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Primary biliary cirrhosis in the mouse: induction by human mycoplasma-like organisms

L Johnson1, E Wirostko, W Wirostko

  • 1Department of Pathology, Columbia-Presbyterian Medical Center, New York, NY 10032.

Insights

Mycoplasma-like organisms (MLO) cause chronic inflammatory eye disease in humans. This study shows MLO also induce progressive liver inflammation in mice, resembling human biliary cirrhosis.

Area of Science:

  • Microbiology
  • Immunology
  • Ophthalmology

Background:

  • Mycoplasma-like organisms (MLO) are implicated in human intraocular and orbital inflammatory diseases.
  • MLO are intracellular, cell-wall deficient bacteria, challenging to culture and diagnose.
  • Current diagnosis relies on transmission electron microscopy to detect MLO within infected cells.

Purpose of the Study:

  • To investigate the pathogenic potential of MLO in a murine model.
  • To characterize the systemic effects of MLO infection, including ocular, orbital, and hepatic manifestations.
  • To explore the potential link between MLO-induced liver disease and human primary biliary cirrhosis.

Main Methods:

  • Inoculation of human MLO into mouse eyelids to induce disease.
  • Histopathological examination of ocular, orbital, and systemic tissues.
  • Microscopic analysis of liver tissues to identify MLO and inflammatory markers.

Main Results:

  • MLO inoculation caused high incidence of orbital and intraocular disease in mice.
  • Systemic dissemination of MLO was observed, with infected leucocytes in all disease sites.
  • Chronic progressive hepatic portal inflammatory disease developed in 11% of infected mice, absent in controls.
  • MLO-parasitized portal leucocytes were found in inflamed livers, suggesting a direct role in hepatic pathology.

Conclusions:

  • MLO can induce severe systemic disease, including chronic progressive liver inflammation in mice.
  • The observed murine liver pathology shares similarities with human primary biliary cirrhosis.
  • These findings highlight MLO as a significant pathogen with potential implications for autoimmune liver diseases.

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