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Bone marrow ‐ mesenchymal stem cells impact on the U937 cells in the presence of staphylococcal enterotoxin B ( SEB )
Author(s) -
Ejtehadifar Mostafa,
Halabian Raheleh,
Ghazavi Ali,
Khansarinejad Behzad,
Mosayebi Ghasem,
Imani Fooladi Abbas Ali
Publication year - 2018
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.12945
Subject(s) - mesenchymal stem cell , bone marrow , enterotoxin , cancer research , immunology , medicine , chemistry , pathology , biochemistry , escherichia coli , gene
Summary The growing resistance against conventional chemotherapy in acute myeloid leukemia ( AML ) is a noticeable clinical concern. Therefore, many researchers are looking for novel substances to overcome drug resistance in cancer. Staphylococcal enterotoxin B ( SEB ) is a superantigen ( SA g) and a promising compound which has lethal effects on malignant cells. In this unprecedented study, SEB was used against U937 cells in a co‐culture system in the presence of human bone marrow‐mesenchymal stem cells ( hBM ‐ MSC s). The effects of hBM ‐ MSC s on the proliferation and survival of U937 cell line with SEB was assessed using MTT assay and AnnexinV/ PI flowcytometry, respectively. Moreover, the expression of IL ‐6, IL ‐10, TGF ‐β, and inhibitor of nuclear factor kappa‐B kinase ( IKK b) was evaluated by real‐time PCR technique. The same experiments were also carried out using hBM ‐ MSC s‐conditioned medium ( hBM ‐ MSC s‐ CM ). The results showed that SEB reduced the proliferation and survival of U937 cell line, but hBM ‐ MSC s or hBM ‐ MSC s‐ CM suppressed the effects of SEB . Furthermore, real‐time PCR demonstrated that SEB could decrease the expression of IL ‐6, IL ‐10, and TGF ‐β in hBM ‐ MSC s ( P < .05), while the production of IKK b was increased in comparison with the control group. These findings help us to have a broader understanding ofthe usage of SEB in the treatment of haematological malignancies, especially if it is targeted against hBM ‐ MSC s to disrupt their supportive effects on malignant cells.