Epithelial response to intestinal anaphylaxis in rats: goblet cell secretion and enterocyte damage

1984 ◽  
Vol 247 (6) ◽  
pp. G632-G637 ◽  
Author(s):  
M. H. Perdue ◽  
J. F. Forstner ◽  
N. W. Roomi ◽  
D. G. Gall
Keyword(s):  
Goblet Cell ◽  
Immunoglobulin E ◽  
Periodic Acid ◽  
Goblet Cells ◽  
High Serum ◽  
Cell Secretion ◽  
Periodic Acid Schiff ◽  
Cellular Debris ◽  
Ige Mediated

The effects of immunoglobulin E (IgE)-mediated reactions on the intestinal epithelium were examined during intestinal anaphylaxis in the rat. Rats sensitized by intraperitoneal injection of egg albumin (EA) plus alum developed high serum titers of IgE anti-EA antibodies after 14 days; sham-treated littermate controls had no anti-EA antibodies. Two isolated loops of jejunum were prepared in vivo in anesthetized rats. The loops were injected with EA in saline or saline alone, and intraluminal contents of each loop were examined after 4 h. Mucosal histamine decreased in sensitized rat intestine exposed to EA. Luminal mucin, measured by radioimmunoassay, was not increased by antigen challenge. In contrast, DNA, protein, and sucrase activities were elevated in contents from the isolated segments exposed to EA in sensitized rats. Histology revealed that periodic acid-Schiff-stained material was contained in goblet cells in sections prepared from these segments after antigen exposure. Cellular debris was present over the tips of the villi. These findings suggest that IgE-mediated reactions in the intestine cause epithelial damage and loss of material from cells other than goblet cells. The results indicate that release of goblet cell mucus is not a feature of intestinal anaphylaxis.

Agarose plug instillation causes goblet cell metaplasia by activating EGF receptors in rat airways

2000 ◽  
Vol 278 (1) ◽  
pp. L185-L192 ◽  
Author(s):  
Heung-Man Lee ◽  
Kiyoshi Takeyama ◽  
Karim Dabbagh ◽  
James A. Lausier ◽  
Iris F. Ueki ◽  
...  
Keyword(s):  
Alcian Blue ◽  
Goblet Cell ◽  
Kinase Inhibitor ◽  
Periodic Acid ◽  
Goblet Cells ◽  
Secretory Cells ◽  
Egf Receptors ◽  
Periodic Acid Schiff ◽  
Egfr Expression ◽  
Goblet Cell Metaplasia

We hypothesized that foreign bodies in airways cause inflammation leading to goblet cell metaplasia. Instilled agarose plugs lodged in the bronchi of pathogen-free rats caused a time-dependent increase in Alcian blue-periodic acid-Schiff staining that was detected within 24 h and markedly increased at 72 h. Control bronchi contained no pregoblet or goblet cells, but plugged bronchi contained many pregoblet and goblet cells and a decrease in nongranulated secretory cells. In situ hybridization showed no expression of MUC5AC in control airways, but plugged airways showed a marked expression. Control bronchi showed sparse staining for epidermal growth factor receptor (EGFR) protein, but plugged bronchi showed intense EGFR staining in the epithelium. Pretreatment with an EGFR tyrosine kinase inhibitor (BIBX1522) prevented Alcian blue-periodic acid-Schiff staining and MUC5AC gene expression in plugged bronchi. Pretreatment with tumor necrosis factor-α neutralizing antibody or pretreatment with cyclophosphamide abolished plug-induced EGFR protein expression and goblet cell metaplasia. Thus instillation of agarose plugs induces profound goblet cell metaplasia by causing EGFR expression and activation.

scholarly journals Morpho-histological characterisation of the alimentary canal of an important food fish, Asian seabass (Lates calcarifer)

PeerJ ◽  
2016 ◽  
Vol 4 ◽  
pp. e2377 ◽  
Author(s):  
Kathiresan Purushothaman ◽  
Doreen Lau ◽  
Jolly M. Saju ◽  
Syed Musthaq SK ◽  
Declan Patrick Lunny ◽  
...  
Keyword(s):  
Goblet Cell ◽  
Periodic Acid ◽  
Goblet Cells ◽  
Lates Calcarifer ◽  
Gastric Glands ◽  
Periodic Acid Schiff ◽  
Asian Seabass ◽  
Cell Numbers ◽  
Food Fish ◽  
Mucus Cells

Asian seabass (Lates calcarifer) is a food fish of increasing aquaculture importance. In order to improve our understanding on the digestive system and feeding of this species, morphological and histological features of the gut were studied. Morphologically, the Asian seabass gut is defined by a short and muscular esophagus, well-developed stomach and comparatively short intestine. Mucous secreting goblet cells reactive to PAS (Periodic Acid Schiff) and AB (Alcian Blue) stain were present throughout the esophagus. The stomach was sac-like and could be distinguished into the cardiac, fundic and pyloric regions. Gastric glands and mucus cells were predominately present in the cardiac and fundic regions. Five finger-like pyloric caeca were present between the stomach and intestine. The intestine was a short, tubular structure with no morphological differences between the various regions. Histologically, the intestinal regions were similar, the main difference being in the number of goblet cells that increased from anterior to posterior intestine, with 114 ± 9, 153 ± 7 and 317 ± 21 goblet cells in the anterior, mid and posterior regions, respectively. The intestinal epithelium stained positively for PAS, but the staining was stronger for acidic glycoproteins. The rectum was similar to intestine, except for increased goblet cell numbers (anterior rectum: 529 ± 26; posterior rectum: 745 ± 29). Gut morpho-histology did not respond to salinity changes, however, there was a significant reduction of mucosal height, goblet cell numbers and muscularis thickness upon food deprivation.

Goblet Cell Density of the Inferior Turbinates in Patients with Perennial Allergic and Nonallergic Rhinitis

1997 ◽  
Vol 11 (3) ◽  
pp. 233-236 ◽  
Author(s):  
Gilead Berger ◽  
Zvi Marom ◽  
Dov Ophir
Keyword(s):  
Goblet Cell ◽  
Periodic Acid ◽  
Inferior Turbinate ◽  
Goblet Cells ◽  
Nonallergic Rhinitis ◽  
Periodic Acid Schiff ◽  
Mucus Production ◽  
The Mean ◽  
Normal Controls ◽  
Goblet Cell Density

Nasal mucus production is regulated by submucosal glands and epithelial goblet cells. The role and especially the number of the latter are quite debatable. The present study compares the distribution and density of goblet cells in the inferior turbinates of patients with perennial allergic and nonallergic rhinitis to normal controls. The periodic acid Schiff-alcian blue whole-mount method was used to identify and count their number. Goblet cell distribution was found nonhomogeneous, and considerable variations were observed among adjacent localities of the same specimen. The mean number of goblet cells per mm2 was 6499 in normal controls (n = 12), 6818 in patients with perennial allergic rhinitis (n = 13), and 6801 in patients with perennial nonallergic rhinitis (n = 18). Statistical analysis confirmed that the density of goblet cells did not differ significantly between patients with and without allergy, as well as between each group of patients and controls. Therefore, it could be concluded that the number of goblet cells in the inferior turbinate is not influenced by the presence of perennial allergic or nonallergic rhinitis.

Lipopolysaccharide-induced goblet cell hypersecretion in the guinea pig trachea: inhibition by macrolides

1997 ◽  
Vol 272 (1) ◽  
pp. L15-L19 ◽  
Author(s):  
J. Tamaoki ◽  
K. Takeyama ◽  
I. Yamawaki ◽  
M. Kondo ◽  
K. Konno
Keyword(s):  
Guinea Pig ◽  
Goblet Cell ◽  
Periodic Acid ◽  
Maximal Response ◽  
Dependent Manner ◽  
Cell Secretion ◽  
Neutrophil Accumulation ◽  
Tracheal Mucosa ◽  
Periodic Acid Schiff ◽  
Dose Dependent

We studied the effects of macrolides on lipopolysaccharide (LPS)-induced airway goblet cell secretion in the guinea pig trachea. The goblet cell secretion was assessed in histological sections of the tracheal mucosa stained with alcian blue and periodic acid Schiff by arbitrarily determining mucus score, which is inversely related to the magnitude of mucus discharge. Inhalation of Escherichia coli LPS (5 mg/kg) caused a time-dependent decrease in mucus score, with the maximal response being from 542 +/- 49 to 92 +/- 20 arbitrary units (P < 0.001) after 3 h, which was accompanied by an increase in the number of neutrophils in the tracheal mucosa. The LPS-induced mucus discharge was inhibited by oral clarithromycin and erythromycin in a dose-dependent manner (5 and 10 mg/kg), whereas amoxicillin and cefaclor had no effect. Each dose of clarithromycin and erythromycin, but not amoxicillin or cefaclor, likewise attenuated the LPS-induced recruitment of neutrophils. These results suggest that LPS stimulates goblet cell secretion and neutrophil accumulation in the airways and that macrolides may be of value in protecting against neutrophil-associated airway hypersecretion.

13 ASTROVIRUS ALTERS THE GUT MUCUS BARRIER AND REDUCES COLONIZATION TO ENTEROPATHOGENIC E. COLI

2020 ◽  
Vol 26 (Supplement_1) ◽  
pp. S28-S28
Author(s):  
Valerie Cortez ◽  
Bridgett Sharp ◽  
Brandi Livingston ◽  
Hannah Rowe ◽  
Ramzi Alsallaq ◽  
...  
Keyword(s):  
Periodic Acid ◽  
Enteric Virus ◽  
Goblet Cells ◽  
Gut Health ◽  
Cell Secretion ◽  
Periodic Acid Schiff ◽  
E Coli ◽  
Degrading Bacteria ◽  
Human Astroviruses ◽  
Mucus Barrier

Abstract Goblet cells, specialized epithelial cells that produce mucus, are essential for gut health. Dysfunctional goblet cell secretion can weaken the mucus barrier, bringing commensal microbes and other lumenal contents in contact with the epithelial barrier, triggering inflammation. We recently discovered that murine astroviruses infect goblet cells in the small intestine, making it the first enteric virus in which this tropism has been recognized in vivo. To first determine whether astrovirus infection alters mucus production in goblet cells, we used periodic acid-Schiff staining of small intestinal tissues and found a thicker mucus layer in infected compared to mock-infected animals (1.85 to 2.51-fold, p&lt;0.001). Because changes to the mucus barrier can alter the microbial environment in the gut, we used 16S metagenomic to characterize the microbiome after infection. We found that the relative frequency of well-characterized mucus-degrading bacteria significantly increased after infection (p&lt;0.001). Using phylogenetic edge principal components analysis, we also identified distinct microbiome shifts between 0 and 14 days post-infection, corresponding to peak infection. Finally, to determine the extent to which these changes in the mucus barrier could have a functional consequence to host disease susceptibility, we developed a neonatal model for astrovirus and tested whether animals inoculated with enteropathogenic E. coli (EPEC), an adherent bacterial pathogen, would be protected from colonization. In comparison to animals inoculated with EPEC alone, co-infected animals had significantly reduced EPEC colonization (p&lt;0.01). Together, these studies reveal a new avenue of enteric virus regulation of gut homeostasis and immunity via goblet cells and highlight astroviruses as a novel model to study the mucus barrier. Future studies are needed to determine whether astrovirus-induced increases in the mucus barrier protect from other gastrointestinal diseases and how these data translate to human astroviruses, which predominately infect children &lt;1-year-old and coincides with the development of gut immunity.

Regulation of intestinal goblet cell secretion. I. Role of parasympathetic stimulation

1982 ◽  
Vol 242 (4) ◽  
pp. G370-G379 ◽  
Author(s):  
R. D. Specian ◽  
M. R. Neutra
Keyword(s):  
Molecular Weight ◽  
High Molecular Weight ◽  
Goblet Cell ◽  
Gel Filtration ◽  
Goblet Cells ◽  
Mucus Secretion ◽  
Cell Secretion ◽  
Intestinal Mucus ◽  
Compound Exocytosis

The in vivo effects of the parasympathomimetic drug pilocarpine on rat intestinal goblet cells were analyzed by autoradiography, light microscopy (LM), and electron microscopy (EM). Pilocarpine accelerated the release of mucus by compound exocytosis from crypt (but not surface) goblet cells throughout the small and large intestine. Pilocarpine-induced mucus secretion was blocked by atropine alone in ileum and colon, but total inhibition in proximal small intestine required a combination of atropine and tubocurarine. The sensitivity of morphological-autoradiographic methods for detection of goblet cell secretion was compared with that of a biochemical detection method, separation of labeled high-molecular-weight glycoproteins by Sepharose 4B gel filtration of luminal washings. Even when secretion of labeled mucus by compound exocytosis was clearly demonstrated by LM, EM, and autoradiography, gel filtration assay of luminal washings from pilocarpine-injected rats failed to reveal an increase in labeled high-molecular-weight glycoproteins. Autoradiographs of mucosal tissue after luminal washing showed that newly secreted, labeled mucus was retained in the crypts and was thus unavailable to the biochemical assay. Thus, direct observation of exocytosis in individual goblet cells provides a qualitative, but sensitive, assay for short-term acceleration of intestinal mucus secretion.

scholarly journals Th2 cytokines-DUOX2-ROS-HMGB1 translocation axis is important in the pathogenesis of allergic rhinitis

2021 ◽  
Vol 135 (3) ◽  
pp. 483-494
Author(s):  
Hyun Jin Min ◽  
Joon Soon Park ◽  
Kyung Soo Kim ◽  
Seung Yong Park ◽  
Honghwan Choi ◽  
...  
Keyword(s):  
Allergic Rhinitis ◽  
Murine Model ◽  
Immunoglobulin E ◽  
Periodic Acid ◽  
High Mobility ◽  
Upper Airway ◽  
Th2 Cytokines ◽  
Periodic Acid Schiff ◽  
Th2 Cytokine

Abstract The function of high-mobility group box 1 (HMGB1) varies according to its location. However, the translocation mechanism behind HMGB1 remains unclear. We hypothesize that type 2 helper T cell (Th2) cytokines are involved in the translocation of HMGB1 in the upper airway epithelium. We investigated the mechanism behind HMGB1 translocation using Th2 cytokine stimulation and examined the clinical significance of HMGB1 translocation in allergic rhinitis (AR). Cytoplasmic and extracellular HMGB1 were increased in AR. Inhibiting HMGB1 translocation with glycyrrhizic acid (GA) decreased the level of antigen-specific immunoglobulin E (IgE), the degree of Periodic Acid–Schiff (PAS), and Sirius Red staining in the murine model. The in vivo reactive oxygen species (ROS) level in the nasal mucosa was higher in the mice with AR than in the controls. Th2 cytokine-induced up-regulation of the ROS and translocation of HMGB1 by Th2 cytokines was dependent on the generated ROS. The ROS level also increased in the murine model. We suggest that the Th2 cytokine-dual oxidase (DUOX)2-ROS-HMGB1 translocation axis is important in AR pathogenesis.

Dynamic regulation of mucus gel thickness in rat duodenum

2000 ◽  
Vol 279 (2) ◽  
pp. G437-G447 ◽  
Author(s):  
Yasutada Akiba ◽  
Paul H. Guth ◽  
Eli Engel ◽  
Igor Nastaskin ◽  
Jonathan D. Kaunitz
Keyword(s):  
Periodic Acid ◽  
Goblet Cells ◽  
Mucus Secretion ◽  
Periodic Acid Schiff ◽  
Dynamic Regulation ◽  
Brunner's Glands ◽  
Brunner’S Glands ◽  
Mucus Gel ◽  
Rat Duodenum

We examined the dynamic regulation of mucus gel thickness (MGT) in vivo in rat duodenum in response to luminal acid, cyclooxygenase (COX) inhibition, and exogenous PGE2. An in vivo microscopic technique was used to measure MGT with fluorescent microspheres in urethan-anesthetized rats. Duodenal mucosa was topically superfused with pH 7.0 or pH 2.2 solutions with or without PGE2and indomethacin treatments. Glycoprotein concentration of duodenal loop perfusates was measured with periodic acid/Schiff (PAS) or Alcian blue (AB) staining. MGT and perfusate glycoprotein concentration were stable during a 35-min perfusion with pH 7.0 solution. Acid exposure increased MGT and PAS- and AB-positive perfusate glycoprotein concentrations. Indomethacin pretreatment increased both PAS- and AB-positive perfusate glycoprotein at baseline; subsequent acid superfusion decreased perfusate glycoproteins and gel thickness. PGE2(1 mg/kg iv) simultaneously increased MGT and PAS-positive perfusate glycoprotein concentrations followed by a transient increase in AB-positive glycoprotein concentration, suggesting contributions from goblet cells and Brunner's glands. Parallel changes in MGT and perfusate glycoprotein concentration in response to luminal acid and PGE2suggest that rapid MGT variations reflect alterations in the balance between mucus secretion and exudation, which in turn are regulated by a COX-related pathway. Luminal acid and PGE2augment mucus secretion from goblet cells and Brunner's glands.

scholarly journals Ectopic atrial arrhythmias arising from canine thoracic veins during in vivo stellate ganglia stimulation

2008 ◽  
Vol 295 (2) ◽  
pp. H691-H698 ◽  
Author(s):  
Alex Y. Tan ◽  
Shengmei Zhou ◽  
Byung Chun Jung ◽  
Masahiro Ogawa ◽  
Lan S. Chen ◽  
...  
Keyword(s):  
Pulmonary Vein ◽  
Sinus Node ◽  
Periodic Acid ◽  
Sympathetic Innervation ◽  
Sympathetic Nerves ◽  
Atrial Arrhythmias ◽  
Periodic Acid Schiff ◽  
Stellate Ganglia ◽  
Ectopic Beats

The purpose of the present study was to determine whether thoracic veins may act as ectopic pacemakers and whether nodelike cells and rich sympathetic innervation are present at the ectopic sites. We used a 1,792-electrode mapping system with 1-mm resolution to map ectopic atrial arrhythmias in eight normal dogs during in vivo right and left stellate ganglia (SG) stimulation before and after sinus node crushing. SG stimulation triggered significant elevations of transcardiac norepinephrine levels, sinus tachycardia in all dogs, and atrial tachycardia in two of eight dogs. Sinus node crushing resulted in a slow junctional rhythm (51 ± 6 beats/min). Subsequent SG stimulation induced 20 episodes of ectopic beats in seven dogs and seven episodes of pulmonary vein tachycardia in three dogs (cycle length 273 ± 35 ms, duration 16 ± 4 s). The ectopic beats arose from the pulmonary vein ( n = 11), right atrium ( n = 5), left atrium ( n = 2), and the vein of Marshall ( n = 2). There was no difference in arrhythmogenic effects of left vs. right SG stimulation (13/29 vs. 16/29 episodes, P = nonsignificant). There was a greater density of periodic acid Schiff-positive cells ( P < 0.05) and sympathetic nerves ( P < 0.05) at the ectopic sites compared with other nonectopic atrial sites. We conclude that, in the absence of a sinus node, thoracic veins may function as subsidiary pacemakers under heightened sympathetic tone, becoming the dominant sites of initiation of focal atrial arrhythmias that arise from sites with abundant sympathetic nerves and periodic acid Schiff-positive cells.

scholarly journals The potential renal toxicity of silver nanoparticles after repeated oral exposure and its underlying mechanisms

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Hamed Nosrati ◽  
Manijeh Hamzepoor ◽  
Maryam Sohrabi ◽  
Massoud Saidijam ◽  
Mohammad Javad Assari ◽  
...  
Keyword(s):  
Silver Nanoparticles ◽  
Molecular Mechanisms ◽  
Renal Toxicity ◽  
Periodic Acid ◽  
Critical Role ◽  
Oral Exposure ◽  
Control Group ◽  
Rt Pcr ◽  
Periodic Acid Schiff

Abstract Background Silver nanoparticles (AgNPs) can accumulate in various organs after oral exposure. The main objective of the current study is to evaluate the renal toxicity induced by AgNPs after repeated oral exposure and to determine the relevant molecular mechanisms. Methods In this study, 40 male Wistar rats were treated with solutions containing 30, 125, 300, and 700 mg/kg of AgNPs. After 28 days of exposure, histopathological changes were assessed using hematoxylin-eosin (H&E), Masson’s trichrome, and periodic acid-Schiff (PAS) staining. Apoptosis was quantified by TUNEL and immunohistochemistry of caspase-3, and the level of expression of the mRNAs of growth factors was determined using RT-PCR. Results Histopathologic examination revealed degenerative changes in the glomeruli, loss of tubular architecture, loss of brush border, and interrupted tubular basal laminae. These changes were more noticeable in groups treated with 30 and 125 mg/kg. The collagen intensity increased in the group treated with 30 mg/kg in both the cortex and the medulla. Apoptosis was much more evident in middle-dose groups (i.e., 125 and 300 mg/kg). The results of RT-PCR indicated that Bcl-2 and Bax mRNAs upregulated in the treated groups (p < 0.05). Moreover, the data related to EGF, TNF-α, and TGF-β1 revealed that AgNPs induced significant changes in gene expression in the groups treated with 30 and 700 mg/kg compared to the control group. Conclusion Our observations showed that AgNPs played a critical role in in vivo renal toxicity.

Sign in / Sign up

Export Citation Format

Share Document