Biomedical subjects
Publications and source records attributed to H Verschueren.
DPD inactivates the edges of cultured mouse embryo cells. Pseudopodal activity is inhibited and spreading is reduced. Concomitantly, the growth rate of the cells is reduced. The interference reflection image shows very large close contacts under DPD treated cells. The translocation speed of the cells is unaffected. DPD penetrates into the cytoplasm, but less or not into the nucleus.
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A simple monolayer invasion assay (MIA) was recently developed using confluent fibroblastic cells as a target and variants of the BW5147 murine T-cell lymphoma as invading cells. Metastatic variants were consistently invasive in the MIA whereas non-metastatic cells were not. In this paper it is reported that pertussis toxin (PT) treatment of a highly metastatic and invasive variant caused a marked delay of invasion in the MIA at concentrations from 50 pg/ml upwards. Surprisingly, PT treatment of the non-metastatic, non-invasive parental BW5147 cells induced a moderate but significant level of invasion. Morphometric analysis showed that PT provoked an increased pseudopodal activity in cells in which it also caused increased invasive potential, and a decreased motility in cells with decreased invasiveness. This finding strengthens the perception that invasive potential and the capability to perform shape changes are related characteristics in these lymphoma cells.
Using an in vitro monolayer assay (MIA) we analyzed the invasive behaviour of a panel of B-cell hybridomas prepared by the fusion of non-invasive, non-metastatic NSO plasmacytoma cells and normal murine B-cells. Interaction of these hybridomas with fibroblast-like monolayers consisted mostly of adhesion on top of the monolayers, whereas only a fraction of these cells penetrated through the monolayer. This is in sharp contrast with the highly invasive properties displayed by T-cell hybridomas. Whereas T-cell hybridomas highly infiltrated monolayers of rat hepatocyte in vitro, B-cell hybridomas neither adhered to nor infiltrated hepatocyte monolayers. We found a good correlation between the degree of adhesion of B-cell hybridomas to fibroblast-like monolayers and their metastatic capabilities upon i.v. injection into syngeneic animals. Unlike T-cell hybridomas which formed diffuse metastasis in liver and spleen, B-cell hybridomas generated nodular metastatic lesions. . When normal LPS-stimulated B-lymphocytes were tested in the fibroblast-MIA, only part of the population infiltrated the monolayers. This again contrasts with T-lymphocytes where a majority of the cells penetrated through the monolayers. These results suggest that (i) B-lymphocytes express invasive properties, albeit to a lesser extent than T-lymphocytes, (ii) non-invasive B-lymphoma cells can acquire invasiveness following cell fusion with a normal B-cell, (iii) these invasive properties contribute to the malignancy of the hybridomas when tested in recipient animals.
BW-O-Li1 murine T-lymphoma cells display target preference for invasion in two different in vitro models. In the precultured chick heart fragment (PHF) assay, BW-O-Li1 preferentially invaded into aggregates of MCF-7 mammary carcinoma cells rather than into PHFs. In a monolayer invasion assay (MIA), BW-O-Li1 cells preferentially invaded under 10 T1/2 mouse embryo cell monolayers rather than under MCF-7 monolayers. Thus, although BW-O-Li1 cells were perfectly able to invade into any of the targets presented, they migrated and accumulated preferentially in one of the targets when a choice was offered. We suggest that this in vitro 'homing' phenomenon can be exploited to investigate certain aspects of organ-specific metastasis.
The metastatic phenotype (M+) is determined by the expression of the invasive (I+) and growth (G+) phenotypes at various sites along the metastatic pathway. The G, I and M phenotypes are not confined to tumor cells and may be expressed by normal cells, such as leukocytes, under certain physiological conditions. The study of the I and M phenotypes of leukocytes may yield valuable information on common mechanisms, underlying invasion and metastasis of normal and malignant cells. In this review we summarize experimental approaches that were developed for the analysis of the I and M phenotypes of normal and malignant leukocytes.
The occurrence of pili has been assessed for 85 strains of Neisseria meningitidis belonging to different serogroups and serotypes, isolated from nasopharyngeal carriers and patients with acute disease. The evolution of piliation on multiple subcultivation has been followed for 16 strains. Almost all the strains were piliated, regardless of their origin, serogroup or serotype. Piliation was generally maintained, although to a variable extent, through more than 50 passages. Type, regulation and possible function in vivo of the described pili are discussed.