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    In: International Journal of Experimental Pathology, Wiley, Vol. 90, No. 5 ( 2009-10), p. 538-548
    Abstract: The aim of this work was to study alterations in the extracellular matrix of liver in dogs naturally infected with Leishmania ( Leishmania ) chagasi that are correlated with clinical aspects and with histological, parasitological and immunological findings. The study was carried out on 30 dogs, 10 uninfected (control group) and 20 infected. The infected animals were further divided into two groups: an asymptomatic group of 10 dogs without clinical signs of the disease; and a symptomatic group of 10 dogs with classical clinical signs. All thirty animals were mongrel dogs of undefined age, obtained from the municipality of Belo Horizonte, MG, metropolitan area. During necropsy, liver fragments were collected and fixed in 10% buffered formaldehyde for histological examination. Paraffined sections of the tissues were stained with haematoxylin–eosin, Gomori’s ammoniacal silver stain for reticular fibres and strepto‐avidin peroxidase for immunohistochemical detection of Leishmania amastigotes. Frozen tissue sections were stained by immunofluorescence for fibronectin (FN) and laminin (LN). Liver collagen deposition was significantly greater in the infected than the control animals and differed significantly between the symptomatic and asymptomatic dogs. There was a positive correlation between the parasite load and liver collagen deposition. The increased collagen deposition in infected animal livers may be associated with the parasite burden. Adhesive FN and LN fibres were significantly more highly expressed in the livers of symptomatic than of asymptomatic dogs. Our results demonstrate that canine visceral leishmaniasis causes fibrogenesis in liver, associated with the parasite load and degenerative processes.
    Type of Medium: Online Resource
    ISSN: 0959-9673 , 1365-2613
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2009
    detail.hit.zdb_id: 1016006-1
    detail.hit.zdb_id: 2010007-3
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