Pathology of the spleen in hepatosplenic schistosomiasis. Morphometric evaluation and extracellular matrix changes

Freitas, Carla Rangel Leite; Barbosa, Alynne da Silva; Fernandes, André L. M.; Andrade, Zilton A.

doi:10.1590/s0074-02761999000600019

Cited by 19 publications

(14 citation statements)

References 7 publications

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“…In addition, the present work showed dilatation and disruption of the wall of the splenic vessels which contained eosinophilic material and numerous inflammatory cells. This was in accordance with [37] as they suggested that these changes were probably due to portal hypertension and as a response to chronic passive congestion and increased blood pressure within the splenic vessels. Moreover, some researchers [38] hypothesized that TNF-α was expressed by both Th1 and Th2 type cells.…”

Section: Discussionsupporting

confidence: 90%

Histological study on the possible therapeutic role of bone marrow derived mesenchymal stem cells in a model of Schistosoma mansoni infestation of spleen of mice

Raafat

Gawad

Fikry

2017

Egyptian Journal of Histology

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Background: Hepatosplenomegaly is a characteristic feature of Schistosoma infestation. However, splenic injury had received little scientific researches than the well-known liver injury. Moreover, the role of bone marrow derived mesenchymal stem cells (BMMSCs) in treatment of splenic injury due to schistosomiasis has not yet been investigated. Aim of the work: To explore the structural changes which might occur to spleen during chronic infestation with schistosomiasis and the possible therapeutic role of (BMMSCs) in ameliorating these changes. Materials & Methods: Fifty female Swiss Albino mice, weighing about 25 gm were classified into group A (control group) and group B (experimental group). Animals in group A were equally subdivided into subgroup AI which served as donors for stem cells obtained from their bone marrow, and subgroup AII which were injected with phosphate buffer saline (PBS) and used to collect control spleen samples. Whereas, animals in group B, were all infected with S. mansoni cercariae (60/ mouse) by subcutaneous injection, then subdivided into three subgroups; subgroup BI sacrificed after eight weeks, subgroup BII treated intraperitoneally with 2x106 MSCs suspended in PBS per mouse at eighth week after infestation hen scarified four weeks later, and subgroup BIII allowed to survive for twelve weeks without treatment then sacrificed. Results: Histological examination of spleen sections of subgroup BI showed structural changes including deposition of eggs which were surrounded by inflammatory cells and collagen fibers. Subgroup BIII showed more extensive structural changes. This was associated with significant increase in collagen fibers and TNF-α immunological reaction compared to control. However, (BMMSCs) treated subgroup BII illustrated improvement of splenic structure. Conclusions: Chronic Schistosoma mansoni infestation has a deleterious effect on the structure of the spleen. Bone marrow derived mesenchymal stem cells have a relevant therapeutic potential on the spleen of an animal model of Schistosoma mansoni.

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Section: Discussionsupporting

confidence: 90%

Histological study on the possible therapeutic role of bone marrow derived mesenchymal stem cells in a model of Schistosoma mansoni infestation of spleen of mice

Raafat

Gawad

Fikry

2017

Egyptian Journal of Histology

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“…We also detected the clinical parameters, such as spleen weight, portal venous pressure and serum ALT. The results showed that clinical symptoms, such as splenomegaly [42], [43], portal hypertension [44], [45] and dysregulated liver function [46], [47] were ameliorated by anti-fibrosis treatment with PZQ. Low dose treatment with PZQ did not show significant effects on hepatic fibrosis, which may be due to the quick metabolism of this drug in liver [48].…”

Section: Discussionmentioning

confidence: 99%

New Insight into the Antifibrotic Effects of Praziquantel on Mice in Infection with Schistosoma japonicum

et al. 2011

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BackgroundSchistosomiasis is a parasitic disease infecting more than 200 million people in the world. Although chemotherapy targeting on killing schistosomes is one of the main strategies in the disease control, there are few effective ways of dealing with liver fibrosis caused by the parasite infection in the chronic and advanced stages of schistosomiasis. For this reason, new strategies and prospective drugs, which exert antifibrotic effects, are urgently required.Methods and FindingsThe antifibrotic effects of praziquantel were assessed in the murine models of schistosomiasis japonica. Murine fibrosis models were established by cutaneous infection with 14±2 Schistosoma japonicum cercariae. Then, the mice of both chronic (8 weeks post-infection) and advanced (15 weeks post-infection) schistosomiasis were treated by gavage of praziquantel (250 mg/kg, once daily for 3 days) to eliminate worms, and followed by praziquantel anti-fibrosis treatment (300 mg/kg, twice daily for 30 days). The fibrosis-related parameters assessed were areas of collagen deposition, content of hydroxyproline and mRNA expressions of Col1α1, Col3α1, α-SMA, TGF-β, MMP9, TIMP1, IL-4, IL-10, IL-13 and IFN-γ of liver. Spleen weight index, alanine aminotransferase activity and liver portal venous pressure were also measured. The results showed that anti-fibrosis treatment improved liver fibrosis, splenomegaly, hepatic function, as well as liver portal hypertension. In order to confirm the anti-fibrotic properties of praziquantel, we established a CCL4-induced model and revealed that CCL4-induced liver fibrosis was inhibited by PZQ treatment for 30 days. Furthermore, we analyzed the effects of praziquantel on mouse primary hepatic stellate cells (HSCs). It is indicated that mRNA expressions of Col1α1, Col3α1, α-SMA, TGF-β, MMP9 and TIMP1 of HSCs were all inhibited after praziquantel anti-parasite treatments.ConclusionsThe significant amelioration of hepatic fibrosis by praziquantel treatment validates it as a promising drug of anti-fibrosis and offers potential of a new chemotherapy for hepatic fibrosis resulting from schistosomiasis.

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“…8A), in the spleen, type IV collagen could be identified only in the structural portion of the red pulp and white pulp, most likely corresponding to the basement membranes of the marginal sinuses and central arterioles (Fig. 8B) (29,30). CD8…”

Section: Vla-1 ϩ Cd8 T Cells Have Enhanced Access To Type IV Collagenmentioning

confidence: 97%

The α1β1 Integrin and TNF Receptor II Protect Airway CD8+ Effector T Cells from Apoptosis during Influenza Infection

Richter

Topham

2007

The Journal of Immunology

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Primary viral infections of the lung induce potent effector CD8 T cell responses. To function in the influenza-infected airways, CD8 T cells must be able to resist cell death. The majority of the CD8 T cells in the airways and lung parenchyma expressed CD49a, the α-chain of the type IV collagen receptor VLA-1, and these cells were highly activated, producing both IFN-γ and TNF-α. In the airways, where type IV collagen is abundant, but not the spleen, the CD49a+ CD8 cells had reduced proportions of annexin V and caspase 8, and >80% expressed the TNF-α receptor II, while Fas, TNFR-I, and CD27 expression were similar to CD49a− cells. Furthermore, the CD49a+, but not CD49a−, CD8 T cells from the airways were resistant to active induction of apoptosis in the presence of type IV collagen and TNF-α in vitro. We propose that TNFR-II and the VLA-1 synergize to protect effector CD8 T cells in the infected airways from apoptosis during the acute infection.

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Pathology of the spleen in hepatosplenic schistosomiasis. Morphometric evaluation and extracellular matrix changes

Abstract: Histological, ultrastructural, morphometric and immunohistochemical

Cited by 19 publications

References 7 publications

Histological study on the possible therapeutic role of bone marrow derived mesenchymal stem cells in a model of Schistosoma mansoni infestation of spleen of mice

Histological study on the possible therapeutic role of bone marrow derived mesenchymal stem cells in a model of Schistosoma mansoni infestation of spleen of mice

New Insight into the Antifibrotic Effects of Praziquantel on Mice in Infection with Schistosoma japonicum

The α1β1 Integrin and TNF Receptor II Protect Airway CD8+ Effector T Cells from Apoptosis during Influenza Infection

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