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The Nature of the Collagen in Hepatic Fibrosis in Advanced Murine Schistosomiasis

✍ Scribed by Catherine H. Wu; Marie-Adele Giambrone; David J. Howard; Marcos Rojkind; George Y. Wu


Publisher
John Wiley and Sons
Year
2007
Tongue
English
Weight
641 KB
Volume
2
Category
Article
ISSN
0270-9139

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✦ Synopsis


Livers from CF 1 mice infected with Schistosoma mansoni, 50 cercariae each, were examined 8 weeks postinfection. The collagen content of the livers was increased about 18-fold over that for normal control animals. Quantitation of the collagen types in pepsin-solubilized collagen showed a change in the ratio of Type I to Type I11 from 2:l in normal mice to 1:l in the fibrotic animals. The change in ratio resulted from a very large accumulation of Type I11 collagen and, accordingly, may provide an important model for study of the possible reversibility of fibrotic lesion.

Hepatic fibrosis is a disease state defined by the excessive accumulation of collagen fibers in the liver. One of the major causes of hepatic fibrosis in humans is schistosomal infection. The cellular reaction to parasite eggs trapped in the portal venules results in granuloma formation and ultimately marked periportal fibrosis. In hepatic fibrosis, collagen deposition is considered to be the final common pathway of wound repair in response to injury. However, fibrosis results from more than simple activation of a normal synthetic process since the proportion of the collagen types is altered (1) as well as the anatomical distribution and the ultrastructural organization. The collagen type composition in fibrosis is significant for several reasons. First, different types of collagen have different physical properties. For example, in pulmonary fibrosis where an absolute and relative increase in Type I collagen is found, the tissue was determined to be much less distensible than normal as measured by lung compliance (2). In the Ehlers-Danlos, Type IV syndrome, there is a deficiency of collagen Type


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