Affiliations 

  • 1 QIMR Berghofer Medical Research Institute, Brisbane, Qld 4006, Australia; School of Veterinary Sciences, The University of Queensland, Gatton, Qld 4343, Australia; School of Medical Sciences, Universiti Sains Malaysia, 16150 Kelantan, Malaysia
  • 2 School of Veterinary Sciences, The University of Queensland, Gatton, Qld 4343, Australia
  • 3 QIMR Berghofer Medical Research Institute, Brisbane, Qld 4006, Australia
  • 4 QIMR Berghofer Medical Research Institute, Brisbane, Qld 4006, Australia. Electronic address: Geoffrey.Gobert@qimrberghofer.edu.au
Int J Parasitol, 2016 Apr;46(4):239-52.
PMID: 26812024 DOI: 10.1016/j.ijpara.2015.12.004

Abstract

For hepatic schistosomiasis the egg-induced granulomatous response and the development of extensive fibrosis are the main pathologies. We used a Schistosoma japonicum-infected mouse model to characterise the multi-cellular pathways associated with the recovery from hepatic fibrosis following clearance of the infection with the anti-schistosomal drug, praziquantel. In the recovering liver splenomegaly, granuloma density and liver fibrosis were all reduced. Inflammatory cell infiltration into the liver was evident, and the numbers of neutrophils, eosinophils and macrophages were significantly decreased. Transcriptomic analysis revealed the up-regulation of fatty acid metabolism genes and the identification of Peroxisome proliferator activated receptor alpha as the upstream regulator of liver recovery. The aryl hydrocarbon receptor signalling pathway which regulates xenobiotic metabolism was also differentially up-regulated. These findings provide a better understanding of the mechanisms associated with the regression of hepatic schistosomiasis.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.