Gastroesophageal reflux disease does not lead to changes in the secretory leukocyte protease inhibitor expression in esophageal mucosa

Wex, Thomas; Mönkemüller, Klaus; Kuester, Doerthe; Weise, Susanne; Kropf, Siegfried; Fry, Lucía C.; Stahr, Antje; Völkel, Simone; Roessner, Albert; Malfertheiner, Peter

doi:10.1097/meg.0b013e32830e4905

Cited by 5 publications

(7 citation statements)

References 31 publications

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“…This supports the concept that chemically induced inflammatory responses in the gastrointestinal tract differ in their immune regulation from other infectious-mediated inflammation [31]. Moreover, the distinct involvement of FOXP3-positive T cells in GERD-and H. pylori-associated inflammation might give rise to new biomarkers that help to differentiate between the two etiologies in cardiac inflammation and contribute to a better clinical management of cardia-related pathologies.…”

Section: Discussionsupporting

confidence: 75%

Chronic Mucosal Inflammation of the Gastric Cardia in Gastroesophageal Reflux Disease Is Not Regulated by FOXP3-Expressing T cells

et al. 2009

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Section: Discussionsupporting

confidence: 75%

Chronic Mucosal Inflammation of the Gastric Cardia in Gastroesophageal Reflux Disease Is Not Regulated by FOXP3-Expressing T cells

et al. 2009

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“…Demographic data of the subgroups for immunohistochemical analysis were comparable, except for a higher mean age in the control group, which reached borderline significance ( P = 0.04), and very low‐level or absent H. pylori infection Table 1B. The histomorphological characterization of the study groups was described in detail recently 31,32 . Therefore, primary data are not given in this article.…”

Section: Resultsmentioning

confidence: 93%

“…Note that all patients diagnosed with NERD had typical reflux‐related symptoms and responded to PPI therapy. Further details of study design, inclusion criteria and exclusion criteria were published recently 31,32 …”

Section: Methodsmentioning

confidence: 99%

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Gastro‐oesophageal reflux disease is associated with up‐regulation of desmosomal components in oesophageal mucosa

et al. 2012

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“…Notably, several subgroups of the study cohort were published in regard to inflammatory mediators (e.g. cytokines, Protease-activated receptor 2) [34,36], molecules related to barrier functions [37,38], desmosomal proteins [39] and histopathological alterations [34]. …”

Section: Methodsmentioning

confidence: 99%

Role of tight junction proteins in gastroesophageal reflux disease

et al. 2012

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Background: Gastroesophageal reflux disease (GERD) is associated with impaired epithelial barrier function that is regulated by cell-cell contacts. The aim of the study was to investigate the expression pattern of selected components involved in the formation of tight junctions in relation to GERD. Methods: Eighty-four patients with GERD-related symptoms with endoscopic signs (erosive: n = 47) or without them (non-erosive: n = 37) as well as 26 patients lacking GERD-specific symptoms as controls were included. Endoscopic and histological characterization of esophagitis was performed according to the Los Angeles and adapted Ismeil-Beigi criteria, respectively. Mucosal biopsies from distal esophagus were taken for analysis by histopathology, immunohistochemistry and quantitative reverse-transcription polymerase chain reaction (RT-PCR) of five genes encoding tight junction components [Occludin, Claudin-1, -2, Zona occludens (ZO-1, -2)]. Results: Histopathology confirmed GERD-specific alterations as dilated intercellular spaces in the esophageal mucosa of patients with GERD compared to controls (P < 0.05). Claudin-1 and −2 were 2-to 6-fold upregulation on transcript (P < 0.01) and in part on protein level (P < 0.015) in GERD, while subgroup analysis of revealed this upregulation for ERD only. In both erosive and non-erosive reflux disease, expression levels of Occludin and ZO-1,-2 were not significantly affected. Notably, the induced expression of both claudins did not correlate with histopathological parameters (basal cell hyperplasia, dilated intercellular spaces) in patients with GERD. Conclusions: Taken together, the missing correlation between the expression of tight junction-related components and histomorphological GERD-specific alterations does not support a major role of the five proteins studied in the pathogenesis of GERD.

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Gastroesophageal reflux disease does not lead to changes in the secretory leukocyte protease inhibitor expression in esophageal mucosa

Cited by 5 publications

References 31 publications

Chronic Mucosal Inflammation of the Gastric Cardia in Gastroesophageal Reflux Disease Is Not Regulated by FOXP3-Expressing T cells

Chronic Mucosal Inflammation of the Gastric Cardia in Gastroesophageal Reflux Disease Is Not Regulated by FOXP3-Expressing T cells

Gastro‐oesophageal reflux disease is associated with up‐regulation of desmosomal components in oesophageal mucosa

Role of tight junction proteins in gastroesophageal reflux disease

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