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

Abstract EN

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.