r iu Chronic pancreatitis MOLECULAR PAIN

Full list of author information is available at the end of the articleBackground Sustained/chronic sensitization of sensory neurons, resulting in pathological pain, can be induced by various components of the inflammatory milieu including physico-chemical factors (temperature, acid) as well as a variety of small molecules, cytokines, growth factors, other peptides and enzymes that are a hallmark of chronic inflammation [1]. Transforming growth factor beta (TGFβ) is also prominently expressed in such situations and plays a key role in wound healing and promoting fibrosis. TGFβ and other members of its superfamily including activin and bone morphogenetic proteins (BMP) are recognized as playing critical roles in the development, survival and repair of neurons in the peripheral and central nervous systems (CNS) [2,3]. Intact and injured dorsal root ganglia (DRG) neurons produce TGFβ and express TGFβ receptors [4,5], and endogenous TGF potentiates the trophic effect of other growth factors on DRG neurons [6,7]. Despite this knowledge, the role of TGFβ on peripheral noccieptor sensitization remains unknown