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Factors influencing the effects of murine cytomegalovirus on the pancreas.

AbstractBACKGROUND:
As human cytomegalovirus (HCMV) infections are implicated in insulin-dependent diabetes mellitus (IDDM), the effects of murine (M)CMV infection of inbred mice on the pancreas are of interest.
RESULTS:
Inflammation and periacinar oedema peaked on day 3 and were replaced by a focal inflammation, but infected cells were rare. The islets were spared in C57BL mice. Insulitis normally seen in non-obese diabetic (NOD) mice was accelerated, but infected NOD mice did not become glycosuric. Isotypes of total and autoreactive antibodies suggested a shift to a Th 1 response (IgG2a) in all MCMV-infected mice. MCMV-induced pancreatitis was not affected by MHC genes but was similar or less severe in BALB/c mice. As these lack the Cmv1 gene, which provides a protective natural killer (NK) cell response in C57BL congenic mice, the C57BL background may carry a pancreatitis susceptibility gene able to counter NK-mediated restriction of viral replication. Consistently, congenic mice expressing Cmvl on a BALB/c background did not display pancreatitis, unless depleted of NK cells. In vivo treatment with soluble cytokine receptors suggested that interleukin 1 (IL-1) and/or tumour necrosis factor alpha contribute to acinar necrosis in C57BL mice.
AuthorsP Price, A G Baxter, R N Allcock, J M Papadimitriou
JournalEuropean journal of clinical investigation (Eur J Clin Invest) Vol. 28 Issue 7 Pg. 546-53 (Jul 1998) ISSN: 0014-2972 [Print] England
PMID9726035 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Autoantibodies
  • Interleukin-1
  • Receptors, Interleukin-1
  • Receptors, Tumor Necrosis Factor
  • Tumor Necrosis Factor-alpha
Topics
  • Animals
  • Autoantibodies (blood)
  • Cytomegalovirus (pathogenicity, physiology)
  • Cytomegalovirus Infections (pathology)
  • Diabetes Mellitus, Type 1 (virology)
  • Female
  • Humans
  • Hypergammaglobulinemia (pathology, virology)
  • Interleukin-1 (physiology)
  • Islets of Langerhans (pathology, virology)
  • Killer Cells, Natural (immunology)
  • Liver (pathology, virology)
  • Lymphocyte Depletion
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Mice, Inbred NOD
  • Necrosis
  • Pancreas (pathology, virology)
  • Pancreatitis (pathology, virology)
  • Receptors, Interleukin-1 (administration & dosage, physiology)
  • Receptors, Tumor Necrosis Factor (administration & dosage, physiology)
  • Tumor Necrosis Factor-alpha (physiology)
  • Virus Replication

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