title: Morphological and immunohistochemical comparison of intrapancreatic nerves between chronic pancreatitis and type 1 autoimmune pancreatitis.
abstract: OBJECTIVE
  The abdominal pain associated with chronic pancreatitis (CP) may be related to the increased number and size of intrapancreatic nerves. On the other hand, patients with type 1 autoimmune pancreatitis (AIP) rarely suffer from the pain syndrome, and there are no previous studies concerning the histopathological findings of intrapancreatic nerves in patients with type 1 AIP. The current study is aimed at investigating the differences in the histopathological and immunohistochemical findings of intrapancreatic nerves in patients with CP and type 1 AIP.
  
  
  METHODS
  Neuroanatomical differences between CP and type 1 AIP were assessed by immunostaining with a pan-neuronal marker, protein gene product 9.5 (PGP9.5). The number (neural density) and area (neural hypertrophy) of PGP9.5-immunopositive nerves were quantitatively analyzed. Furthermore, the expression of nerve growth factor (NGF), and a high affinity receptor for NGF, tyrosine kinase receptor A (TrkA), was assessed by immunohistochemistry.
  
  
  RESULTS
  Both neural density and hypertrophy were significantly greater in pancreatic tissue samples from patients with CP than those with normal pancreas or type 1 AIP. NGF expression was stronger in type 1 AIP than in CP, whereas TrkA expression in type 1 AIP was poorer than in CP.
  
  
  CONCLUSIONS
  Although CP and type 1 AIP are both characterized by the presence of sustained pancreatic inflammation, they are different in terms of the density and hypertrophy of intrapancreatic nerve fibers. It is possible that this may be related to the difference in the activity of the NGF/TrkA-pathway between the two types of pancreatitis.
authors.affiliation: The Third Department of Internal Medicine, Kansai Medical University, Osaka, Japan.
authors.forename: Kota
authors.initials: K
authors.lastname: Kato
authors.affiliation: The Third Department of Internal Medicine, Kansai Medical University, Osaka, Japan.
authors.forename: Tsukasa
authors.initials: T
authors.lastname: Ikeura
authors.affiliation: The Third Department of Internal Medicine, Kansai Medical University, Osaka, Japan.
authors.forename: Masato
authors.initials: M
authors.lastname: Yanagawa
authors.affiliation: The Third Department of Internal Medicine, Kansai Medical University, Osaka, Japan.
authors.forename: Takashi
authors.initials: T
authors.lastname: Tomiyama
authors.affiliation: The Third Department of Internal Medicine, Kansai Medical University, Osaka, Japan.
authors.forename: Toshiro
authors.initials: T
authors.lastname: Fukui
authors.affiliation: The Third Department of Internal Medicine, Kansai Medical University, Osaka, Japan.
authors.forename: Kazushige
authors.initials: K
authors.lastname: Uchida
authors.affiliation: The Third Department of Internal Medicine, Kansai Medical University, Osaka, Japan.
authors.forename: Makoto
authors.initials: M
authors.lastname: Takaoka
authors.affiliation: The Third Department of Internal Medicine, Kansai Medical University, Osaka, Japan.
authors.forename: Akiyoshi
authors.initials: A
authors.lastname: Nishio
authors.affiliation: Department of Pathology, Kansai Medical University, Osaka, Japan.
authors.forename: Yoshiko
authors.initials: Y
authors.lastname: Uemura
authors.affiliation: Department of Surgery, Kansai Medical University, Osaka, Japan.
authors.forename: Sohei
authors.initials: S
authors.lastname: Satoi
authors.affiliation: Department of Anatomy and Cell Science, Kansai Medical University, Osaka, Japan.
authors.forename: Hisao
authors.initials: H
authors.lastname: Yamada
authors.affiliation: The Third Department of Internal Medicine, Kansai Medical University, Osaka, Japan. Electronic address: okazaki@hirakata.kmu.ac.jp.
authors.forename: Kazuichi
authors.initials: K
authors.lastname: Okazaki
mesh_terms: D000328:Adult; D000368:Aged; D001327:Autoimmune Diseases / Q000378:metabolism / Q000473:pathology*; D015415:Biomarkers; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D009412:Nerve Fibers / Q000473:pathology; D020932:Nerve Growth Factor / Q000378:metabolism; D010146:Pain / Q000209:etiology; D010179:Pancreas / Q000294:innervation* / Q000378:metabolism / Q000473:pathology*; D010195:Pancreatitis / Q000378:metabolism / Q000473:pathology*; D050500:Pancreatitis, Chronic / Q000378:metabolism / Q000473:pathology*; D010525:Peripheral Nerves / Q000473:pathology; D020917:Receptor, trkA / Q000378:metabolism; D043222:Ubiquitin Thiolesterase / Q000032:analysis / Q000378:metabolism
chemical_list: D015415:Biomarkers; C482860:UCHL1 protein, human; D020932:Nerve Growth Factor; D020917:Receptor, trkA; D043222:Ubiquitin Thiolesterase
keywords: Autoimmune pancreatitis; Chronic pancreatitis; Nerve; Nerve growth factor; Pain