Decreased membrane "fluidity" of T lymphocytes from untreated patients with Hodgkin's disease.
Plasma membrane "fluidity" of peripheral blood T lymphocytes from untreated patients with Hodgkin's disease (HD) and healthy controls was studied using the fluorescent probes 1,6-diphenyl-1,3,5-hexatriene (DPH) and 1-(4(trimethylamino)phenyl)-6-phenyl-1,3,5-hexatriene (TMA-DPH). In 13 consecutive patients a significant increase of T lymphocyte plasma membrane microviscosity was observed with both DPH and TMA-DPH. These alterations seemed unrelated to the cholesterol (Chol) and phospholipid (PL) content of HD T lymphocytes since the Chol/PL ratio was comparable in both HD and control cells. Since prostaglandin E2 (PGE2) from monocytic origin has been claimed to be responsible for the impairment of cell-mediated immunity (CMI) associated with HD, we studied the effect of exogeneously added PGE2 (0.1 microM) on control subjects T lymphocyte membrane "fluidity". Using the fluorescent probe DPH and the spin labelled fatty acid probe 16 NMS for electron paramagnetic resonance study, we observed a PGE2-induced fluidization of control T lymphocyte membranes which is specifically located in the inner part of the plasma membrane, whereas the plasma membrane surface seemed unaffected by PGE2 as judged by the TMA-DPH probe. Thus, PGE2 does not appear to be responsible for the alterations of T lymphocyte membranes observed in HD. Intrinsic alterations and/or other mediators might be involved.
D000328:Adult; D002784:Cholesterol / Q000032:analysis; D015232:Dinoprostone; D005260:Female; D005454:Fluorescence Polarization; D006689:Hodgkin Disease / Q000378:metabolism*; D006801:Humans; D008297:Male; D008560:Membrane Fluidity / Q000187:drug effects; D008875:Middle Aged; D010743:Phospholipids / Q000032:analysis; D011458:Prostaglandins E / Q000494:pharmacology; D013601:T-Lymphocytes / Q000032:analysis / Q000378:metabolism*; D013696:Temperature
D010743:Phospholipids; D011458:Prostaglandins E; D002784:Cholesterol; D015232:Dinoprostone