Several chemical effectors were used to induce changes in spleen B cell membrane fluidity.
Membrane fluidity was monitored by fluorescence polarization analysis of the hydrophobic
probe 1,6-diphenyl-1,3,5-hexatriene (DPH) and cell viability was checked not to be
affected by the treatments. Membrane immunoglobulin (Ig) endocytosis by the living
B cells with modified or unmodified membranes was quantitatively measured by flow
cytometry, using a previously described method (Métézeau et al., 1982, 1984). The
kinetics of endocytosis of membrane Ig was not affected by chemical effectors increasing
membrane fluidity. On the contrary, increasing membrane microviscosity resulted in
the slowing down and eventually the blocking of membrane Ig endocytosis. It is suggested
that a step depending on membrane microviscosity is involved in the process of endocytosis;
this step may become rate limiting when membranes are artificially rendered or naturally
become (i.e. for pathological or particularly differentiated cells) more viscous.