Gastric Parietal Cell and Intestinal Goblet Cell Secretion: a Novel Cell-Mediated In Vivo Metal Nanoparticle Metabolic Pathway Enhanced with Diarrhea Via Chinese Herbs

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.

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Club Cell Secretion Protein 16 (CC16) Improve Chronic Obstructive Pulmonary Disease In Vivo Study

Journal of Biomaterials and Tissue Engineering ◽

10.1166/jbt.2022.2907 ◽

2022 ◽

Vol 12 (2) ◽

pp. 279-286

Author(s):

Zhihong Qiu ◽

Li Yan ◽

Juan Xu ◽

Xiaojun Qian

Keyword(s):

Protein Expression ◽

Goblet Cell ◽

Inflammatory Cells ◽

Cell Number ◽

Chronic Obstructive ◽

Model Group ◽

Cell Secretion ◽

Down Regulation ◽

Club Cell

Purpose: The purpose of this study was to evaluate CC16 in COPD treatment and relative mechanism by vivo study. Materials and methods: The mice were divided into Normal, Model and CC16 groups. Measuring Pathology and goblet cell number by HE or AB/PAS staining; Evaluating apoptosis cell number by TUNEL assay; using flow separation to analysis inflammatory cells in difference groups; MAPK and NF-κB(p65) protein expression were evaluated by IHC assay in tissues; Total protein concentration of MUC5AC, CC16, Bax and Bcl-2 were evaluated by Western Blot (WB) assay. Results: Compared with Normal group, the pathology was deteriorate and goblet cell number were significantly up-regulation in Model group, apoptosis goblet cell number were significantly depressed (P < 0.001), lympbocyte rate and hypertrophic rate were significantly down-regulation and Eosinophils rate, Macrophage rate and Neutrophils rate were significantly up-regulation (P < 0.001, respectively) in Model group. By IHC assay, MAPK and NF-κB(p65) proteins expression were significantly increased (P < 0.001, respectively) in Model group; by WB assay, MUC5AC and Bcl-2 protein expression were significantly up-regulation and CC16 and Bax proteins expression were significantly down-regulation (P < 0.001, respectively) in Model group. CC16 supplement, the COPD were significantly improved with relative inflammatory cells rates significantly improving and relative proteins improving. Conclusion: CC16 could improve COPD by inducing goblet cell apoptosis increasing via regulation MAPK/NF-κB(p65) pathway In Vivo study.

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

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1982.242.4.g370 ◽

1982 ◽

Vol 242 (4) ◽

pp. G370-G379 ◽

Cited By ~ 5

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.

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Computer modeling of gastric parietal cell: significance of canalicular space, gland lumen, and variable canalicular [K+]

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00431.2015 ◽

2016 ◽

Vol 310 (9) ◽

pp. G671-G681 ◽

Cited By ~ 5

Author(s):

James M. Crothers ◽

John G. Forte ◽

Terry E. Machen

Keyword(s):

Acid Secretion ◽

Parietal Cell ◽

Driving Forces ◽

Short Circuit ◽

Open Circuit ◽

Cell Secretion ◽

Gastric Parietal Cell ◽

Atpase Inhibitors ◽

Long Time ◽

Cellular Components

A computer model, constructed for evaluation of integrated functioning of cellular components involved in acid secretion by the gastric parietal cell, has provided new interpretations of older experimental evidence, showing the functional significance of a canalicular space separated from a mucosal bath by a gland lumen and also shedding light on basolateral Cl− transport. The model shows 1) changes in levels of parietal cell secretion (with stimulation or H-K-ATPase inhibitors) result mainly from changes in electrochemical driving forces for apical K+ and Cl− efflux, as canalicular [K+] ([K+]can) increases or decreases with changes in apical H+/K+ exchange rate; 2) H-K-ATPase inhibition in frog gastric mucosa would increase [K+]can similarly with low or high mucosal [K+], depolarizing apical membrane voltage similarly, so electrogenic H+ pumping is not indicated by inhibition causing similar increase in transepithelial potential difference ( Vt) with 4 and 80 mM mucosal K+; 3) decreased H+ secretion during strongly mucosal-positive voltage clamping is consistent with an electroneutral H-K-ATPase being inhibited by greatly decreased [K+]can (Michaelis-Menten mechanism); 4) slow initial change (“long time-constant transient”) in current or Vt with clamping of Vt or current involves slow change in [K+]can; 5) the Na+-K+-2Cl− symporter (NKCC) is likely to have a significant role in Cl− influx, despite evidence that it is not necessary for acid secretion; and 6) relative contributions of Cl−/HCO3− exchanger (AE2) and NKCC to Cl− influx would differ greatly between resting and stimulated states, possibly explaining reported differences in physiological characteristics of stimulated open-circuit Cl− secretion (≈H+) and resting short-circuit Cl− secretion (>>H+).

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The Physiology of the Gastric Parietal Cell

Physiological Reviews ◽

10.1152/physrev.00016.2019 ◽

2020 ◽

Vol 100 (2) ◽

pp. 573-602 ◽

Cited By ~ 4

Author(s):

Amy C. Engevik ◽

Izumi Kaji ◽

James R. Goldenring

Keyword(s):

Acid Secretion ◽

Gastric Acid Secretion ◽

Gastric Acid ◽

Parietal Cell ◽

Duodenal Mucosa ◽

Parietal Cells ◽

Apical Surface ◽

Cell Secretion ◽

Gastric Parietal Cell ◽

Glucagon Like Peptide 1

Parietal cells are responsible for gastric acid secretion, which aids in the digestion of food, absorption of minerals, and control of harmful bacteria. However, a fine balance of activators and inhibitors of parietal cell-mediated acid secretion is required to ensure proper digestion of food, while preventing damage to the gastric and duodenal mucosa. As a result, parietal cell secretion is highly regulated through numerous mechanisms including the vagus nerve, gastrin, histamine, ghrelin, somatostatin, glucagon-like peptide 1, and other agonists and antagonists. The tight regulation of parietal cells ensures the proper secretion of HCl. The H+-K+-ATPase enzyme expressed in parietal cells regulates the exchange of cytoplasmic H+ for extracellular K+. The H+ secreted into the gastric lumen by the H+-K+-ATPase combines with luminal Cl− to form gastric acid, HCl. Inhibition of the H+-K+-ATPase is the most efficacious method of preventing harmful gastric acid secretion. Proton pump inhibitors and potassium competitive acid blockers are widely used therapeutically to inhibit acid secretion. Stimulated delivery of the H+-K+-ATPase to the parietal cell apical surface requires the fusion of intracellular tubulovesicles with the overlying secretory canaliculus, a process that represents the most prominent example of apical membrane recycling. In addition to their unique ability to secrete gastric acid, parietal cells also play an important role in gastric mucosal homeostasis through the secretion of multiple growth factor molecules. The gastric parietal cell therefore plays multiple roles in gastric secretion and protection as well as coordination of physiological repair.

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Anemia, hematinic deficiencies, hyperhomocysteinemia, and serum gastric parietal cell antibody positivity in atrophic glossitis patients with or without microcytosis

Journal of the Formosan Medical Association ◽

10.1016/j.jfma.2019.06.004 ◽

2019 ◽

Vol 118 (10) ◽

pp. 1401-1407 ◽

Cited By ~ 8

Author(s):

Chun-Pin Chiang ◽

Julia Yu-Fong Chang ◽

Yi-Ping Wang ◽

Yang-Che Wu ◽

Yu-Hsueh Wu ◽

...

Keyword(s):

Parietal Cell ◽

Gastric Parietal Cell ◽

Cell Antibody ◽

Antibody Positivity ◽

Parietal Cell Antibody

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Baicalin Represses Type Three Secretion System of Pseudomonas aeruginosa through PQS System

Molecules ◽

10.3390/molecules26061497 ◽

2021 ◽

Vol 26 (6) ◽

pp. 1497

Author(s):

Pansong Zhang ◽

Qiao Guo ◽

Zhihua Wei ◽

Qin Yang ◽

Zisheng Guo ◽

...

Keyword(s):

Pseudomonas Aeruginosa ◽

Virulence Factors ◽

Mammalian Cells ◽

Secretion System ◽

Chinese Herbs ◽

Infection Model ◽

Lung Pathology ◽

Promising Alternative ◽

The Impact

Therapeutics that target the virulence of pathogens rather than their viability offer a promising alternative for treating infectious diseases and circumventing antibiotic resistance. In this study, we searched for anti-virulence compounds against Pseudomonas aeruginosa from Chinese herbs and investigated baicalin from Scutellariae radix as such an active anti-virulence compound. The effect of baicalin on a range of important virulence factors in P. aeruginosa was assessed using luxCDABE-based reporters and by phenotypical assays. The molecular mechanism of the virulence inhibition by baicalin was investigated using genetic approaches. The impact of baicalin on P. aeruginosa pathogenicity was evaluated by both in vitro assays and in vivo animal models. The results show that baicalin diminished a plenty of important virulence factors in P. aeruginosa, including the Type III secretion system (T3SS). Baicalin treatment reduced the cellular toxicity of P. aeruginosa on the mammalian cells and attenuated in vivo pathogenicity in a Drosophila melanogaster infection model. In a rat pulmonary infection model, baicalin significantly reduced the severity of lung pathology and accelerated lung bacterial clearance. The PqsR of the Pseudomonas quinolone signal (PQS) system was found to be required for baicalin’s impact on T3SS. These findings indicate that baicalin is a promising therapeutic candidate for treating P. aeruginosa infections.

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