PubMed · 4265193
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S D Lawler. 1972. Leukaemia.. https://doi.org/10.1136/jcp.25.11.1008-a
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Growth of human connective tissue progenitor cells (CTPs) was characterized on smooth and microtextured polydimethylsiloxane (PDMS) surfaces. Human bone-marrow-derived cells were cultured for 9 days under conditions promoting osteoblastic differentiation on smooth PDMS surfaces and on PDMS post microtextures that were 6 microm high and 5, 10, 20, and 40 microm in diameter, respectively. Glass tissue-culture dishes were used as controls. The number of viable cells was determined, and an alkaline phosphatase stain was used as a marker for osteoblastic phenotype. CTPs attached, proliferated, and differentiated on all surfaces. Cells on the smooth PDMS and control surfaces spread and proliferated as colonies in proximity to other cells and migrated in random directions, with cell process lengths of up to 80 microm. In contrast, cells on the PDMS post microtextures grew as sparsely distributed networks of cells, with processes, occasionally up to 300 microm, that appeared to interact with the posts. Cell counts revealed that there were fewer (50%) CTPs on the smooth PDMS surface than were on the glass control surfaces. However, there were consistently more (>144%) CTPs on the PDMS post textures than on the controls. In particular, the 10-microm-in-diameter posts (268%) exhibited a significantly (p < 0.05) greater cell number than did the smooth PDMS.
Placental/umbilical cord blood (PCB) is a source of hematopoietic stem cells for bone marrow reconstitution. Engraftment speed and survival are related to the total nucleated cell (TNC) dose of the graft. This study explored the possible influence on engraftment of nucleated red blood cells (NRBCs) in the graft. Automated hematology analyzers were used to enumerate TNCs. NRBCs were counted by visual examination or by using an automated analyzer. Hematopoietic progenitor cells were enumerated as either colony-forming cells or CD34(+) cells. Transplant centers reported on transplant outcome in 1112 patients given PCB grafts through September 2001. NRBCs correlated with progenitor cell numbers. Both white blood cell and NRBC dose were independently predictive of myeloid engraftment speed. Because NRBC dose predicted engraftment speed, inclusion of NRBCs in the TNC count does not reduce the effectiveness of the prefreezing TNC count as an index of the quality of a PCB unit as a graft. The correlation between the number of NRBCs and the number of hematopoietic progenitor cells probably reflects the involvement of early stem cells in erythroid responses.
BACKGROUND: Cadaver donor bone marrow cells (DBMC) are capable of a low-grade response to allogeneic stimulation in vitro, indicating their potential ability to cause graft versus host disease (GvHD). However, at this center, we have observed a lack of GvHD in kidney transplant recipients who received DBMC perioperatively. Therefore, we questioned whether an intrinsic immunoregulatory function of (subpopulations of) DBMC might play a role in this observation. METHODS: In in vitro assays, DBMC was added to autologous splenic responder cells taking part in allogeneic mixed lymphocyte reaction (MLR) and cell-mediated lympholysis (CML) reactions. RESULTS: When compared with autologous donor irradiated spleen cells as control modulators, DBMC significantly inhibited the CML, but to a much lesser extent than MLR, of autologous responding cells stimulated with allogeneic irradiated cells in a dose dependent manner. The down-regulation of CML responses was observed even in the presence of pharmacological concentrations FK506, mycophenolic acid, or cyclosporine-A. The inhibition could not be overcome by the addition of exogenous helper factors. Moreover, in contrast with findings previously reported from this laboratory of the in vitro inhibitory effect of DBMC on allogeneic responding cells in MLR and CML reactions to stimulating cells of the DBMC donor (allogeneic host versus graft inhibition), the following unique observations were made using DBMC inhibiting autologous reactions (GvH): (1) optimal restimulation of autologous responder cells in secondary cultures could not abrogate this inhibition; even activated responder cells could be inhibited by autologous DBMC, and (2) soluble factors were at least partially operative in this autologous (GvH) inhibition as indicated by experiments in transwells and by the CML inhibition caused by 50% supernatants from DBMC cultures. CONCLUSION: These in vitro results indicate that DBMC treatment brings about a marked down-regulation of autologous immunocompetent cells in cytotoxicity reactions, partially at least through secreted soluble factor(s), (and in presence of immunosuppressive drugs in vivo) thereby preventing overt clinical GvHD.