Histochemical Changes in Mucus in Duodenal Ulceration

Sm, Morrissey; Pm, Ward; Ap, Jayaraj; Fi, Tovey

doi:10.1007/978-1-4615-9254-9_36

Cited by 3 publications

(3 citation statements)

References 1 publication

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“…Therefore, esophageal acid exposure is associated with production of neutral mucosubstances of the submucosal apocrine glands of the adjacent trachea. Acid mucosubstances are produced and secreted by mucosal cells in a position to provide defense against bacteria, e.g., the colon (45), whereas neutral mucosubstances are produced and secreted primarily by submucosal glands in a position to defend against acid, e.g., the duodenum (38,46). Therefore, the increased production of PAS-stained mucus from submucosal glands of the trachea with acid exposure of the adjacent esophagus is the appropriate response to the possible threat of acid exposure of the airway.…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of airway responses to esophageal acidification in cats

Lang

Haworth

Medda

et al. 2016

Journal of Applied Physiology

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Acid in the esophagus causes airway constriction, tracheobronchial mucous secretion, and a decrease in tracheal mucociliary transport rate. This study was designed to investigate the neuropharmacological mechanisms controlling these responses. In chloralose-anesthetized cats (n = 72), we investigated the effects of vagotomy or atropine (100 μg·kg(-1)·30 min(-1) iv) on airway responses to esophageal infusion of 0.1 M PBS or 0.1 N HCl at 1 ml/min. We quantified 1) diameter of the bronchi, 2) tracheobronchial mucociliary transport rate, 3) tracheobronchial mucous secretion, and 4) mucous content of the tracheal epithelium and submucosa. We found that vagotomy or atropine blocked the airway constriction response but only atropine blocked the increase in mucous output and decrease in mucociliary transport rate caused by esophageal acidification. The mucous cells of the mucosa produced more Alcian blue- than periodic acid-Schiff (PAS)-stained mucosubstances, and the mucous cells of the submucosa produced more PAS- than Alcian blue-stained mucosubstances. Selective perfusion of the different segments of esophagus with HCl or PBS resulted in significantly greater production of PAS-stained mucus in the submucosa of the trachea adjacent to the HCl-perfused esophagus than in that adjacent to the PBS-perfused esophagus. In conclusion, airway constriction caused by esophageal acidification is mediated by a vagal cholinergic pathway, and the tracheobronchial transport response is mediated by cholinergic receptors. Acid perfusion of the esophagus selectively increases production of neutral mucosubstances of the apocrine glands by a local mechanism. We hypothesize that the airway responses to esophageal acid exposure are part of the innate, rather than acute emergency, airway defense system.

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Section: Discussionmentioning

confidence: 99%

Mechanisms of airway responses to esophageal acidification in cats

Lang

Haworth

Medda

et al. 2016

Journal of Applied Physiology

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“…Pyloric gland or gastric metaplasia, with characteristic diastase PAS-positive mucin staining [6], has long been recognized in association with duodenal ulcers [7]. Duodenal ulcers are often surrounded by gastric-type epithelia with distinct microvillar patterns similar to the antrum [8].…”

Section: Figurementioning

confidence: 99%

Pyloric metaplasia, pseudopyloric metaplasia, ulcer‐associated cell lineage and spasmolytic polypeptide‐expressing metaplasia: reparative lineages in the gastrointestinal mucosa

Goldenring

2018

The Journal of Pathology

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Summary The gastrointestinal mucosae provide a critical barrier between the external and internal milieu. Thus, damage to the mucosa requires an immediate response to provide appropriate wound closure and healing. Metaplastic lineages with phenotypes similar to the mucous glands of the distal stomach or Brunner’s glands have been associated with various injurious scenarios in the stomach, small bowel and colon. These lineages have been assigned various names including pyloric metaplasia, pseudopyloric metaplasia, Ulcer-associated cell lineage (UACL) and spasmolytic polypeptide-expressing metaplasia (SPEM). A re-examination of the literature on these various forms of mucous cell metaplasia suggests that pyloric type mucosal gland lineages may provide a ubiquitous response to mucosal injury throughout the gastrointestinal tract as well as in the pancreas, esophagus and other mucosal surfaces. While the cellular origin of these putative reparative lineages likely varies in different regions of the gut, their final phenotypes may converge on a pyloric type gland dedicated to mucous secretion. In addition to their healing properties in the setting of acute injury, these pyloric type lineages may also represent precursors to neoplastic transitions in the face of chronic inflammatory influences. Further investigations are needed to determine how discrete molecular profiles relate to the origin and function of pyloric-type metaplasias previously described by histological characteristics in multiple epithelial mucosal systems in the setting of acute and chronic damage.

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“…Pearson and Brownlee (2010) also noted that the normal functionality and biochemistry of the mucous barrier appears to be lost in diseases of the colorectal mucosa. In peptic ulcer, the deficiency of gel forming polymeric mucins of the antral adherent mucous barrier (Allen et al, 1988) and the reduction of acid mucosubstances in goblet cells (Morrissey et al, 1983) have also been reported.…”

Section: Introductionmentioning

confidence: 99%

Histochemical demonstration of mucosubstances in the mouse gastrointestinal tract treated with Origanum hypericifolium O. Schwartz and P.H. Davis extract

Keskin¹,

İli²,

Sahin³

2012

Afr. J. Biotechnol.

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Glycoconjugate-containing mucous in the gastrointestinal tract has lubricant and cytoprotective effects. This study was performed to demonstrate the intensity of mucous in the stomach, small and large intestine tissues of female BALB/c mice injected intraperitoneally with 0.2 ml of the Origanum hypericifolium extract for six weeks. The staining procedures employed were Alcian Blue (AB) at pH 1 and 2.5, periodic acid-Schiff (PAS) and lectins including Galanthus nivalis agglutinin (GNA), Arachis hypogaea (PNA, Peanut Agglutinin) and Maackia amurensis leucoagglutinin (MAL). The mucous glands in the large intestine of the experimental groups were found to show stronger positive reaction for AB at pH 2.5 and PAS when compared with the controls. In lectin histochemistry, the mucous glands which reacted with lectins exhibited less density for PNA in the stomach and for MAL and PNA in the small intestine in the experimental groups than the controls. In the large intestine of the experimental groups, less staining pattern of GNA was observed on the surface epithelium of villi when compared with the controls. The results suggest that O. hypericifolium extract increases acidic and neutral mucosubstances in the large intestine and also changes some glycan structures in the gastrointestinal tract.

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Histochemical Changes in Mucus in Duodenal Ulceration

Cited by 3 publications

References 1 publication

Mechanisms of airway responses to esophageal acidification in cats

Mechanisms of airway responses to esophageal acidification in cats

Pyloric metaplasia, pseudopyloric metaplasia, ulcer‐associated cell lineage and spasmolytic polypeptide‐expressing metaplasia: reparative lineages in the gastrointestinal mucosa

Histochemical demonstration of mucosubstances in the mouse gastrointestinal tract treated with Origanum hypericifolium O. Schwartz and P.H. Davis extract

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