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Cytokines released in vitro by stromal cells from autologous bone marrow transplant patients with lymphoid malignancy
Author(s) -
Roingeard Françoise,
Binet Christian,
Lecron JeanClaude,
Truglio Danielle,
Colombat Philippe,
Domenech Jorge
Publication year - 1998
Publication title -
european journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.904
H-Index - 84
eISSN - 1600-0609
pISSN - 0902-4441
DOI - 10.1111/j.1600-0609.1998.tb01068.x
Subject(s) - stromal cell , bone marrow , granulocyte macrophage colony stimulating factor , cytokine , granulocyte , medicine , immunology , cancer research , haematopoiesis , transforming growth factor , leukemia inhibitory factor , growth factor , stem cell , interleukin 6 , biology , receptor , genetics
Marrow stromal cells of patients treated by autologous bone marrow transplantation (ABMT) for malignancies have been assessed for their ability to secrete granulocyte colony‐stimulating factor (G–CSF), granulocyte‐macrophage colony‐stimulating factor (GM–CSF), stem cell factor (SCF), leukemia inhibitory factor (LIF), interleukin‐6 (IL‐6), transforming growth factor β1 (TGFβ1) and macrophage inflammatory protein‐1α (MIP‐1α). Long‐term marrow cultures were established from 10 patients prior to and 3 months after ABMT, from 7 patients 1 yr after ABMT and from 11 controls. Cytokines in culture supernatants of stromal layers (SL) were evaluated by enzyme‐linked immunosorbent assay (ELISA). Significant differences between patient groups and controls were apparent in baseline production of GM–CSF, SCF, MlP‐1α and TGFβ1. After IL‐1β addition in cultures, G–CSF production was reduced in pretransplant and post‐transplant patients compared to controls. The production of TGFβ1, LIF, IL‐6 and more particularly SCF were reduced in post‐transplant patients, while elevated levels of GM–CSF and MIP‐1α were observed in these patients only when the values were corrected for the number of cells growing in the SL. These results indicate a prolonged stromal defect in growth factor production following ABMT for the early‐stage acting cytokines IL‐6, LIF and SCF as well as for G–CSF, but not for GM–CSF, while the production of the 2 inhibitors shows different pathways.