Gastroenterology
Volume 136, Issue 2 , Pages 425-440, February 2009

Roles of Infection, Inflammation, and the Immune System in Cholesterol Gallstone Formation

  • Kirk J. Maurer

      Affiliations

    • Division of Gastroenterology, Brigham and Women's Hospital, Department of Medicine, Harvard Medical School, Boston, Massachusetts
    • Division of Comparative Medicine, Massachusetts Institute of Technology, Cambridge, Massachusetts
    • Corresponding Author InformationAddress requests for reprints to: Kirk J. Maurer, DVM, PhD, Cornell Center for Animal Resources and Education, College of Veterinary Medicine, Cornell University, Ithaca, New York. fax: (607) 253-3527
  • ,
  • Martin C. Carey

      Affiliations

    • Division of Gastroenterology, Brigham and Women's Hospital, Department of Medicine, Harvard Medical School, Boston, Massachusetts
  • ,
  • James G. Fox

      Affiliations

    • Division of Comparative Medicine, Massachusetts Institute of Technology, Cambridge, Massachusetts
    • Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, Massachusetts

Received 16 July 2008; accepted 8 December 2008. published online 24 December 2008.

John P. Lynch and David C. Metz, Section Editors

Cholesterol gallstone formation is a complex process mediated by genetic and environmental factors. Until recently, the role of the immune system in the pathogenesis of cholesterol gallstones was not considered a valid topic of research interest. This review collates and interprets an extensive body of basic literature, some of which is not customarily considered to be related to cholelithogenesis, describing the multiple facets of the immune system that appear to be involved in cholesterol cholelithogenesis. A thorough understanding of the immune interactions with biliary lipids and cholecystocytes should modify current views of the pathogenesis of cholesterol gallstones, promote further research on the pathways involved, and lead to novel diagnostic tools, treatments, and preventive measures.

Abbreviations used in this paper: EGF, epidermal growth factor, EGFR, epidermal growth factor receptor, FXR, farnesoid X receptor, IL, interleukin, LPS, lipopolysaccharide, MyD88, myeloid differentiation protein 88, TGF, transforming growth factor, TLR, toll-like receptor, TNF, tumor necrosis factor, PCR, polymerase chain reaction

 

 M.C.C. and J.G.F. contributed equally to this work.

 K.J.M. was supported by grant K08-DK07728, J.G.F. was supported by grants P30-ES02109 and R01-CA067529, and M.C.C. was supported by grants R01-DK073687 and R37-DK036588.

 The authors disclose no conflicts.

PII: S0016-5085(08)02187-2

doi:10.1053/j.gastro.2008.12.031

Gastroenterology
Volume 136, Issue 2 , Pages 425-440, February 2009