Bile-pancreatic juice exclusion increases cholinergic M3 and CCK-A receptor expression and interleukin-6 production in ligation-induced acute pancreatitis - 25/08/11
, Asgar Zaheer, Ph.D. a, Smita Zaheer, Ph.D. b, Rory A. Fisher, Ph.D. cAbstract |
Background |
Using an original model, the Donor Rat Model, we showed that bile-pancreatic juice (BPJ) exclusion from gut exacerbates ligation-induced acute pancreatitis in rats. We also showed that muscarinic cholinergic M3 and CCK-A receptor expression is induced following duct ligation. Increased receptor number potentially could exacerbate cytokine production. We hypothesize that BPJ exclusion is responsible for M3 and CCK-A receptor induction and increased interleukin-6 (IL-6) production.
Methods |
M3 and CCK-A receptor expression and IL-6 production were compared in rat pancreata 1 to 3 hours after duct ligation with or without BPJ replacement.
Results |
Our studies showed that BPJ replacement attenuates duct ligation–induced increases in M3 and CCK-A receptor expression and IL-6 production.
Conclusions |
In this model, BPJ exclusion from gut induces M3 and CCK-A receptor expression and increases IL-6 production. In this experimental corollary of gallstone pancreatitis, BPJ exclusion from gut may play a key role in the mechanism of disease pathogenesis.
Le texte complet de cet article est disponible en PDF.Keywords : Acute pancreatitis, donor rat model, CCK-A receptor, cholinergic M3 receptor, cytokines, interleukin-6
Plan
| Supported by an American College of Surgeons Faculty Research Fellowship and a National Institutes of Health NIDDK Career Development Award (Grant K08-DK062805) to I.S. |
Vol 188 - N° 5
P. 511-515 - novembre 2004 Retour au numéro
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