Myofibroblasts in Schistosomal Portal Fibrosis of Man

Andrade, Zilton de Araújo; Guérret, Sylviane; Fernandes, André L. M.

doi:10.1590/s0074-02761999000100018

Cited by 29 publications

(22 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The role a peculiar contractile tissue like this could play on the mechanisms of portal hypertension appeared obvious. However, our own data showed that myofibroblasts in schistosomal portal fibrosis were focally accumulated around damaged portal veins, since they originated from dissociation of the muscular coat of portal vein walls, followed by dispersion of smooth muscle cells and their further differentiation into myofibroblasts (Andrade et al 1998). It was also observed that these myofibroblasts behaved as transient cells, some becoming fibroblasts and others disappearing, probably undergoing apoptosis.…”

Section: Is Schistosomal Portal Fibrosis Peculiar?mentioning

confidence: 83%

“…Electron microscopy, 4400X; B: collagen degradation in advanced schistosomiasis: area of fibrosis showing dissolution of a large amount of collagen fibers, giving origin to empty spaces ("lytic change"). Electron microscopy, 4400X; C: even when examined by light microscopy, schistosomal fibrosis may reveal rarefaction of collagen fibers; D: this aspect can be compared with the usual compact appearance of the fibrous tissue in other areas of the same liver; Picro Sirius-red method for collagen, 200X (Andrade et al 1998). itself can cause a certain degree of chronic hepatitis, probably of a reactive nature. The presence of this hepatitis in experimental animals can be easily observed.…”

Section: The Significance Of Chronic Hepatitismentioning

confidence: 99%

See 1 more Smart Citation

Schistosomal hepatopathy

Andrade

2004

Mem. Inst. Oswaldo Cruz

Self Cite

View full text Add to dashboard Cite

Advanced schistosomiasis produces in man one of the most characteristic gross picture presentation of hepatic pathology. On the cut surface of the liver this lesion appears as whitish fibrous plaques replacing portal spaces on a background of normal looking hepatic parenchyma (Fig. 1C, D). Exactly one century ago, Symmers (1904) classically described this picture after performing autopsies in Egypt. It represents the anatomical counterpart of the clinical condition known as hepatosplenic schistosomiasis. A cursory gross and microscopic examination of the lesion will reveal important clues about its pathogenesis. It can then be noted that the lesion resulted from the deposition of numerous schistosome eggs along the periportal tissues, which provoked chronic granulomatous inflammation with consequent fibrous expansion of the portal spaces and intrahepatic portal vein obstruction. The parenchyma usually maintains its normal architecture, in a good correlation with the preservation of the normal hepatic function, as usually exhibited by the patients. The presence of numerous eggs points to the pathogenetic importance of worm load. Thus, schistosomal hepatopathy seems a good example of a straightforward condition, with a simple, characteristic, and understandable pathology.Although these main lines mentioned above are correct, they say little about the complexities that this unique type of chronic hepatopathy discloses when more closely and properly investigated. A closer view of its physiopathology will reveal several points of interests that are usually overlooked, but that are important for the understanding of the disease in patients and so are worth discussing here. Schistosomal hepatopathy represents a special type of a chronic liver disease. Its pathology contains unique features, one of the most important refers to its vascular changes, which differs from those found in cirrhosis, and are key factors for the understanding of the fundamental pathogenesis and the clinical potential for evolution presented by hepatosplenic schistosomiasis.

show abstract

Section: Is Schistosomal Portal Fibrosis Peculiar?mentioning

confidence: 83%

Section: The Significance Of Chronic Hepatitismentioning

confidence: 99%

Schistosomal hepatopathy

Andrade

2004

Mem. Inst. Oswaldo Cruz

Self Cite

View full text Add to dashboard Cite

show abstract

“…Secondary biliary cirrhosis with bile duct proliferation and portal fibrosis can be induced by bile duct occlusion after injection in a retrograde manner with the sclerosant sodium amidotriazoate (Ethibloc, Ethicon, Norderstedt, Germany) (Boigk et al, 1997;Cho et al, 2000). In our hands, this model induces an early inflammation due to biliary epithelial cell necrosis; thus, the mech- (Andrade et al, 1999).…”

Section: Myofibroblastic Cells In Liver Pathologymentioning

confidence: 94%

Normal and Pathologic Soft Tissue Remodeling: Role of the Myofibroblast, with Special Emphasis on Liver and Kidney Fibrosis

Desmoulière

Darby

Gabbiani³

2003

Laboratory Investigation

316

279

View full text Add to dashboard Cite

“…Possible roles for hepatic stellate cells (HSCs) in schistosomiasis have been postulated. Experimental studies in mice have shown that activated HSCs participate in the formation of periovular granulomas in portal spaces (Barbosa Junior et al 1993), and some authors have identified liver myofibroblasts in the portal fibrous tissue of human schistosomiasis (Andrade et al 1999). Previous studies have reported that non steroidal antiinflammatory drugs enhance liver pathology as a consequence of the liver metabolism of these drugs in schistosomiasis (Rainsford 1985), while other compounds that can regulate cytokine production proved efficacy in case of S. mansoni-induced liver fibrosis (Allam 2009).…”

Section: Introductionmentioning

confidence: 99%

Prevention and treatment of Schistosoma mansoni-induced liver fibrosis in mice

2011

View full text Add to dashboard Cite

The present study was designed to examine the potential preventive and curative effects of curcumin, resveratrol, imatinib, rosiglitazone, losartan and bosentan (BOS) on Schistosoma mansoni-induced liver fibrosis in mice. Induction of liver fibrosis was produced in male Swiss mice by subcutaneous injection of S. mansoni cercariae per mouse. Mice were left for 28 days before starting the experiment then mice were divided into two main groups. The first group was further subdivided into experimental groups and started drug treatment at day 28 after infection and continued for 2 weeks in order to evaluate the potential preventive effects of the mentioned drugs on S. mansoni-induced liver fibrosis. The second group of mice were left for 2 weeks and then treated with praziquantel for two consecutive days to eradicate the worms and so stop egg disposition and further fibrosis development. Mice were then subdivided into the experimental groups and drug treatment was started for 2 weeks to evaluate their efficacy to decrease the developed fibrosis. At the end of the experiment period, mice were killed and serum was collected for the estimation of alanine aminotransferase (ALT), aspartate aminotransferase (AST), bilirubin and albumin. Liver tissue was taken for the estimation of hepatic hydroxyproline content and histopathological examination to confirm the biochemical results. Results of the study indicate that curcumin and imatinib have potent antifibrotic activity both in suppressing and reversing S. mansoni-induced liver fibrosis, while resveratrol has beneficial effects only in suppressing the development of S. mansoni-induced liver fibrosis.

show abstract

Myofibroblasts in Schistosomal Portal Fibrosis of Man

Cited by 29 publications

References 9 publications

Schistosomal hepatopathy

Schistosomal hepatopathy

Normal and Pathologic Soft Tissue Remodeling: Role of the Myofibroblast, with Special Emphasis on Liver and Kidney Fibrosis

Prevention and treatment of Schistosoma mansoni-induced liver fibrosis in mice

Contact Info

Product

Resources

About