Summary Granulocyte colony-stimulation factor (G-CSF) is a cytokine that selectively promotes growth and maturation of neutrophils and may modulate the cytokine response to inflammatory stimuli. The purpose of this study was to examine the effect of G-CSF on ex vivo peripheral blood mononuclear cell (PBMC) functions. Ten patients with breast cancer were included in a clinical trial in which r-metHuG-CSF was administrered daily for 5 days to mobilize peripheral blood stem cells. Ten healthy women were also included as controls. Our data show that G-CSF treatment induces an increase in peripheral blood leucocyte, neutrophil, lymphocyte and monocyte counts. We have found a modulation in the percentages of CD19+, CD45+CD14+, CD4+CD45RA+ and CD4+CD45RO+ cells in PBMC fractions during G-CSF treatment. We have also found a significant reduction in the proliferative response of PBMC to mitogenic stimulation that reverted 14 days after the fifth and the last dose of G-CSF. Furthermore, it was not associated with significant changes in the pattern of cytokine production. The mechanism of this immunoregulatory effect is probably indirect since G-CSF receptor has not been found in T lymphocytes. This mechanism and its potential clinical applications remain to be elucidated.
Catalase activity in liver homogenates was studied in normal and low endotoxin (LPS)-responder mice treated with various doses of LPS from S. typhimurium B or bearing tumours induced by 3-methylcholanthrene. In normal LPS-responder (C3H/f) mice a dose of 40 micrograms LPS or tumour induction caused a reduction of catalase activity of about 50%. In low responder (C3H/HeJ) mice a reduction of the enzyme activity of over 40% was observed at a dose of 200 micrograms LPS. Tumour induction had no effect. In tumour-bearing mice of both strains the presence of a tumour seemed to interfere with the ability of LPS to depress hepatic catalase activity. Since a reduction of the enzyme activity in response to LPS or tumour induction seemed to be influenced by the LPS responsiveness of the mice, this study suggests that there could be common mediators of this effect. It is also possible that tumour induction might influence host responses to LPS.
The migratory responses of four human melanoma cell lines (A-2058, DEMEL, HTB-63, and HTB-72), using chemotaxis (CTX) and haptotaxis (HPTX) assays, were studied. The attractants were three extracellular matrix components (EMCs), fibronectin, laminin, and collagen type IV. The conditioned media (CM) of each cell line were used to study autocrine and paracrine responses. A screening and sensitive CTX assay was performed, using pertussis toxin (PTX)- treated A-2058 as responder cells; the other melanoma cells and normal cells were used as secretory cells. Autotaxin (ATX), a purified autocrine motility factor, was also used as a chemoattractant. Reverse transcriptase-polymerase chain reaction was used to detect the expression of ATX by all cell lines. The secretion of ATX was determined by Western blot. The invasive capacity of the cell lines was evaluated using Matrigel and ATX as attractant. Chemotaxis responses to EMCs varied. Except for the A-2058 cells, HPTX migration was low. Autocrine and paracrine responses also varied. The migration of PTX-treated A-2058 cells to ATX and to their own CM was abolished. All the melanoma cells expressed ATX, and except for the HTB-72 and normal cells, all secreted ATX. Matrigel was invaded by all the melanoma cell lines except the HTB-72 and normal cells. The migratory properties of human melanoma cells in vitro suggest that they could correlate to their metastatic potential in vivo.
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