved in wound repair and epithelial regeneration are closely interacting and imply extracellular matrix proteins, matrix metalloproteinases (MMPs) and their inhibitors as well as cytokines and growth factors secreted by airway epithelial and mesenchymal cells. The development of in vitro and in vivo models of airway epithelium wound repair allowed the study of the spatio-temporal modulation of these factors during the different steps of epithelial repair and regeneration. In this context, several studies have demonstrated that the matrix and secretory environment are markedly involved in these mechanisms and that their dysregulation may induce remodelling of the airway mucosa. A better knowledge of the mechanisms involved in airway epithelium regeneration may pave the way to regenerative therapeutics allowing the reconstitution of a functional airway epithelium in numerous respiratory diseases such as asthma, chronic obstructive pulmonary diseases, cystic fibrosis and bronchiolitis.

Animals↗

PubMed1987

[Is there a correlation between the degree of proliferation of vaginal and urethral epithelium and the incidence of stress incontinence? A contribution to estrogen therapy in stress incontinence].

The extent of proliferation of the vaginal and urethral epithelium, as well as urodynamic parameters, were studied in 232 patients in order to determine whether there is a relation between the development of stress incontinence and hormone-related epithelial proliferation. A higher build-up of vaginal than of urethral epithelium was found in 74% of the patients. Even in post-menopause patients, epithelial atrophy in the vagina was only found in 29.3%, while in the urethra it was found in 61.3%. Therefore, the vaginal epithelium cannot with confidence be taken as a basis for conclusions concerning the condition of the urethral epithelium. In the group of 145 patients with urinary stress incontinence no link could be established between the extent of proliferation of the urethral epithelium, the urethral occlusion pressure and the functional length of the urethra: The occurrence of an age-related excessively low urethral occlusion pressure (hypotonic urethra) is independent of the extent of proliferation of the vaginal or urethral epithelium. Sedimentation phenomena are also seen equally frequently in cases with atrophic and eutrophic epithelium. Owing to the high percentage of overweight women among those with stress incontinence, the extent of proliferation of the vaginal and urethral epithelium often corresponds to premenopausal cell pictures even in perimenopausal and postmenopausal women; this is a consequence of increased estrogen production in the peripheral fatty tissue. Therefore, estrogen therapy is unsuccessful in women with pure urinary stress incontinence. However, the efficacy of an equivalent therapy, e.g., with estriol, has been confirmed in cases of active and combined incontinence.

Atrophy↗

PubMed1997

Histochemical study of the epithelia of nasal polyps by biotinylated lectins and neoglycoprotein. A comparison with the normal human respiratory epithelium.

Formalin-fixed, paraffin-embedded sections from human nasal polyps and the normal respiratory epithelium were glycohistochemically investigated. Three biotinylated lectins were used: peanut (Arachis hypogaea) agglutinin (PNA) which, binds to terminal galactose (beta 1-3) N-acetylgalactosamine residues that can be unmasked by a neuraminidase digestion; wheat germ (Triticum vulgare) agglutinin (WGA), which binds to N-acetylglucosamine and N-acetylneuraminic acids; and gorse seed (Ulex europaeus) agglutinin (UEA-1), which binds to L-fucose. In addition, the presence of accessible galactose (beta 1-3) N-acetylgalactosamine (T-antigen) glycan receptors (endolectins) was also assessed. The avidin-biotin-peroxidase complex (ABC) and diaminobenzidine (DAB) were used as chromogen. The ciliated cells of the normal respiratory epithelium and those of the pseudostratified epithelium of nasal polyps possess similar glycohistochemical characteristics suggesting no major alterations on the level of lectin-reactive carbohydrate epitopes as indicators of cellular glycosylations. Notably, this parameter can respond sensitively to changes in cell differentiation or activation. The basal and mucus-secreting cells in the two epithelia display different reactivity patterns emphasizing the presence of dissimilar sugar residues. Similarly, the dysplasia reflecting squamous epithelium of nasal polyps shows a distinct staining behaviour, indicative for disparate glycoconjugate display. Thus, quantitative differences in the lectin-selective staining of various cell types are detectable. The expression of T-antigen-bearing neoglycoprotein binding is weak and similar in both the normal epithelium and the pseudostratified epithelium lining nasal polyps. Only the most superficial cells of the squamous epithelium disclose a moderate labelling with this probe. These results indicate that further studies in this field are warranted, employing neoglycoproteins and also endolectins from human tissues to correlate glycobiological properties of the epithelium of the conducting airways and its diseased forms with functional features.

Adult↗