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Mediators of Inflammation
Volume 2012 (2012), Article ID 294070, 8 pages
Research Article

Essential Role of Mast Cells in the Visceral Hyperalgesia Induced by T. spiralis Infection and Stress in Rats

Department of Gastroenterology, Peking University Third Hospital, 49 North Garden Road, Haidian District, Beijing 100191, China

Received 16 September 2011; Accepted 18 December 2011

Academic Editor: Amal O. Amer

Copyright © 2012 Chang-Qing Yang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Mast cells (MCs) deficient rats (Ws/Ws) were used to investigate the roles of MCs in visceral hyperalgesia. Ws/Ws and wild control ( ) rats were exposed to T. spiralis or submitted to acute cold restraint stress (ACRS). Levels of proteinase-activated receptor 2 (PAR2) and nerve growth factor (NGF) were determined by immunoblots and RT-PCR analysis, and the putative signal pathways including phosphorylated extracellular-regulated kinase (pERK1/2) and transient receptor potential vanilloid receptor 1 (TRPV1) were further identified. Visceral hyperalgesia triggered by ACRS was observed only in rats. The increased expression of PAR2 and NGF was observed only in rats induced by T. spiralis and ACRS. The activation of pERK1/2 induced by ACRS occurred only in rats. However, a significant increase of TRPV1 induced by T. spiralis and ACRS was observed only in rats. The activation of PAR2 and NGF via both TRPV1 and pERK1/2 signal pathway is dependent on MCs in ACRS-induced visceral hyperalgesia rats.