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PubMed2001

Intact corneal epithelium is essential for the prevention of stromal haze after laser assisted in situ keratomileusis.

AIMS: To determine the effect of intact corneal epithelium on stromal haze and myofibroblast cell formation after excimer laser surgery. METHODS: Denuded epithelium alone, photorefractive keratectomy (PRK), laser in situ keratomileusis (LASIK), or LASIK with denuded epithelium was performed in rabbit eyes. Postoperative anterior stromal haze was assessed employing a standard scale. Immunohistochemical methods were used to detect alpha smooth muscle actin (alpha-SMA), a marker for myofibroblastic cells, and type III collagen in subepithelial corneal tissue. RESULTS: Three weeks after surgery, the presence of alpha-SMA positive long extended and spindle-shaped stromal cells, and synthesis of type III collagen were observed in the subepithelial stromal layer corresponding to corneal haze in PRK and LASIK with denuded epithelium, but not in denuded epithelium alone and LASIK. CONCLUSION: The intact corneal epithelium may play an important part curbing subepithelial haze and differentiation of myofibroblasts in corneal wound healing.

Actins↗
PubMed1993

Electrogenic Na+ absorption of rat distal colon is confined to surface epithelium: a voltage-scanning study.

There is no quantitative assignment of large intestinal electrogenic Na+ absorption to surface epithelium and crypts so far. We determined the spatial distribution of electrogenic Na+ absorption to crypts and surface epithelium of rat late distal colon using a modified voltage-scanning technique. Voltage deflections resulting from external 30-Hz current were sensed by an extracellular microelectrode stepping at 0.7 Hz above crypt openings or surface epithelium. Local conductances were calculated applying a planar model of electrical field distribution to surface epithelium and a electrostatic disk source model to the crypts. These models were confirmed by methodological experiments where the electrode position was varied in vertical and horizontal direction. Electrogenic Na+ absorption was detected by blocking apical Na+ channels by mucosal 0.1 mM amiloride. Under control conditions surface epithelium contributed 44% (2.0 +/- 0.2 mS/cm2) and crypts 56% (2.6 +/- 0.2 mS/cm2) to the total conductance of 4.6 +/- 0.4 mS/cm2. Electrogenic Na+ absorption was induced by 6 h in vitro incubation in a medium containing 3 nM aldosterone. This caused a short-circuit current (ISC) of 12.1 +/- 0.8 mumol.h-1.cm-2, which was paralleled by a 2.5-fold increase in surface epithelial conductance to 5.1 +/- 0.4 mS/cm2, whereas crypt conductance was not significantly altered (3.0 +/- 0.2 mS/cm2). Amiloride reversed ISC to -0.8 +/- 0.1 mumol.-1.cm-2 and decreased surface epithelium conductance to 2.3 +/- 0.3 mS/cm2 but again had no significant effect on crypt conductance (2.5 +/- 0.3 mS/cm2). Sham incubation (no hormones added) for 6 h neither induced electrogenic transport nor altered local epithelial conductances.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone↗
PubMed1996

Influence of amphotericin B on the sodium pump of porcine lens epithelium.

Active transport by Na(+)-K(+)-ATPase in the monolayer of lens epithelium is vital for the regulation of sodium and potassium levels within the mass of fiber cells that make up the bulk of the lens. In this study, experiments were conducted using porcine lenses to test whether Na(+)-K(+)-ATPase activity in the epithelium is altered when the permeability of lens cell plasma membranes is increased by the ionophore amphotericin B. After 24 h, sodium was significantly (P < 0.01) elevated in lenses exposed to 5 or 10 microM amphotericin B. Amphotericin B stimulated 86Rb uptake, probably through an increase of cytoplasmic sodium concentration due to increased inward sodium leak; the rate of ouabain-sensitive potassium (86Rb) uptake by intact lenses was significantly increased by amphotericin B at 5 microM (P < 0.05) and 10 microM (P < 0.01). After 24 h, the epithelium from lenses exposed to amphotericin B had an Na(+)-K(+)-ATPase activity that was more than twofold higher (P < 0.01) than the Na(+)-K(+)-ATPase activity in control lenses. By immunoblot, there was an increase in Na(+)-K(+)-ATPase catalytic (alpha) subunit immunoreactive polypeptide in the epithelium of lenses exposed to amphotericin B. The increase stemmed from a marked increase of Na(+)-K(+)-ATPase alpha 2-immunoreactive polypeptide but little change in the amount of alpha 1-immunoreactive protein. As judged by immunoblot experiments, the amount of Na(+)-K(+)-ATPase beta 1-immunoreactive polypeptide also appeared to be higher in the epithelium of amphotericin B-treated lenses compared with control lenses. In summary, these results suggest that in response to a permeability challenge with amphotericin B, the porcine lens epithelium is able to increase the activity of Na(+)-K(+)-ATPase. The same permeability challenge also appears to stimulate the biosynthesis of Na(+)-K(+)-ATPase catalytic subunit as well as glycoprotein subunit polypeptides.

Amphotericin B↗
PubMed1995

Hydrogen peroxide contracts human airways in vitro: role of epithelium.

The effects of hydrogen peroxide (H2O2) on human airway smooth muscle tone were determined in vitro. Treatment with H2O2 led to transient concentration-related contractions in the organ bath, amounting to 118 +/- 14 mg (mean +/- SE; n = 12) at 1 mM H2O2, and to greater and more prolonged contractions under superfusion conditions, amounting to 451 +/- 71 mg (n = 17) at 1 mM H2O2. Epithelial removal augmented the response to H2O2 in both systems. Addition of catalase (500 U/ml) abolished the effects of H2O2. Pretreatment of superfused tissues with indomethacin (3 microM) shifted the concentration-effect curve to H2O2 rightward and almost abolished the response to 1 mM H2O2 in epithelium-intact preparations (n = 16; P < 0.05); the response in epithelium-denuded tissues was also significantly inhibited (n = 16; P < 0.05). Pretreatment of the tissues with the TP prostanoid-receptor antagonist GR-32191B (1 microM) also inhibited the contractile effect of H2O2 in epithelium-intact and -denuded tissues. In separate experiments, H2O2 resulted in concentration-related generation of prostaglandin (PG) D2 from isolated airway preparations. The amount of PGD2 released was not different in tissues with intact epithelium compared with those without (n = 9; NS). We conclude that H2O2 exerts on isolated human airways a contractile effect that is augmented by epithelium removal and is largely mediated by prostanoids. The source of PGD2 does not appear to be the epithelium, which we suggest serves mainly as a barrier against H2O2-mediated bronchoconstriction.

Aged↗
PubMed1997

HSP27 elevated in mild allergic inflammation protects airway epithelium from H2SO4 effects.

Inflammation in allergic individuals is hypothesized to elevate stress proteins [heat shock proteins (HSP)] in airway epithelium, which may protect cells from further adverse conditions. Allergic, either asthmatic or not, and normal volunteers participated in a 2-day segmental allergen challenge bronchoscopic procedure. Bronchial epithelium was obtained before and after challenge. Epithelium was exposed to medium with H2SO4 (pH5), returned to medium at pH 7.4, and finally harvested for Western blotting with anti-27-kDa HSP (HSP27) antibody. Prechallenge epithelium of all subjects had significantly inhibited ciliary function by H2SO4 (pH 5) conditions (P < 0.001); only epithelium of normals recovered (P = 0.02). Allergic subjects with mild inflammation (< 50 micrograms/ml increase in albumin in bronchoalveolar lavage) had significantly increased HSP27 postchallenge (P = 0.01) and little ciliary dysfunction at pH 5, whereas subjects with severe inflammation (> 50 micrograms/ml increase in albumin) had little change in HSP27 and significant ciliary inhibition (P = 0.02). Normal epithelium had similar trends in HSP27 and equivalent inhibition of ciliary activity at pH 5 before and after allergen challenge. These data indicate that mild inflammation to allergen elevates HSP27 stress protein levels, thereby potentially protecting epithelial function from additional adverse conditions.

Adult↗
PubMed1990

Epithelium, contractile tone, and responses to relaxing agonists in canine bronchi.

Experiments were conducted in canine bronchi to determine whether the effect of epithelium removal on relaxations was affected by the contractile agent used to induce active force and the degree of contraction. Pairs of fourth-order bronchi with and without epithelium were suspended in organ chambers in physiological salt solution (95% O2-5% CO2, 37 degrees C). The bronchi were contracted to the concentration of acetylcholine or 5-hydroxytryptamine that resulted in a contraction that was 40 or 80% of the response to 10(-4) M of the agonist (ED40 or ED80). Epithelium removal reduced relaxations to isoproterenol and sodium nitroprusside during contraction to the ED80 but not the ED40 of acetylcholine. Responses to forskolin were not affected. Bronchi were significantly more sensitive to relaxing agonists in the presence of 5-hydroxytryptamine; there was no effect on epithelium removal or level of contraction. Thus 1) the influence of epithelium on bronchial relaxation is greatest during high degrees of cholinergic tone and 2) experimental conditions influence the effect of epithelium removal on relaxation.

Acetylcholine↗
PubMed1993

Cationic proteins alter smooth muscle function by an epithelium-dependent mechanism.

Using a perfused guinea pig tracheal tube preparation, which allows the selective application of agonists to either the serosal or luminal surface, we have investigated whether two synthetic cationic proteins, poly-L-arginine and poly-L-lysine, can modify epithelium-dependent responses. With an intact epithelium, methacholine was approximately 150 times less potent when applied intraluminally than when applied extraluminally. This difference was abolished by chemically removing the epithelium with the detergent CHAPS. Intraluminal application of KCl induced a dose-related relaxation of a precontracted trachea, which was also abolished by epithelium removal. Perfusion of the luminal surface with cationic proteins for 1 h (10 micrograms/ml) increased the potency of intraluminally applied methacholine without modifying the responses to extraluminally applied methacholine. Cationic proteins also attenuated the relaxant effects of intraluminally applied KCl. These effects occurred in the absence of any overt epithelial cell damage. In contrast, when the serosal surface of the trachea was treated with poly-L-arginine, there was no modification of either methacholine-induced contraction or KCl-induced relaxation. The effects of poly-L-arginine were inhibited by coperfusion with the polyanions albumin (10 micrograms/ml) or heparin (100 micrograms/ml). In contrast to cationic proteins, intraluminal perfusion with a polyanion, poly-L-aspartate (10 micrograms/ml), failed to modify either methacholine-induced contraction or KCl-induced relaxation. Our data demonstrate that cationic proteins can modify epithelium-dependent responses in the airways. Although the precise mechanisms are unclear, a role is suggested for a charge-mediated interaction with the respiratory epithelium, resulting in airway smooth muscle dysfunction.

Albumins↗
PubMed1998

Calcium-dependent proteolysis in rabbit lens epithelium after oxidative stress.

The purpose of this study was to examine changes in calcium-dependent proteolytic activity in the lens epithelium from whole rabbit lenses exposed to long-term oxidative stress at near physiological levels. Rabbit lenses, incubated in 50 microM H2O2 for 1 or 24 h, were checked for clarity and morphological changes in the epithelium. Proteolytic activity was measured in the epithelium using a fluorogenic synthetic substrate; N-succinyl-Leu-Tyr-7-amino-4-methylocoumarin, both in the presence and the absence of calcium (1 mM Ca2+ and 5 mM EDTA respectively). The effect on transparency and morphology of the epithelium following a 1-hour incubation in 100 microM H2O2 was also studied. Lenses incubated in 50 microM H2O2 were clear even after 24h. After a 1-hour incubation in 50 microM H2O2 the epithelium of the exposed lens appeared normal. However, after 24 h the epithelium cells appeared swollen and microscopical examination showed extensive intracellular and subepithelial vacuolization. Incubation in 100 microM H2O2 for 1 h caused loss of transparency; vacuole formation, globulization of the superficial lens fibers and death of the epithelial cells. There was a 55% increase in calcium-dependent proteolytic activity after 1 h in 50 microM H2O2, implying a role for the calcium-activated protease calpain in oxidatively induced cataract.

Animals↗
PubMed2002

Changes in the epithelium of the vaginal complex during the estrous cycle of the marsupial Monodelphis domestica. 1. Transmission electron microscopy study.

The vaginal complex of marsupials differs from that of eutherians. Cervices open separately in a sinus vaginalis or cul-de-sac. Two lateral vaginae adjoin the sinus vaginalis and fuse at the level of the urethra opening and form the sinus urogenitalis. During the estrous cycle the vaginal epithelium undergoes a number of specified morphological changes. This paper is the first to describe these changes on an ultrastructural level in a marsupial. Investigations in Monodelphis vagina reveal that a cyclic switch exists between a keratinized and a stratified nonkeratinized epithelium. Keratinization starts during proestrus and reaches its maximum during estrus. In the postestrus, desquamation of the stratum corneum takes place, mostly in two steps. In metestrus one to two additional layers of the now nonkeratinized surface cells are shed into the vaginal lumen. Typical cell structures, such as keratin filaments, keratohyalin and membrane-coating granules, are involved in the keratinization process. Keratohyalin is found in the cytoplasm as well as in the nucleus of stratum granulosum cells, a phenomenon which is known from other parakeratinized epithelia of rapid turnover. Membrane-coating granules, responsible for the permeability barrier between the epithelial cells, are of the nonlamellated type in the nonkeratinized epithelium and produce an amorphous material in the intercellular spaces after extrusion. At periods, however, when the epithelium is keratinized, membrane-coating granules are of the lamellated type and form a lamellated barrier structure after extrusion in the intercellular space. The loss of the protective keratinized layers asks for an additional defense mechanism for the epithelium. The migration of leukocytes through the epithelium predominantly during post- and metestrus and their presence in the vaginal lumen may play a protective role together with the bacterial content.

Animals↗
PubMed1987

The transitional zone in the epithelium lining the mouse epiglottis.

The epithelium lining the caudal surface of the mouse epiglottis occupies the transitional zone between the keratinized stratified squamous epithelium, continuing from the oral cavity, and the ciliated columnar epithelium, extending into the laryngeal cavity. The epithelium showed gradations ranging from stratified squamous through stratified cuboidal to ciliated stratified low-columnar type. It is suggested that the epithelium is identical with the 'intermediate epithelium' in the mouse nasopharynx.

Animals↗
PubMed1989

Solute and water transport across the pulmonary epithelium: a new chapter in lung physiology inaugurated by Alfred Jost.

Early experiments by Jost and Policard demonstrated the presence of secretory activity in the lungs of the fetal rabbit. Subsequent work has demonstrated a system of active ion transport across the pulmonary epithelium of the sheep fetus, in which uphill movement of chloride ions to the pulmonary lumen provides the main force for lung liquid secretion. In the last 10-20% of gestation a reabsorptive mechanism in response to beta-adrenergic stimulation is developed which is brought into play in the perinatal period, clearing the lungs of liquid. The development of this response has been shown to require thyroid hormones. The action of adrenaline (or of a directly induced rise in intracellular cAMP) depends on the initiation of active sodium transport from the luminal side of the epithelium. Active glucose-sodium cotransport, maintaining a low glucose concentration in fetal pulmonary liquid, has also been demonstrated in this epithelium. In the postnatal period, sodium absorption continues to be a feature of the lung periphery and the epithelium of the conducting airways is known to be a site of an active ion transport system which features both chloride secretion and sodium absorption. However, this epithelium responds quite differently from the fetal peripheral epithelium to beta-adrenergic stimulation by increasing chloride secretion with little or no change in sodium absorption.

Animals↗
PubMed1989

Toxicity of eosinophil cationic proteins for guinea pig tracheal epithelium in vitro.

We tested the effects of four eosinophil granule cationic proteins: major basic protein (MBP), eosinophil cationic protein (ECP), eosinophil peroxidase (EPO), and eosinophil-derived neurotoxin (EDN), on guinea pig tracheal epithelium in vitro. Examination by inverted microscopy revealed that MBP, both the form stabilized by alkylation of sulfhydryl groups as well as the native form of the molecule, ECP, EPO by itself, as well as EPO + H2O2 + halide, but not EDN, cause dose-related damage to the tracheal epithelium. The lowest concentrations of MBP and ECP causing damage were 10 and 100 micrograms/ml, respectively. In contrast, EDN, although biochemically similar to ECP, did not damage the tracheal epithelium in concentrations of up to 200 micrograms/ml. MBP caused exfoliation, as well as bleb formation and ciliostasis. EPO in the presence of the H2O2-producing enzyme glucose oxidase (GO), Cl-, 0.11 M, and iodide caused ciliostasis, bleb formation, and exfoliation of epithelial cells at concentrations as low as 1 U/ml (3.9 micrograms/ml). EPO + GO in the presence of Cl-, 0.11 M, alone or with Cl- and l-, 10(-4) M, or Cl- and Br-, 5 x 10(-5) M, were all toxic to epithelium. Surprisingly, EPO by itself caused partial ciliostasis, bleb formation, and exfoliation of epithelial cells in a dose-related manner at concentrations as low as 10 to 30 U/ml (39 to 121 micrograms/ml). These results confirm prior observations showing the toxicity of MBP to tracheal epithelium and indicate that ECP and EPO alone, as well as EPO + GO + halide, cause damage. Thus, several eosinophil granule proteins are able to damage respiratory epithelium.

Alkylation↗
PubMed1987

Modulation of rabbit airway smooth muscle responsiveness by respiratory epithelium. Involvement of an inhibitory metabolite of arachidonic acid.

The integrity of the respiratory epithelium may be important in development of bronchial hyperreactivity; however, the mechanisms involved remain unknown. This study was undertaken to determine if epithelium of rabbit intrapulmonary bronchi is capable of modulating the responsiveness of airway smooth muscle to a pharmacologic stimulus, and whether epithelial-derived prostaglandins play a role in this modulatory function. Mechanical removal of the epithelium from bronchial segments, or incubation of intact bronchi with indomethacin (an inhibitor of prostaglandin synthesis) increased the sensitivity of bronchial smooth muscle to bethanechol. Cyclooxygenase was localized within mucosal epithelial cells of intact airways by avidin-biotin immunoperoxidase staining using a monoclonal antibody to the enzyme. Removal of the epithelium significantly reduced the levels of PGE2 and 6-keto-PGF1 alpha accumulated in the media surrounding bronchial explants. In epithelium-intact bronchi precontracted with bethanechol, arachidonic acid evoked an indomethacin-sensitive relaxation response comparable to relaxation induced by exogenous addition of PGE2. Although PGE2 evoked similar responses in epithelium-denuded bronchi, arachidonic acid-induced relaxation responses were negligible. The results suggest epithelial cells of rabbit bronchi modulate the responsiveness to pharmacologic stimuli by production and release of an inhibitory cyclooxygenase metabolite of arachidonic acid.

Animals↗
PubMed1994

Fodrin and actin in the normal, metaplastic, and dysplastic respiratory epithelium and in lung carcinoma.

Distribution of actin and fodrin, a nonerythroid analogue of spectrin, was studied in cytocentrifuge preparations and in tissue sections of normal and pathologic respiratory epithelium by using immunofluorescence and immunoelectron microscopy. In ciliated epithelial cells and in goblet cells of normal bronchial epithelium, fodrin and actin were located in the apical parts and along the lateral walls of the cells. In basal cells, fodrin and actin were also seen diffusely in the cytoplasm. Immunoelectron microscopy showed fodrin in close association with the basal bodies and rootlets of the cilia and microvilli in the ciliated cells. In alveolar epithelium, fodrin and actin were located at the apical membrane in type I pneumocytes and along the apical and lateral membranes in type II pneumocytes. In type II pneumocytes, fodrin was also seen in close association with the secretory vacuoles. In metaplastic and dysplastic bronchial epithelium, a diffuse cytoplasmic and a circumferential, membrane-associated staining for fodrin and actin was seen. In all types of carcinomas, fodrin was seen along the lateral walls and diffusely in the cytoplasm. The staining was more intense than in the normal cells. In immunoblotting of the normal bronchial epithelium, and peripheral lung and lung carcinomas, a single 240 kD band was recognized with antibodies to fodrin. The results show distinct differences in the distribution of fodrin in the various cell types of the respiratory epithelium. In ciliated cells, the close relationship with cytoskeleton suggests a role of fodrin in the establishment of the elaborate structural architecture of the apical compartment. In type II pneumocytes, on the other hand, fodrin probably plays a role in secretion of the surfactant. In basal cells, the diffuse distribution of fodrin probably reflects the high proliferative capacity of this cell compartment. Interestingly, a similar distribution was also seen in premalignant and malignant cells.

Actins↗
PubMed1999

Long-lasting effects of chronic ozone exposure on rat nasal epithelium.

Ozone, the principal oxidant pollutant in photochemical smog, causes airway epithelial injury in the upper and lower respiratory tract of laboratory animals. We have recently reported that long-term inhalation exposure to ozone causes mucous-cell metaplasia (MCM) in the surface epithelium lining the nasal airways of F344 rats. The principal objective of the present study was to determine the persistence of ozone-induced MCM in the nasal epithelium after the end of a chronic exposure. Male F344/N rats were exposed to 0, 0.25, or 0.5 ppm ozone, for 8 h/d, 7 d/wk for 13 wk. Animals were killed 8 h, 4 wk, or 13 wk after the end of the chronic exposure. Ozone-related alterations in the nasal epithelium were qualitatively and quantitatively characterized through histochemistry, image analysis, and morphometric techniques. Some rats were exposed for an additional 8 h to 0.5 ppm ozone at 13 wk after the end of the chronic exposure to determine whether previous ozone exposure results in persistent changes in the sensitivity of nasal epithelium to acute injury. At the end of the chronic exposure, hyperplasia was present in the nasal epithelium of rats exposed to 0.25 and 0.5 ppm ozone. By 13 wk postexposure, this proliferative alteration was still evident only in the rats exposed to 0.5 ppm ozone. Ozone-induced MCM with associated intraepithelial mucosubstances was evident only in the nasal tissues of rats exposed to 0.5 ppm ozone. Though attenuated, these alterations in the nasal mucous apparatus were still detectable at 13 wk after the end of the exposure. At this same time after the chronic exposure, an acute (8 h) exposure to 0.5 ppm ozone induced an additional increase of mucosubstances in the nasal epithelium of rats previously exposed to 0.5 ppm ozone, but not in rats chronically exposed to 0 or 2.5 ppm ozone. The persistent nature of the ozone-induced MCM in rats documented in this report suggests that ozone exposure may have the potential to induce similar long-lasting alterations in the airways of humans.

Animals↗
PubMed1991

Tetrodotoxin does not block the epithelium-dependent release of prostaglandin E2 induced by electrical field stimulation in isolated ferret trachea.

Electrical field stimulation (EFS) has previously been shown to induce the release of prostaglandin (PG) E2 from ferret tracheal epithelium. We have now conducted a study to see whether this effect of EFS is due to the activation of nerves or whether it is a non-neural effect. The release of PGE2 and 6-keto-PGF1 alpha into the bath fluid was assayed in isolated ferret tracheas with (E+) or without (E-) epithelium, stimulated by either EFS or direct vagal nerve stimulation (DNS) repeatedly for 120 min. EFS-stimulated E+ preparations showed a gradual decline in the contractile responses (30 +/- 1% of baseline) and an increase in PGE2 to 296 +/- 38 pg/ml. In EFS-stimulated, epithelium-denuded (E-) preparations, the decline was significantly lower (11 +/- 5%), as well as the final concentration of PGE2 (107 +/- 21 pg/ml). In DNS-stimulated E+ preparations, the contraction decline was 8 +/- 1% and the final concentration of PGE2 was less than 6 pg/ml. Although tetrodotoxin (TTX) abolished the contractile response in EFS-stimulated E+ preparations, it did not significantly reduce the release of PGE2 (260 +/- 6 pg/ml), whereas atropine partly counteracted the release. The bath concentration of 6-keto-PGF1 alpha increased, independently of the electrical stimulation, contractile response, or presence of the epithelium. We conclude that EFS activates the epithelium-dependent release of PGE2 by a TTX-resistant mechanism. This may be due to an activation of TTX-resistant nerves, or possibly to a non-neural effect, such as a direct effect on the epithelial cells. The results indicate that the airway epithelium has the ability to respond to certain stimuli with a pronounced release of PGE2, thereby counteracting bronchoconstriction.

6-Ketoprostaglandin F1 alpha↗
PubMed1995

Effect of HA-1A monoclonal IgM antibody on endotoxin-induced proliferation of cultured rat middle ear epithelium.

The effect of human monoclonal antibody HA-1A (Centoxin) on the effect of endotoxin on cultured rat middle ear epithelium was investigated. The addition of endotoxin to the standard culture medium revealed a concentration-related proliferative effect on cultured rat middle ear epithelium, leading to cobblestone cells, cell tracks, and stratification of epithelium, whereas rat middle ear epithelium cultured in standard medium grew as a monolayer composed of flat polygonal cells. Addition of HA-1A to standard medium supplemented with endotoxin gave rise to a statistically significant suppression of the proliferative effects of endotoxin on these cells. The morphology of rat middle ear epithelium cultured in the presence of HA-1A and endotoxin showed that these cells still had a tendency to form cobblestone-like cells and cell tracks, but to a substantially lower degree. The present results support the hypothesis that HA-1A suppresses the proliferative and morphological effects of endotoxin on rat middle ear epithelium and may play an important role in the pathogenesis of otitis media.

Animals↗
PubMed1989

Expression of neuron-specific enolase, Leu-7, and neuropeptides in human fetal salivary gland epithelium.

The immunoreactivity of anti-neuron-specific enolase (NSE) and anti-Leu-7 on formalin-fixed sections of human fetal salivary gland epithelium was determined by the avidin-biotin-peroxidase complex (ABC) method. In addition, expression of some neuropeptides such as vasoactive intestinal polypeptide (VIP), somatostatin (SRIF), and substance P in the human salivary gland epithelium during the gestational period was observed, whereas the other polypeptides examined, including glucagon, cholecystokinin (CCK), Leu-enkephalin, and calcitonin were absent. NSE and Leu-7 immunoreactivity in the fetal salivary gland epithelium was observed solitarily or in groups commonly restricted to the developing duct epithelium. Positive immunoreactivity was observed in 46 cases with NSE (73%) and 44 cases with Leu-7 (70%) in 63 fetal salivary glands examined. In contrast, the incidence of positive cases stained with neuropeptides was lower than those of NSE and Leu-7 immunoreactivity in the human fetal salivary gland epithelium. These findings indicate that certain neuropolypeptides, as well as VIP, SRIF, and substance P present in the human fetal salivary gland epithelium may play a significant role in the development of the gland.

Antigens, Differentiation↗