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肥大细胞参与小鼠急性酸诱导食管炎症的直接证据。

Direct evidence of mast cell participation in acute acid-induced esophageal inflammation in mice.

作者信息

Morganstern Jeffrey A, Wang Ming-Yu, Wershil Barry K

机构信息

The Children's Hospital at Montefiore and Albert Einstein College of Medicine, Bronx, NY 10467, USA.

出版信息

J Pediatr Gastroenterol Nutr. 2008 Feb;46(2):134-8. doi: 10.1097/MPG.0b013e31815ceaa4.

Abstract

OBJECTIVES

Mast cells have been implicated in the pathogenesis of esophagitis resulting from gastroesophageal acid reflux, but their precise role has been difficult to define. We proposed to directly examine the contribution of mast cells to neutrophil infiltration in a mouse model of acid-induced esophageal injury.

MATERIALS AND METHODS

Normal and mast cell-deficient (Kit) mice underwent either a surgical procedure to induce acute acid reflux injury of the esophagus or sham surgery. Neutrophil infiltration in the esophagus was determined by morphometrical quantification. To further delineate the involvement of mast cells, acid-induced esophageal injury was elicited in mast cell-deficient mice that had undergone mast cell reconstitution by bone marrow transplantation.

RESULTS

Normal mice exhibited significant neutrophil infiltration into the esophagus as a result of acid-induced injury. The neutrophil accumulation was significantly diminished in mast cell-deficient mice. However, the neutrophil infiltration that resulted from acid-induced injury in mast cell-reconstituted Kit mice was similar to that seen in normal mice.

CONCLUSIONS

Our findings provide direct evidence that mast cells participate in the recruitment of neutrophils during acid-induced esophageal injury in mice.

摘要

目的

肥大细胞与胃食管酸反流所致食管炎的发病机制有关,但其确切作用难以界定。我们建议在酸诱导的食管损伤小鼠模型中直接检测肥大细胞对中性粒细胞浸润的作用。

材料与方法

正常小鼠和肥大细胞缺陷(Kit)小鼠接受诱导食管急性酸反流损伤的手术或假手术。通过形态计量学定量测定食管中的中性粒细胞浸润情况。为进一步阐明肥大细胞的作用,对经骨髓移植进行肥大细胞重建的肥大细胞缺陷小鼠诱发酸诱导的食管损伤。

结果

正常小鼠因酸诱导损伤而出现食管中显著的中性粒细胞浸润。肥大细胞缺陷小鼠的中性粒细胞积聚明显减少。然而,经肥大细胞重建的Kit小鼠因酸诱导损伤所致的中性粒细胞浸润与正常小鼠相似。

结论

我们的研究结果提供了直接证据,表明肥大细胞在小鼠酸诱导的食管损伤过程中参与中性粒细胞的募集。

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