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Inflammation and oxidative stress in gastroesophageal reflux disease.

Yoshida N - J Clin Biochem Nutr (2007)

Bottom Line: The etiology of esophageal mucosal injury is complex, since it may involve the reflux of gastric acid, bile acid, and pancreatic juice, external factors such as drugs and alcohol, or functional factors such as esophagogastric motility.In addition, nociceptors such as acid-sensitive vanilloid receptors, protease-activated receptors and substance P have also been implicated in the pathogenesis of neurogenic inflammation in NERD patients with esophageal hypersensitivity.The development of new therapy with anti-inflammatory and anti-oxidant effects is expected to assist in the treatment of intractable NERD/GERD and the prevention of carcinogenesis.

View Article: PubMed Central - PubMed

Affiliation: Molecular Gastroenterology and Hepatology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kamigyo-ku, Kyoto 602-8566, Japan.

ABSTRACT
The etiology of esophageal mucosal injury is complex, since it may involve the reflux of gastric acid, bile acid, and pancreatic juice, external factors such as drugs and alcohol, or functional factors such as esophagogastric motility. The mechanism of esophageal mucosal injury has gradually been understood at the molecular biological level. It is particularly important that pro-inflammatory factors, such as inflammatory cytokines (interleukin-6 and -8), leukocytes and oxidative stress, have been demonstrated to be involved in the development of gastroesophageal reflux disease (GERD) including nonerosive reflux disease (NERD). In addition, nociceptors such as acid-sensitive vanilloid receptors, protease-activated receptors and substance P have also been implicated in the pathogenesis of neurogenic inflammation in NERD patients with esophageal hypersensitivity. The development of new therapy with anti-inflammatory and anti-oxidant effects is expected to assist in the treatment of intractable NERD/GERD and the prevention of carcinogenesis.

No MeSH data available.


Related in: MedlinePlus

Relationship between IL-8 mRNA expression and the endoscopic grade of gastroesophageal reflux disease (GERD) (4). Samples were taken from mucosal breaks in patients with esophagitis. Expression of IL-8 mRNA was quatified by real-time polymerase chain reaction (PCR) using biopsy mucosal materials and was corrected for that of GAPDH mRNA. Endoscopic grading was done according to the Los Angeles (LA) classification. Reprinted with permisson [4]
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Figure 2: Relationship between IL-8 mRNA expression and the endoscopic grade of gastroesophageal reflux disease (GERD) (4). Samples were taken from mucosal breaks in patients with esophagitis. Expression of IL-8 mRNA was quatified by real-time polymerase chain reaction (PCR) using biopsy mucosal materials and was corrected for that of GAPDH mRNA. Endoscopic grading was done according to the Los Angeles (LA) classification. Reprinted with permisson [4]

Mentions: It has recently been demonstrated that inflammatory cytokines, including chemokines, play an important role in inducing early inflammatory changes in patients with GERD. Using esophageal biopsy samples obtained from patients with GERD (including those with NERD), we examined correlations between the expression of various genes (interleukin (IL)-6, IL-8, and monocyte chemoattractant protein 1 (MCP-1)) and the endoscopic findings, histological findings, and symptoms. We found that IL-8 mRNA levels in the esophageal mucosa of patients with GERD were significantly higher than in normal subjects [3, 4]. Regarding the expression of IL-8 mRNA, there was a positive correlation with endoscopic severity (Fig. 2) as well as with the histological neutrophil infiltration score, but there was no clear correlation with the QUEST score (an index of the severity of symptoms). Although an increase of IL-6 (Fig. 3) and MCP-1 was also observed in patients with GERD or NERD, no correlation was detected between the expression of these genes and endoscopic severity. Immunostaining analysis revealed that expression of IL-8 was primarily localized to the basal layer of the esophageal epithelium in patients with GERD. IL-8 is a neutrophil-activating factor that is chiefly produced by leukocytes and vascular endothelial cells. The results of our investigation indicated that esophageal epithelium cells play an important role in the development of mucosal inflammation by producing IL-8. In patients treated with oral PPI therapy for 8 weeks, IL-8 mRNA levels declined quickly as both symptoms and endoscopic findings improved, but there was no change of MCP-1 mRNA levels. These observations indicate that IL-8 is a sensitive marker of esophageal inflammation.


Inflammation and oxidative stress in gastroesophageal reflux disease.

Yoshida N - J Clin Biochem Nutr (2007)

Relationship between IL-8 mRNA expression and the endoscopic grade of gastroesophageal reflux disease (GERD) (4). Samples were taken from mucosal breaks in patients with esophagitis. Expression of IL-8 mRNA was quatified by real-time polymerase chain reaction (PCR) using biopsy mucosal materials and was corrected for that of GAPDH mRNA. Endoscopic grading was done according to the Los Angeles (LA) classification. Reprinted with permisson [4]
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2291500&req=5

Figure 2: Relationship between IL-8 mRNA expression and the endoscopic grade of gastroesophageal reflux disease (GERD) (4). Samples were taken from mucosal breaks in patients with esophagitis. Expression of IL-8 mRNA was quatified by real-time polymerase chain reaction (PCR) using biopsy mucosal materials and was corrected for that of GAPDH mRNA. Endoscopic grading was done according to the Los Angeles (LA) classification. Reprinted with permisson [4]
Mentions: It has recently been demonstrated that inflammatory cytokines, including chemokines, play an important role in inducing early inflammatory changes in patients with GERD. Using esophageal biopsy samples obtained from patients with GERD (including those with NERD), we examined correlations between the expression of various genes (interleukin (IL)-6, IL-8, and monocyte chemoattractant protein 1 (MCP-1)) and the endoscopic findings, histological findings, and symptoms. We found that IL-8 mRNA levels in the esophageal mucosa of patients with GERD were significantly higher than in normal subjects [3, 4]. Regarding the expression of IL-8 mRNA, there was a positive correlation with endoscopic severity (Fig. 2) as well as with the histological neutrophil infiltration score, but there was no clear correlation with the QUEST score (an index of the severity of symptoms). Although an increase of IL-6 (Fig. 3) and MCP-1 was also observed in patients with GERD or NERD, no correlation was detected between the expression of these genes and endoscopic severity. Immunostaining analysis revealed that expression of IL-8 was primarily localized to the basal layer of the esophageal epithelium in patients with GERD. IL-8 is a neutrophil-activating factor that is chiefly produced by leukocytes and vascular endothelial cells. The results of our investigation indicated that esophageal epithelium cells play an important role in the development of mucosal inflammation by producing IL-8. In patients treated with oral PPI therapy for 8 weeks, IL-8 mRNA levels declined quickly as both symptoms and endoscopic findings improved, but there was no change of MCP-1 mRNA levels. These observations indicate that IL-8 is a sensitive marker of esophageal inflammation.

Bottom Line: The etiology of esophageal mucosal injury is complex, since it may involve the reflux of gastric acid, bile acid, and pancreatic juice, external factors such as drugs and alcohol, or functional factors such as esophagogastric motility.In addition, nociceptors such as acid-sensitive vanilloid receptors, protease-activated receptors and substance P have also been implicated in the pathogenesis of neurogenic inflammation in NERD patients with esophageal hypersensitivity.The development of new therapy with anti-inflammatory and anti-oxidant effects is expected to assist in the treatment of intractable NERD/GERD and the prevention of carcinogenesis.

View Article: PubMed Central - PubMed

Affiliation: Molecular Gastroenterology and Hepatology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kamigyo-ku, Kyoto 602-8566, Japan.

ABSTRACT
The etiology of esophageal mucosal injury is complex, since it may involve the reflux of gastric acid, bile acid, and pancreatic juice, external factors such as drugs and alcohol, or functional factors such as esophagogastric motility. The mechanism of esophageal mucosal injury has gradually been understood at the molecular biological level. It is particularly important that pro-inflammatory factors, such as inflammatory cytokines (interleukin-6 and -8), leukocytes and oxidative stress, have been demonstrated to be involved in the development of gastroesophageal reflux disease (GERD) including nonerosive reflux disease (NERD). In addition, nociceptors such as acid-sensitive vanilloid receptors, protease-activated receptors and substance P have also been implicated in the pathogenesis of neurogenic inflammation in NERD patients with esophageal hypersensitivity. The development of new therapy with anti-inflammatory and anti-oxidant effects is expected to assist in the treatment of intractable NERD/GERD and the prevention of carcinogenesis.

No MeSH data available.


Related in: MedlinePlus