Dilated intercellular space in the larynx and esophagus of a rabbit reflux model

Hu, Ying; Xü, Xinsheng; Lei, Xu; Lai, Chuijin; Zhang, Tianyu

doi:10.1016/j.anl.2012.09.010

Cited by 11 publications

(7 citation statements)

References 21 publications

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“…In LPR, there are several studies which have focused on DIS in laryngeal mucosa [8][9][10], but research on claudins in LPR is absent. In the present study, we have shown that esophageal and laryngeal expression of claudin-3 in a rat reflux model is significantly lower in the study group when compared with the control group.…”

Section: Discussionmentioning

confidence: 99%

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Expression of claudin-3 in the esophagus and larynx of rat reflux model

Wang

et al. 2014

Auris Nasus Larynx

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Section: Discussionmentioning

confidence: 99%

“…A markedly dilated intercellular space (DIS) and reduction in the number of TJs were observed in several studies on GERD and LPR [8][9][10]. It has been suggested that dissociation and dispersion of claudin-3 from the tight junction could be one of the most sensitive indicators of reflux esophagitis in rats [11].…”

Section: Introductionmentioning

confidence: 99%

Expression of claudin-3 in the esophagus and larynx of rat reflux model

Wang

et al. 2014

Auris Nasus Larynx

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“…19,[31][32][33] Significant changes in the intercellular space were also found in the esophageal and laryngeal samples of a rabbit reflux model induced by total cardiomyectomy. 27 Park et al found that both LPR patients with and without GERD had a dilated intercellular space in esophageal tissues (0.95 ± 0.44 m and 0.61 ± 0.47 m, respectively), compared to the control group (0.35 ± 0.27 m). 20 In the present study, we studied the mucosal ultrastructure changes in this LPR model.…”

Section: Discussionmentioning

confidence: 98%

“…However, the LPR animal model has been reported limitedly. Hu et al 27 induced LPR by total cardiomyectomy on albino rabbits in New Zealand to study the association between LPR and GERD. But they did not monitor the objective evidence of reflux, for example the pH value.…”

Section: Discussionmentioning

confidence: 99%

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A Bama Minipig Model of Laryngopharyngeal Reflux and the Change of Laryngopharyngeal Mucosal Ultrastructure

Feng

Zhang²,

Chun-yan

et al. 2015

J Neurogastroenterol Motil

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Background/Aims To establish an animal model of laryngopharyngeal reflux (LPR) and study the effect of LPR on the laryngopharyngeal mucosal ultrastructure. Methods Ten Bama minipigs were randomly divided into control group and stent group. Every pig underwent endoscope, and baseline pH was monitored for 4 hours at laryngopharynx and distal esophagus, then specimens from laryngopharyngeal mucosa were biopsied. For the control group, these procedures were repeated on the 14th day. In the stent group, a custom-designed esophageal stent suit was implanted into esophagus, laryngopharyngeal and distal esophageal pH monitoring lasted for 2 hours, then stent suit was removed 3 days later. At last, the same procedures were done as the control group on the 14th day. Specimens were observed under transmission electron microscope to measure the intercellular space and desmosome number. Results In the control group, there was no laryngopharyngeal reflux on the first day and 14th day. Before the stent was implanted, there was also no laryngopharyngeal reflux in the stent group. In both 2 hours and 14 days after stent implantation, the num -ber of reflux, reflux time, and percentage time of pH < 4.0 were significantly increased ( P < 0.05) in the stent group. There was no difference in intercellular space and desmosomes in the control group between baseline and 14th day. In the stent group, intercellular space of laryngopharyngeal mucosa was significantly increased (0.37 μm vs 0.96 μm, P = 0.008), and the number of desmosomes was significantly decreased (20.25 vs 9.5, P = 0.003). Conclusions A Bama minipig model of LPR was established by implanting a custom-designed stent suit. LPR might destroy the laryngophar yngeal mucosal barrier.

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Narrative review of the role of inflammation in gastroesophageal reflux disease. Can food allergies play a part?

Swain

2021

Lifestyle Medicine

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Acid suppression is the accepted treatment for gastroesophageal reflux disease, despite being ineffective in one third of patients. Certain conditions presenting as reflux may later be attributed to food allergy (infant cow's milk allergy; eosinophilic esophagitis), but the role of food allergy in adult reflux disease has rarely been investigated. The mechanisms of gastroesophageal reflux disease are examined to explore potential subgroups within the population, such as undisclosed food allergy, which may determine the responsiveness to treatment. The relevant literature was searched systematically using ProQuest Dialog, yielding 113 papers that were evaluated for quality. The extracted evidence was formed into a mechanistic diagram representing the processes of disease. As yet, insufficient research exists to evaluate the relationship between food allergies and reflux in adults. Of significance, however, is the potential for multiple variables to affect the integrity of the esophageal mucosa, thereby allowing symptoms to emerge which are independent of acid exposure. Where nonacidic drivers of inflammation exist, acid suppression is unlikely to offer adequate symptom resolution and may serve to explain the high proportion of nonresponders in this group. The review concludes that symptoms of gastroesophageal reflux may emerge in response to the coexistence of physiological reflux and esophageal mucosal inflammation. The latter may arise due to reflux‐induced acid erosion, or due to alternative endogenous sources of inflammation. When a patient presents with refractory reflux and a history of allergic disease, the role of antigen‐induced inflammation should be considered for further investigation. Nonallergic individuals presenting with refractory reflux symptoms may benefit from further analysis of relevant co‐morbidities that have the capacity to compromise mucosal integrity, including obesity or psychological stress. The identification of specific mediators of inflammation in refractory reflux disease may enable the development of personalized treatment regimes which improve outcomes and reduce the reliance on acid suppressants.

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Dilated intercellular space in the larynx and esophagus of a rabbit reflux model

Cited by 11 publications

References 21 publications

Expression of claudin-3 in the esophagus and larynx of rat reflux model

Expression of claudin-3 in the esophagus and larynx of rat reflux model

A Bama Minipig Model of Laryngopharyngeal Reflux and the Change of Laryngopharyngeal Mucosal Ultrastructure

Narrative review of the role of inflammation in gastroesophageal reflux disease. Can food allergies play a part?

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