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瘦素介导艰难梭菌毒素A诱导的小鼠肠炎。

Leptin mediates Clostridium difficile toxin A-induced enteritis in mice.

作者信息

Mykoniatis Andreas, Anton Pauline M, Wlk Michael, Wang Chi Chung, Ungsunan Linda, Blüher Susann, Venihaki Maria, Simeonidis Simos, Zacks Jeff, Zhao Dezheng, Sougioultzis Stavros, Karalis Katia, Mantzoros Christos, Pothoulakis Charalabos

机构信息

Divisions of Gastroenterology and Endocrinology, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215, USA.

出版信息

Gastroenterology. 2003 Mar;124(3):683-91. doi: 10.1053/gast.2003.50101.

DOI:10.1053/gast.2003.50101
PMID:12612907
Abstract

BACKGROUND & AIMS: Leptin regulates energy homeostasis and participates in the regulation of the hypothalamic-pituitary-adrenal axis. Although hyperleptinemia is described in experimental colitis, its role in the pathophysiology of enterotoxin-mediated diarrhea and inflammation remains unclear. We examined the role of leptin in the inflammatory diarrhea induced by toxin A from Clostridium difficile, the causative agent of antibiotic-related colitis.

METHODS

Toxin A (10 microg) or buffer were administered in ileal loops of leptin-deficient (ob/ob), leptin-resistant (db/db), or wild-type mice and enterotoxic responses were measured.

RESULTS

In toxin A-treated wild-type mice, circulating leptin and corticosterone levels were increased compared with buffer-injected animals. Toxin A also stimulated increased mucosal expression of the Ob-Rb at the messenger RNA (mRNA) and protein level. Ob/ob and db/db mice were partially protected against toxin A-induced intestinal secretion and inflammation, and this effect was reversed by leptin administration in ob/ob, but not db/db, mice. Basal- and toxin A-stimulated plasma corticosterone levels in ob/ob and db/db mice were higher compared with toxin A-treated wild-type mice. To assess whether the effect of leptin in intestinal inflammation is mediated by corticosteroids we performed adrenalectomy experiments in db/db and wild-type mice. Our results suggested that the diminished intestinal response to toxin A in db/db mice was related only in part to increased levels of corticosteroids.

CONCLUSIONS

Leptin plays an important role in regulating the severity of enterotoxin-mediated intestinal secretion and inflammation by activating both corticosteroid-dependent and -independent mechanisms.

摘要

背景与目的

瘦素调节能量平衡,并参与下丘脑 - 垂体 - 肾上腺轴的调节。尽管在实验性结肠炎中已描述有高瘦素血症,但其在肠毒素介导的腹泻和炎症病理生理学中的作用仍不清楚。我们研究了瘦素在艰难梭菌毒素A诱导的炎性腹泻中的作用,艰难梭菌是抗生素相关性结肠炎的病原体。

方法

将毒素A(10微克)或缓冲液注入瘦素缺乏(ob/ob)、瘦素抵抗(db/db)或野生型小鼠的回肠肠袢中,并测量肠毒性反应。

结果

与注射缓冲液的动物相比,毒素A处理的野生型小鼠循环瘦素和皮质酮水平升高。毒素A还刺激了信使核糖核酸(mRNA)和蛋白质水平上Ob-Rb的粘膜表达增加。Ob/ob和db/db小鼠对毒素A诱导的肠道分泌和炎症有部分保护作用,在ob/ob小鼠中给予瘦素可逆转这种作用,但在db/db小鼠中则不能。与毒素A处理的野生型小鼠相比,ob/ob和db/db小鼠的基础及毒素A刺激的血浆皮质酮水平更高。为了评估瘦素在肠道炎症中的作用是否由皮质类固醇介导,我们在db/db和野生型小鼠中进行了肾上腺切除术实验。我们的结果表明,db/db小鼠对毒素A的肠道反应减弱仅部分与皮质类固醇水平升高有关。

结论

瘦素通过激活皮质类固醇依赖性和非依赖性机制,在调节肠毒素介导的肠道分泌和炎症严重程度中起重要作用。

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