Anti-Inflammatory Protein ofSchistosoma japonicumDirects the Differentiation of the WEHI-3B JCS Cells and Mouse Bone Marrow Cells to Macrophages

Zhongdao Wu,Shaomin Hu,Ming Chiu Fung,Linlin Yang,Kwok Nam Leung,Nai Ki Mak

doi:10.1155/2010/867368

Abstract

Sj16 is an anti-inflammatory protein identified from Schistosoma japonicum. Our previous studies showed that recombinant Sj16 (rSj16) could suppress host's inflammatory responses and inhibit macrophage maturation. In the present study, the effects of rSj16 on the differentiation of the murine myeloid leukemia WEHI-3B JCS cell line and on mouse hematopoiesis were investigated. Our data demonstrated that rSj16 expressed and purified from Escherichia coli could suppress the proliferation of the WEHI-3B JCS cells in a time- and concentration-dependent manner, while not affect the viability of the cells. Further studies indicated that rSj16 induced macrophage differentiation of the WEHI-3B JCS cells, and arrested the cell cycle in the G1/G0 and G2/M phases. The macrophage differentiation of the rSj16-treated WEHI-3B JCS cells was confirmed by their expression of macrophage specific antigen F4/80 and phagocytic activity. Furthermore, our results revealed that rSj16 biased the colony formation of mouse bone marrow cells towards macrophage linage.

Highlights

Leukemia occurs when the normal hematopoietic process fails, and the leukemic cells retain the proliferative capacity of progenitor cells and unable to spontaneously undergo terminal maturation [1]
The results indicated that the viability of WEHI-3B JCS cells was not affected after 0.5 μg/ml of recombinant Sj16 (rSj16) treatment for 24 hours (98.51 ± 0.14% versus 98.86 ± 0.28% viability, P > .2; rSj16 treatment versus untreated; n = 4), 48 hours (97.80% ± 0.35% versus 97.36 ± 0.43%, P > .2; n = 4) and 72 hours (96.48% ± 0.57% versus 97.43% ± 0.51%, P > .2; n = 4). recombinant glutathione-Stransferase (rGST) did not show any effects on WEHI-3B JCS viability
Previous studies reported that Sm16 could suppress the host immune responses by inhibiting the antigen-induced

Summary

Introduction

Leukemia occurs when the normal hematopoietic process fails, and the leukemic cells retain the proliferative capacity of progenitor cells and unable to spontaneously undergo terminal maturation [1]. Plenty of studies have demonstrated that the schistosome-originated substances could modulate the host’s immune system [5, 6]. An IL-4 inducing factor identified from Schistosoma mansoni (S. mansoni) egg has been demonstrated to skew the immune response to Th2 [8]. Another apoptosis inducing factor produced by skin-stage schistosomula of S. mansoni could cause apoptosis of T cells [9]. Trottein et al have reported that substances from S. mansoni suppressed host’s inflammation by activating host microvascular endothelial cells [10]. Up to now, little is reported about the immunomodulatory effects of schistosome-derived substances on leukemia and hematopoiesis. We reported the effects of rSj16 on the proliferation and differentiation of the WEHI-3B JCS and on mouse hematopoiesis.

Materials and Methods

Results

Findings

Discussion