Cytosolic double-stranded DNA as a damage-associated molecular pattern induces the inflammatory response in rat pancreatic stellate cells

A plausible mechanism for tissue injury-associated pancreatitis

Taichi Nakamura, Tetsuhide Ito, Hisato Igarashi, Masahiko Uchida, Masayuki Hijioka, takamasa ono, Nao Fujimori, Yusuke Niina, Koichi Suzuki, Robert T. Jensen, Ryoichi Takayanagi

研究成果: ジャーナルへの寄稿記事

11 引用 (Scopus)

抄録

Pancreatitis is an inflammatory disease of unknown causes. There are many triggers causing pancreatitis, such as alcohol, common bile duct stone, virus and congenital or acquired stenosis of main pancreatic duct, which often involve tissue injuries. Pancreatitis often occurs in sterile condition, where the dead/dying pancreatic parenchymal cells and the necrotic tissues derived from self-digested-pancreas were observed. However, the causal relationship between tissue injury and pancreatitis and how tissue injury could induce the inflammation of the pancreas were not elucidated fully until now. This study demonstrates that cytosolic double-stranded DNA increases the expression of several inflammatory genes (cytokines, chemokines, type I interferon, and major histocompatibility complex) in rat pancreatic stellate cells. Furthermore, these increase accompanied the multiple signal molecules genes, such as interferon regulatory factors, nuclear factor-kappa B, low-molecular-weight protein 2, and transporter associated with antigen processing 1. We suggest that this phenomenon is a plausible mechanism that might explain how cell damage of the pancreas or tissue injury triggers acute, chronic, and autoimmune pancreatitis; it is potentially relevant to host immune responses induced during alcohol consumption or other causes.

元の言語英語
記事番号504128
ジャーナルInternational Journal of Inflammation
2012
DOI
出版物ステータス出版済み - 11 7 2012

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Pancreatic Stellate Cells
Pancreatitis
DNA
Wounds and Injuries
Pancreas
Interferon Regulatory Factors
Interferon Type I
NF-kappa B
Pancreatic Ducts
Chronic Pancreatitis
Antigen Presentation
Common Bile Duct
Major Histocompatibility Complex
Chemokines
Alcohol Drinking
Genes
Pathologic Constriction
Molecular Weight
Alcohols
Cytokines

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy

これを引用

Cytosolic double-stranded DNA as a damage-associated molecular pattern induces the inflammatory response in rat pancreatic stellate cells : A plausible mechanism for tissue injury-associated pancreatitis. / Nakamura, Taichi; Ito, Tetsuhide; Igarashi, Hisato; Uchida, Masahiko; Hijioka, Masayuki; ono, takamasa; Fujimori, Nao; Niina, Yusuke; Suzuki, Koichi; Jensen, Robert T.; Takayanagi, Ryoichi.

:: International Journal of Inflammation, 巻 2012, 504128, 07.11.2012.

研究成果: ジャーナルへの寄稿記事

Nakamura, Taichi ; Ito, Tetsuhide ; Igarashi, Hisato ; Uchida, Masahiko ; Hijioka, Masayuki ; ono, takamasa ; Fujimori, Nao ; Niina, Yusuke ; Suzuki, Koichi ; Jensen, Robert T. ; Takayanagi, Ryoichi. / Cytosolic double-stranded DNA as a damage-associated molecular pattern induces the inflammatory response in rat pancreatic stellate cells : A plausible mechanism for tissue injury-associated pancreatitis. :: International Journal of Inflammation. 2012 ; 巻 2012.
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abstract = "Pancreatitis is an inflammatory disease of unknown causes. There are many triggers causing pancreatitis, such as alcohol, common bile duct stone, virus and congenital or acquired stenosis of main pancreatic duct, which often involve tissue injuries. Pancreatitis often occurs in sterile condition, where the dead/dying pancreatic parenchymal cells and the necrotic tissues derived from self-digested-pancreas were observed. However, the causal relationship between tissue injury and pancreatitis and how tissue injury could induce the inflammation of the pancreas were not elucidated fully until now. This study demonstrates that cytosolic double-stranded DNA increases the expression of several inflammatory genes (cytokines, chemokines, type I interferon, and major histocompatibility complex) in rat pancreatic stellate cells. Furthermore, these increase accompanied the multiple signal molecules genes, such as interferon regulatory factors, nuclear factor-kappa B, low-molecular-weight protein 2, and transporter associated with antigen processing 1. We suggest that this phenomenon is a plausible mechanism that might explain how cell damage of the pancreas or tissue injury triggers acute, chronic, and autoimmune pancreatitis; it is potentially relevant to host immune responses induced during alcohol consumption or other causes.",
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