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J S Trier

Publications and source records attributed to J S Trier.

At least 37 records · Page 2Linked to original sources
PubMed1987

Demonstration of microtubules in the terminal web of mature absorptive cells from the small intestine of the rat.

The terminal web (TW) region of mature absorptive cells in the small intestine of the rat contains an elaborate cytoskeleton which supports the apical microvillus membrane. In studies regarding the structural organization of the cytoskeleton and associated proteins in the small intestine, microtubules have not been mentioned as components of the TW. By transmission electron microscopy of conventional resin-embedded sections of rat small intestine, we observe many microtubule profiles in the TW of mature absorptive cells. These microtubules are found in various orientations, although most course parallel to the long axis of the cell, and many microtubule profiles are seen in close association with smooth-surfaced vesicles.

Animals↗
PubMed1987

Ethanol-induced damage to mucosal capillaries of rat stomach. Ultrastructural features and effects of prostaglandin F2 beta and cysteamine.

Impairment of the mucosal microcirculation may contribute to ethanol-induced gastric mucosal damage. In this report, we describe diffuse and severe ultrastructural damage to the capillaries of the gastric glandular mucosa of the rat that occurred within 1 min after intragastric instillation of 100% ethanol. There was a gradient of damage in that endothelial cell structure was most severely disrupted in profiles of capillaries located close to the luminal surface but some morphologic evidence of damage was evident in the wall of capillary profiles to a mean depth of 256 micron. Capillary structure was generally normal in the deeper regions of the mucosa. Pretreatment with intragastric cysteamine, 30 mg/100 g, or intragastric prostaglandin F2 beta, 0.5 mg/100 g, significantly reduced the depth in the mucosa to which damage to capillaries extended. Pretreatment with intragastric prostaglandin F2 beta, 0.2 mg/100 g, afforded no significant protection. We conclude that a 1-min exposure to 100% ethanol induces striking damage to the microcirculation of glandular mucosa of the rat stomach with severe damage to capillary profiles near the lumen and sparing of capillary profiles near the muscularis mucosa, and pretreatment with the sulfhydryl agent, cysteamine, or with a large dose of prostaglandin F2 beta reduces the extent of but does not abolish ethanol-induced damage to gastric mucosal capillaries.

Animals↗
PubMed1987

Adherence to and penetration of the intestinal epithelium by reovirus type 1 in neonatal mice.

In 10-day-old suckling and adult mice, reovirus type 1 adheres selectively to and penetrates membranous epithelial (M) cells. To determine when M cells first appear, when they first transport reovirus, and if reovirus adheres to and is endocytosed by other epithelial cells in the first postnatal week, we examined neonatal mouse intestine by transmission electron microscopy after reovirus type 1 exposure. At 2 days M cells accounted for 0.9% of dome epithelial cells. By 9 days M cells had increased to 7.4%. Reovirus type 1 adherence to the surface of villus and dome epithelial cells showed marked variation in 2-6-day-old animals, but by 7 days only a few absorptive cell profiles had adherent reovirus. Adherence to greater than 50% of M-cell profiles occurred in all but 2 animals, but adherence to the majority of Peyer's patch absorptive cell profiles was present only in some 4- and 5-day-old animals. Adherence to a majority of undifferentiated cell profiles occurred in some animals at all ages. Membranous epithelial cells endocytosed reovirus at all ages but only at 2 days did rare villus and dome absorptive cells endocytose reovirus into the apical cytoplasm. Thus, adherence of reovirus to the apical surface of mucosal epithelial cells is nonselective in newborn mice but becomes more selective within the first postnatal week with adherence by day 7 to most M-cell profiles, to a substantial but variable number of undifferentiated cell profiles, but to few absorptive cell profiles.

Animals↗
PubMed1986

Structural features of absorptive cell and microvillus membrane preparations from rat small intestine.

Absorptive cells of the small intestine are highly polarized cells with distinct microvillus membrane (MVM) and basolateral plasma membrane domains. We compared membrane structure in the following preparations of rat small intestine commonly used for in vitro study of MVM function: epithelial sheets, isolated epithelial cells, and four different MVM vesicle preparations, using electron microscopy of thin sections and freeze fracture replicas. We also quantitated mean vesicle diameter of the four MVM preparations by quasielastic light scattering and determined their actin content. Epithelial sheets maintained their plasma membrane polarity as judged by intramembrane particle (IMP) distribution for at least 30 min after isolation. In contrast, the plasma membrane of isolated cells showed redistribution of IMPs, indicating considerable loss of polarity in the few minutes required for cell recovery. The P-face IMPs in MVM prepared by Ca++ precipitation were randomly distributed but became aggregated after exposure to potassium thiocyanate, which removed approximately 50% of core actin. The P-face IMPs in Mg++ precipitated MVM were aggregated whether or not core actin was depleted with potassium thiocyanate. The shape and size of MVM vesicles differed considerably with different preparative techniques. The extremely rapid loss of plasma membrane polarity of isolated intestinal epithelial cells and the striking structural heterogeneity of MVM vesicles prepared by commonly used techniques should be considered in the interpretation of functional studies with these preparations.

Animals↗
PubMed1986

Early microcirculatory stasis in acute gastric mucosal injury in the rat and prevention by 16,16-dimethyl prostaglandin E2 or sodium thiosulfate.

We used in vivo microscopy and laser-Doppler velocimetry to examine the effects on the gastric mucosal microcirculation and in gastric mucosal blood flow of agents that induce acute gastric mucosal damage. In vivo microscopic observation of superficial mucosal capillaries revealed vascular stasis within a mean of 54, 81, or 61 s after 100% ethanol, 0.6 N HCl, or 0.2 N NaOH, with the subsequent development of hemorrhagic mucosal lesions. Mucosal blood flow estimated by laser-Doppler velocimetry decreased by 30% at 5 min after luminal application of 100% ethanol, and decreased further to about 40% of basal levels by 15 min. The decreased mucosal blood flow 15 min after application of 50% ethanol correlated with the extent of hemorrhagic mucosal lesions. Examination of the submucosal vessels that supply and drain the mucosa showed moderate dilation of small arterioles 1, 3, and 6 min after exposure to 100% ethanol but there were no consistent changes in venules. Mild vasoconstriction of small- and medium-sized venules could be detected 6, 10, and 15 min after NaOH but not after exposure to HCl. Pretreatment with 16,16-dimethyl prostaglandin E2 or sodium thiosulfate before exposure of the mucosa to ethanol prevented capillary stasis, maintained mucosal blood flow, and prevented the development of hemorrhagic gastric mucosal lesions. Topical mucosal application of 16,16-dimethyl prostaglandin E2 decreased, whereas topical exposure to sodium thiosulfate increased gastric mucosal blood flow, indicating that change in blood flow per se is an unlikely mediator of protection.

16,16-Dimethylprostaglandin E2↗
PubMed1986

Alterations in blood vessels during gastric injury and protection.

Recent investigations suggest that the mucosal vascular endothelium is not a passive bystander, and that alterations within the blood vessel wall actively participate in the pathogenesis of gastric mucosal injury. We review here our data on rapidly developing vascular injury as detected by monastral blue deposition and increased vascular permeability measured by Evan's blue extravasation in dose- and time-dependent experiments with ethanol, HCl, and NaOH in the rat. In addition, using in vivo microscopy and laser-Doppler velocimetry, we demonstrate circulatory stasis in the superficial capillaries within about 1 min after topical application of damaging agents, and a gradual decrease in blood flow that correlates with the extent of hemorrhagic erosions. Prostaglandins or sulfhydryl agents prevented the circulatory standstill and the development of hemorrhagic mucosal lesions. We conclude that microvascular damage, increased vascular permeability, and capillary stasis precede the development of hemorrhagic mucosal lesions.

Animals↗
PubMed1985

A quantitative method for assessing the extent of experimental gastric erosions and ulcers.

Evaluation of acute gastric erosions and ulcers induced by chemicals such as ethanol or aspirin is difficult because these lesions are predominantly multiple and irregularly shaped. A commercially available, relatively inexpensive microprocessor-linked planimeter (Micro-Plan II) with a stereomicroscope was used to measure the area of gastric mucosa damaged following intragastric administration of various doses of ethanol or aspirin. An enlarged image of rat glandular stomach was projected from the stereomicroscope onto a planimeter on which the perimeter of the entire glandular stomach and each lesion was traced with an electronic cursor. An attached printer recorded the area of stomach assessed, the number of lesions, the surface area of each lesion and the total area of mucosal damage. The technique was compared with semiquantitative methods used previously to assess experimentally induced gastric mucosal damage. The quantitative morphometric method was sufficiently sensitive to demonstrate a dose-response effect of ethanol and aspirin. The stereomicroscope--planimeter combination provides a sensitive method to quantitate either a few small, or numerous large, regularly or irregularly shaped hemorrhagic and nonhemorrhagic gastric mucosal lesions.

Animals↗
PubMed1985

Early vascular injury and increased vascular permeability in gastric mucosal injury caused by ethanol in the rat.

The hypothesis that vascular injury contributes to the development of hemorrhagic erosions after intragastric administration of ethanol has been examined in the rat using vascular tracers. Extravasation of intravenously injected Evans blue into the gastric wall and into gastric contents was used as an indicator of vascular permeability. India ink and monastral blue, which label damaged blood vessels, were used to demonstrate vascular injury morphologically. Intragastric instillation of 75% and 100% ethanol induced increased vascular permeability within 1-3 min and resulted in monastral blue labeling of vessels in 13% and 17%, respectively, of the glandular mucosa within 1 min. After 1 h of 100% ethanol exposure, the areal density of monastral blue-stained blood vessels did not increase compared with that seen at 1 min, but the areal density of grossly visible hemorrhagic lesions increased strikingly and approximated that of vessel staining. The hemorrhagic erosions consistently occurred in regions of glandular mucosa where vessels were stained with monastral blue. Pretreatment with prostaglandin F2 beta or cysteamine reduced ethanol-induced Evans blue extravasation and monastral blue staining of mucosal blood vessels but did not reduce histologic evidence of gastric surface cell damage in the glandular mucosa. As increased vascular permeability and morphologically detectable vascular lesions consistently preceded the development of grossly visible hemorrhagic erosions in the glandular mucosa, we suggest that vascular injury is an early pathogenetic factor in the development of ethanol-induced gastric hemorrhagic erosions. The data also indicate that the degree of vascular damage, unlike the injury to surface epithelial cells, is reduced by pretreatment with prostaglandin F2 beta or the sulfhydryl cysteamine.

Animals↗
PubMed1985

Glucocorticoid receptors in isolated intestinal epithelial cells in rats.

There is evidence that glucocorticoid hormones influence a variety of epithelial cell functions in the small intestine. To exert their effect, glucocorticoids bind to cytoplasmic glucocorticoid receptors (GR), which, following translocation to the nucleus, stimulate mRNA transcription and then protein synthesis and ultimately trigger hormonal actions. To determine the distribution of GR in small intestinal villus and crypt cells, we measured GR activity in enriched villus and crypt cell fractions by use of [3H]dexamethasone. In normal rats GR activity was present in all cell fractions but was lowest in fully mature villus cells of the upper villus and greatest in immature crypt cells. In contrast, 1 wk after adrenalectomy and ovariectomy or sham operation, both of which reduced plasma corticosterone levels, GR activities were comparable in enriched villus cell and enriched crypt cell fractions. Kinetic studies indicated a single class of binding sites with comparable Kd values in villus and crypt cells of normal and steroid-depleted animals, suggesting that there are more glucocorticoid-binding sites in crypt than in villus cells of normal animals. Immature crypt cells may be more susceptible to glucocorticoid modulation than fully mature villus cells in normal rats in view of their higher GR activity.

Adrenalectomy↗
PubMed1984

Esophageal, gastric, and intestinal candidiasis.

Gastrointestinal Candida infection is more prevalent than previously recognized. It is most often seen in patients with underlying impairment of the immune system but may also occur in apparently normal individuals. Esophageal involvement is most common, presenting with odynophagia, dysphagia, or bleeding. Gastric Candida infection may cause diffuse mucosal involvement or focal invasion of benign gastric ulcers. Intestinal candidiasis is uncommon and poorly characterized. The diagnosis is usually established by visualizing the characteristic yeast or mycelial forms in endoscopic brushings and biopsies. Oral nystatin is effective therapy in many patients, but other antifungal agents may be needed in extensive or persistent disease, especially in immunocompromised patients.

Candidiasis↗
PubMed1984

Flounder intestinal absorptive cells have abundant gap junctions and may be coupled.

We noted that, unlike mammalian intestinal absorptive cells, cells of the winter flounder (Pseudopleuronectes americanus) displayed abundant gap junctions on the lateral plasma membrane. We compared the distribution of gap junctions in winter flounder to that in rabbit intestinal epithelium. We also examined for evidence of gap junction-mediated intercellular coupling by comparing the cell-to-cell variation of electrical potential difference across winter flounder intestinal cell apical membranes with that in rabbit small intestinal epithelium in which gap junctions are rare. Gap junctions were seen in 95% of flounder absorptive cells and were localized largely to the apical third of the lateral membrane. Individual gap junctions often contained several hundred uniform 9-nm intramembrane particles. Gap junction size and structure was independent of the position of individual absorptive cells on mucosal folds. These findings sharply contrasted flounder intestinal absorptive cells with rabbit small intestinal absorptive cells, in which gap junctions were rarely detected and when present consisted of few intramembrane particles. Correlating with this distribution of morphologically detectable gap junctions, rabbit small intestinal epithelial cells demonstrated marked variability in potential difference across their apical membranes, whereas those in flounder small intestine showed little variation in apical membrane potential difference. Thus, in contrast to intestinal epithelium of rabbits, flounder intestinal epithelium demonstrates morphological and functional characteristics, suggesting a substantial degree of electrical coupling.

Animals↗
PubMed1984

Structural features of and cholesterol distribution in M-cell membranes in guinea pig, rat, and mouse Peyer's patches.

Evidence suggests that M cells, which are antigen-sampling epithelial cells that overlie the domes of Peyer's patches, have an apical plasma membrane that differs from that of absorptive cells. We examined the structural features of rat, mouse, and guinea pig M-cell apical membranes and compared them with those of dome and villus absorptive cell apical membranes using electron microscopy of thin sections and freeze-fracture replicas. We also determined the distribution of morphologically detectable cholesterol in M-cell plasma and intracellular membranes in dome epithelium exposed to the polyene antibiotic, filipin. The areal density of P-face intramembrane particles was significantly less on M-cell microvilli than on microvilli of dome absorptive cells and villus absorptive cells. Areal densities of E-face intramembrane particles were similar on M-cell and absorptive-cell microvilli. M-cell apical plasma membranes were rich in cholesterol, displaying numerous filipin-induced membrane lesions in thin sections and freeze-fracture replicas. In contrast, apical membrane endocytic pits and coated vesicles in M cells failed to show filipin-induced membrane lesions. These findings suggest that, compared with the apical membranes of absorptive cells, those of M cells have a low protein to lipid ratio and an abundance of morphologically detectable cholesterol except in domains involved in endocytosis. Additionally, a subpopulation of dome epithelial cells displayed distinctive tight junctions with high strand counts and unusual depth. Although the cell type associated with these modified tight junctions could not be identified with certainty, their interspecies frequency paralleled the interspecies frequency of M cells in dome epithelium. These expanded tight junctions may result from physical tension caused by epithelial shape changes induced by intraepithelial lymphoid trafficking or, alternatively, may help buttress M cells that have attenuated cytoplasmic processes due to the presence of central hollows.

Animals↗
PubMed1984

Structure, distribution, and origin of M cells in Peyer's patches of mouse ileum.

The derivation of membranous epithelial (M) cells, which are specialized antigen sampling cells overlying the lymphoid follicles of Peyer's patches, is unknown; it has been suggested recently, however, that M cells differentiate from absorptive cells on the follicular epithelium. To examine whether M cells, like other intestinal epithelial cells, derive directly from undifferentiated crypt cells, we studied the structure, selected functional features, proliferation, and distribution of Peyer's patch M cells in the ileum of adult mice. We observed a spectrum of M-cell structure ranging from mature to immature-appearing M cells. Most immature-appearing M cells lacked the central cytoplasmic hollow found in those mature M cells that contained lymphoid cells. The microvilli of immature-appearing M cells were more numerous and regular appearing than those of mature M cells, but they were sparser and shorter, and some were wider than those of absorptive cells. Many immature-appearing M cells contained more free ribosomes than did mature M cells. Both mature and immature-appearing M cells were observed on all regions of follicular domes, including the base near the mouths of surrounding crypts. Type 1 reovirions adhered with considerable selectivity to the apical membrane of mature and immature-appearing M cells but were observed in endocytic vesicles only in mature M cells. Neither mature nor immature-appearing M cells showed evidence of lipid absorption, in contrast to adjacent absorptive cells. Both mature and immature-appearing M cells internalized more bound cationized ferritin than did absorptive cells. Only mature M cells transported cationized ferritin to the intercellular spaces. Nuclei of a few immature-appearing M cells were labeled 24 h after injection of [3H]thymidine in concert with the appearance of labeled absorptive cell nuclei. These observations strongly suggest that many, if not all, M cells derive directly from undifferentiated crypt cells.

Animals↗
PubMed1984

Distribution of filipin-sterol complexes in villus goblet cell membranes of rat small intestine.

The polyene antibiotic, filipin, was used as a morphologic probe to determine the distribution of cholesterol in plasma and intracellular membranes in freeze fracture replicas of villus goblet cells from rat small intestine. Endoplasmic reticular and cis-face Golgi membranes displayed only rare filipin-sterol complexes. Membranes of the Golgi trans-face and adjacent nascent secretory granules revealed a moderate number of complexes. Membranes of mature secretory granules contained numerous filipin-sterol complexes, especially in sites where adjacent granules abutted. Complexes were so abundant on the apical plasma membrane that they approached confluence. The areal density of filipin-sterol complexes on the lateral plasma membrane was less than on the apical membrane but varied from goblet cell to goblet cell. The number of complexes on the lateral membrane of cells that appeared to be actively secreting mucus at the time of fixation was greater than on cells that showed no evidence of active mucus secretion. Thus, in villus goblet cells of rat small intestine (a) mucous granule membranes and the apical plasma membrane with which they fuse during secretion appear strikingly enriched with cholesterol, (b) cholesterol appears to be incorporated into mucous granule membranes during and shortly after their formation at the Golgi trans-face, and (c) the cholesterol content of the lateral plasma membrane of secreting goblet cells appears to be greater than that of nonsecreting cells.

Animals↗
PubMed1983

The sigma 1 protein determines the extent of spread of reovirus from the gastrointestinal tract of mice.

After intragastric inoculation of adult mice, type 1 reovirus was initially concentrated in Peyer's patches over the first 4 hr after inoculation, then spread sequentially to the mesenteric lymph nodes and spleen. For type 3 reovirus, however, initial entry into Peyer's patches in adult mice was followed by loss of viral infectivity so that by 4 hr after inoculation virtually no infectious virus was detected in the intestine, and spread to extraintestinal tissues did not occur. In 10-day-old mice, type 3 was capable of spread to the mesenteric lymph nodes but not the spleen. Thus, as animals aged there was a greater restriction of the spread of type 3 from the intestine. Studies using a field isolate of type 3 reovirus that is resistant to intestinal proteases, and genetic studies utilizing type 1 x type 3 viral reassortants, revealed that the viral sigma 1 protein determined the capacity of reovirus to spread from the intestine in both adult and 10-day-old mice. Thus, the interaction of reovirus with host defense mechanisms, and the age-dependent restriction of spread of type 3 reovirus from the intestine are mediated by the viral sigma 1 protein.

Aging↗
PubMed1983

Determinants of reovirus interaction with the intestinal M cells and absorptive cells of murine intestine.

Reovirus type 1 penetrates the gastrointestinal tract in suckling mice via specialized epithelial cells, designated membranous cells, or M cells, located in the epithelium overlying Peyer's patches. We have examined whether the interaction of reovirus with murine mucosa of in situ closed ileal loops is influenced by mouse age or strain or reovirus serotype. Neither mouse age (suckling or adult), strain (C3H/HeJ or Balb/cJ), nor reovirus serotype (types 1 and 3) affected reovirus adherence to and transport through M cells. In all conditions, reovirions adhered to the M-cell surface and were transported across M cells in endocytic vesicles. The adherence to and endocytosis by M cells of type 1 reovirus and reassortants with the viral hemagglutinin of type 1 were selective in suckling mice; type 1 virus was not adherent to nor endocytosed by absorptive cells. In adult mice, type 1 reovirions adhered to the surface of a minority of absorptive cells but were never seen within absorptive cell cytoplasm. In contrast, type 3 reovirus and reassortants with the viral hemagglutinin of type 3 adhered to and were endocytosed not only by M cells but also by absorptive cells of suckling mice. Virions accumulated within lysosomelike bodies in absorptive cells but transport of virions across absorptive cells was not observed. These studies indicate that (a) adherence of reovirus to the apical surface of and transcellular transport by M cells is independent of viral serotype or viral surface proteins, (b) adherence of reovirus to and transcellular transport by M cells is independent of mouse age after 9 days and comparable in two mouse strains, and (c) adherence of reovirus to and their endocytosis by absorptive cells of suckling mice is determined by the viral hemagglutinin (sigma 1 protein).

Age Factors↗