title: The conspiracy of autophagy, stress and inflammation in acute pancreatitis.
abstract: OBJECTIVE
  Acute pancreatitis is associated with alcohol abuse, gallstones and bacterial infection. Its basic cause is tissue destruction accompanied by an innate immune response, which induces epithelial stress pathways. Recent studies have focused on some of the integral cellular pathways shared between multiple pancreatitis models that also suggest new approaches to detection and treatment.
  
  
  RESULTS
  Several models of pancreatitis have been associated with stress responses, such as endoplasmic reticulum and oxidative stress together with the induction of a defective autophagic pathway. Recent evidence reinforces the critical role of these cellular processes in pancreatitis. A member of the toll-like receptor family, toll-like receptor 4, which is known to contribute to disease pathology in many models of experimental pancreatitis, has been found to be a promising target for treatment of pancreatitis. Interestingly, a direct activator of toll-like receptor 4, the bacterial cell wall component in gram-negative bacteria lipopolysaccharide, contributes to the onset and severity of disease when combined with additional stressors, such as chronic alcohol feeding; however, recent studies have shown that acute infection of mice with live bacteria is alone sufficient to induce acute pancreatitis.
  
  
  CONCLUSIONS
  In the last several months, the convergent roles of acinar cell stress, autophagy and proinflammatory signaling initiated by the toll-like receptors have been emphatically reinforced in the onset of acute pancreatitis.
authors.affiliation: Department of Cancer Biology, Mayo Clinic, Jacksonville, Florida, USA.
authors.forename: Jason C
authors.initials: JC
authors.lastname: Hall
authors.forename: Howard C
authors.initials: HC
authors.lastname: Crawford
mesh_terms: D000818:Animals; D001343:Autophagy; D006801:Humans; D007111:Immunity, Cellular; D018384:Oxidative Stress / Q000502:physiology*; D019283:Pancreatitis, Acute Necrotizing / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D015398:Signal Transduction