Peripheral lymphocyte membrane fluidity after thermal injury

Serum cortisol levels are increased in patients after thermal injury. Lymphocyte function is altered in these patients, which renders them susceptible to infections. Elevated cortisol levels may contribute to this compromised state. In this study, we have demonstrated that cortisol directly affects lymphocyte membrane fluidity as measured by the polarization of fluorescence from the membrane-associated probe diphenylhexatriene in peripheral blood lymphocytes. Membrane fluidity increased in vitro with short- or long-term cortisol exposure. However, membranes of control peripheral blood lymphocytes that were previously exposed to cortisol became resistant to the fluidizing effect of cortisol, which implies membrane adaptation to long-term cortisol exposure. Cortisol effects were similar to those associated with ethanol, a known membrane-fluidizing agent, in peripheral blood lymphocytes and cytotoxic T lymphocytes. Membrane fluidity was compared in peripheral blood lymphocytes from thermally injured patients and peripheral blood lymphocytes from normal (control) subjects. Peripheral blood lymphocyte membrane fluidity increased in major thermal injury. Our data suggest that cortisol affects lymphocyte membrane fluidity in vitro in a manner similar to the membrane fluidity alterations that are observed in vivo after thermal injury. These observations reflect a direct membrane effect of cortisol, which may explain, in part, the cellular dysfunction and immunologic suppression that is observed after thermal injury.