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Acinar Cell Production of Leukotriene B4 Contributes to Development of Neurogenic Pancreatitis in Mice.

Publication ,  Journal Article
Shahid, RA; Vigna, SR; Layne, AC; Romac, JM-J; Liddle, RA
Published in: Cell Mol Gastroenterol Hepatol
January 2015

BACKGROUND & AIMS: In the pancreas, activation of primary sensory nerves through the transient receptor potential ion channel TRPV1 contributes to the early stages of development of pancreatitis. Little is known about the mechanism by which this occurs. We investigated whether leukotriene B4 (LTB4) is an endogenous agonist of TRPV1 and mediates pancreatitis. METHODS: Acute inflammation was induced in the pancreata of Trpv1-/- mice and their wild-type littermates by retrograde infusion of the main pancreatic duct with 2% sodium taurocholate (NaT) or intraperitoneal injections of caerulein. Mice were also given injections of resiniferatoxin (an excitotoxin that desensitizes TRPV1) or MK886 (a drug that inhibits LTB4 biosynthesis). Pancreatic tissues and plasma were collected and analyzed. RESULTS: Retrograde perfusion of the main pancreatic ducts of wild-type mice with NaT caused severe acute pancreatitis; severity was reduced by co-administration of resiniferatoxin. Trpv1-/- mice developed a less severe pancreatitis following NaT administration than controls. Administration of MK886 before perfusion with NaT also significantly reduced the severity of pancreatitis in wild-type mice. Pancreatic tissues from mice given NaT had a marked increase in the level of 5-lipoxygenase immunoreactivity specifically in acinar cells. Bile acid and caerulein induced secretion of LTB4 by cultured pancreatic acinar cells; MK886 inhibited this process. CONCLUSIONS: Administration of caerulein or intraductal bile acids in mice causes production of LTB4 by pancreatic acinar cells. This activates TRPV1 on primary sensory nerves to induce acute pancreatitis.

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Published In

Cell Mol Gastroenterol Hepatol

DOI

ISSN

2352-345X

Publication Date

January 2015

Volume

1

Issue

1

Start / End Page

75 / 86

Location

United States

Related Subject Headings

  • 3202 Clinical sciences
  • 3101 Biochemistry and cell biology
 

Citation

APA
Chicago
ICMJE
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Shahid, R. A., Vigna, S. R., Layne, A. C., Romac, J.-J., & Liddle, R. A. (2015). Acinar Cell Production of Leukotriene B4 Contributes to Development of Neurogenic Pancreatitis in Mice. Cell Mol Gastroenterol Hepatol, 1(1), 75–86. https://doi.org/10.1016/j.jcmgh.2014.11.002
Shahid, Rafiq A., Steven R. Vigna, Amanda C. Layne, Joelle M-J Romac, and Rodger A. Liddle. “Acinar Cell Production of Leukotriene B4 Contributes to Development of Neurogenic Pancreatitis in Mice.Cell Mol Gastroenterol Hepatol 1, no. 1 (January 2015): 75–86. https://doi.org/10.1016/j.jcmgh.2014.11.002.
Shahid RA, Vigna SR, Layne AC, Romac JM-J, Liddle RA. Acinar Cell Production of Leukotriene B4 Contributes to Development of Neurogenic Pancreatitis in Mice. Cell Mol Gastroenterol Hepatol. 2015 Jan;1(1):75–86.
Shahid, Rafiq A., et al. “Acinar Cell Production of Leukotriene B4 Contributes to Development of Neurogenic Pancreatitis in Mice.Cell Mol Gastroenterol Hepatol, vol. 1, no. 1, Jan. 2015, pp. 75–86. Pubmed, doi:10.1016/j.jcmgh.2014.11.002.
Shahid RA, Vigna SR, Layne AC, Romac JM-J, Liddle RA. Acinar Cell Production of Leukotriene B4 Contributes to Development of Neurogenic Pancreatitis in Mice. Cell Mol Gastroenterol Hepatol. 2015 Jan;1(1):75–86.
Journal cover image

Published In

Cell Mol Gastroenterol Hepatol

DOI

ISSN

2352-345X

Publication Date

January 2015

Volume

1

Issue

1

Start / End Page

75 / 86

Location

United States

Related Subject Headings

  • 3202 Clinical sciences
  • 3101 Biochemistry and cell biology