Gastroesophageal reflux disease does not lead to changes in the secretory leukocyte protease inhibitor expression in esophageal mucosa
Gastroesophageal reflux disease does not lead to changes in the secretory leukocyte protease inhibitor expression in esophageal mucosa
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胃食管反流病不会导致食管粘膜分泌性白细胞蛋白酶抑制剂表达的变化
DOI：
10.1097/meg.0b013e32830e4905
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发表时间：
2009
影响因子：
2.1
通讯作者：
Malfertheiner P.
中科院分区：
文献类型：
--
作者：
Mönkemüller K;Kuester D;Weise S;Kropf S;Fry LC;Stahr A;Völkel S;Roessner A;Malfertheiner P.
目的分泌性白细胞蛋白酶抑制剂（SLPI）在炎症反应中起着对抗丝氨酸蛋白酶的“防御盾牌”作用。胃食管反流病（GERD）与胃食管连接部和食管粘膜的慢性炎症和组织形态学改变有关。在这里，它是调查是否存在胃食管反流病与黏膜SLPI expression.Methods的变化95例胃食管反流病相关症状和27例患者缺乏这些症状。根据洛杉矶和更新的悉尼分类进行内镜和组织学评价。从每例患者的胃和食管粘膜采集多个活检组织进行组织学、免疫组织化学（IHC）和分子分析。SLPI的表达进行了分析，定量逆转录-PCR，酶联免疫测定，和IHC，数据进行了统计分析，内镜和临床parameters.Results 44例非糜烂性和51糜烂性反流病，分别。胃食管反流病患者胃黏膜慢性炎症反应明显加重（P= 0.04），细胞间隙、基底细胞增生、乳头长度明显改变（P< 0.05）。胃窦、贲门和食管的粘液SLPI水平相当，范围为95 - 165 pg/μg蛋白，不受GERD的影响，而GERD患者的食管SLPI转录水平是诱导的3倍（P= 0.002）。免疫组化结果显示，正常食管和贲门黏膜SLPI表达主要来源于上皮细胞，而慢性炎症组织SLPI表达主要来源于浸润的免疫细胞。
Objectives Secretory leukocyte protease inhibitor (SLPI) serves as a ‘defense shield’against serine proteases in inflammation. Gastroesophageal reflux disease (GERD) is associated with chronic inflammation and histomorphological alterations of the gastroesophageal junction and esophageal mucosa. Here, it was investigated whether the presence of GERD was associated with changes of mucosal SLPI expression.Methods Ninety-five patients with GERD-related symptoms and 27 patients lacking those symptoms were included. Endoscopic and histological evaluation was done according to the Los Angeles and updated Sydney classifications. Multiple biopsies were taken from gastric and esophageal mucosa of each patient for histology, immunohistochemistry (IHC), and molecular analyses. SLPI expression was analyzed by quantitative reverse transcriptase-PCR, enzyme-linked immunoassay, and IHC, and the data were statistically analyzed with respect to endoscopic and clinical parameters.Results Forty-four patients had nonerosive and 51 erosive reflux diseases, respectively. Histology revealed higher chronic inflammation (P= 0.04) and significant alterations of the intercellular spaces, basal cell hyperplasia, and length of papilla (P< 0.05) in patients with GERD. Mucosal SLPI levels were comparable among antrum, cardia, and esophagus ranging from 95 to 165 pg/μg protein and were not affected by the presence of GERD, whereas esophageal SLPI-transcript levels were three-fold induced in patients with GERD (P= 0.002). IHC identified epithelial cells as major cellular source of mucosal SLPI expression in normal cardiac and esophageal mucosa, whereas infiltrating immune cells contributed to the SLPI expression in chronically inflamed tissue.Conclusion GERD, a chemically induced inflammation, does not affect mucosal SLPI expression in gastroesophageal mucosa.
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DOI：
10.1016/j.prp.2007.09.003
发表时间：
2007
期刊：
Pathology, research and practice
影响因子：
--
作者：
T. Guenther;A. Hackelsberger;D. Kuester;P. Malfertheiner;A. Roessner
通讯作者：
A. Roessner
分泌性白细胞蛋白酶抑制剂在各类胃炎中的表达：幽门螺杆菌感染的特定作用
DOI：
--
发表时间：
2006
期刊：
European Journal of Gastroenterology and Hepathology
影响因子：
--
作者：
I. Hritz;D. Kuester;M. Vieth;L. Herszényi;M. Stolte;A. Roessner;Z. Tulassay;T. Wex;P. Malfertheiner
通讯作者：
P. Malfertheiner
影响因子：
9.8
作者：
Isomoto, H;Saenko, VA;Kohno, S
通讯作者：
Kohno, S
胃食管反流病中，与未暴露的鳞状上皮相比，暴露于酸的鳞状上皮中 COX-2 mRNA 表达显着增加
影响因子：
3.2
作者：
G. Lurje;D. Vallbohmer;P. Collet;H. Xi;S. Baldus;J. Brabender;R. Metzger;Michaela Heitmann;S. Neiss;Ute Drebber;A. Holscher;P. Schneider
通讯作者：
P. Schneider
影响因子：
3.1
作者：
Nagahama, K;Yamato, M;Takeuchi, K
通讯作者：
Takeuchi, K