Antifibrotic effect of adipose- versus bone marrow-derived mesenchymal stem cells in chronically infected mice with Schistosoma mansoni after Praziquantel treatment

Document Type : Original Article

Authors

Medical Parasitology Department, Faculty of Medicine, Suez Canal University, Ismailia, Egypt

Abstract

Background: Despite the effective infection treatment with Praziquantel (PZQ), hepatic fibrosis represents
the leading cause of schistosomiasis-related morbidity and mortality. Mesenchymal stem cells (MSCs)
have emerged as a potential therapeutic candidate for schistosomiasis-induced hepatic fibrosis.
Objective: To evaluate and compare the effect of bone marrow (BM) derived MSCs and adipose (AD)
derived MSCs in ameliorating liver fibrosis in S. mansoni chronically infected mice treated with PZQ.
Material and Methods: S. mansoni chronically infected mice were treated with PZQ on the ninth week
post-infection (pi), followed after four weeks by BM- or AD-MSCs administration. In addition to the two
treated groups, three control groups (uninfected, infected untreated, infected and PZQ-treated) were
employed. Mice were sacrificed two- and four-weeks post-MSCs treatment (wpt). The antifibrotic effect
of MSCs was assessed by measuring liver function tests, hepatic tissue histopathological examination, and
alpha-smooth muscle actin (α-SMA) immunohistochemical staining.
Results: Both types of MSCs significantly attenuated S. mansoni-induced liver damage four wpt compared
to PZQ-treated control group. This was apparent in marked improvement of liver functions and overall
hepatic histopathological changes with significant reduction of collagen content and α-SMA positive cells.
However, the best results were achieved following AD-MSCs administration with statistically significant
differences compared to BM-MSCs.
Conclusion: It was concluded that AD-MSCs are a potentially more potent therapeutic candidate than BMMSCs
in combating hepatic fibrosis in chronic murine schistosomiasis mansoni.

Keywords

Parasitologists United Journal
Volume 16, Issue 3
December 2023
Pages 220-229

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