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Peripheral lymphocyte membrane fluidity after thermal injury

M V Tolentino1, M M Sarasua, O A Hill

  • 1Department of Surgery, MetroHealth Medical Center, Cleveland, OH.

The Journal of Burn Care & Rehabilitation
|November 1, 1991
PubMed

Insights

Serum cortisol increases lymphocyte membrane fluidity, potentially explaining immune suppression after thermal injury. Adaptation occurs with long-term exposure, suggesting a direct membrane effect.

Area of Science:

  • Immunology
  • Cell Biology
  • Biochemistry

Background:

  • Patients with thermal injury exhibit elevated serum cortisol levels.
  • Altered lymphocyte function in these patients increases infection susceptibility.
  • Elevated cortisol may contribute to this compromised immune state.

Purpose of the Study:

  • To investigate the direct effect of cortisol on lymphocyte membrane fluidity.
  • To compare in vitro cortisol effects with in vivo observations in thermally injured patients.

Main Methods:

  • Measured lymphocyte membrane fluidity using fluorescence polarization of diphenylhexatriene.
  • Exposed peripheral blood lymphocytes to cortisol in vitro (short- and long-term).
  • Compared membrane fluidity in lymphocytes from thermally injured patients and healthy controls.

Main Results:

  • Cortisol increased lymphocyte membrane fluidity in vitro.
  • Long-term cortisol exposure led to membrane adaptation, reducing cortisol's fluidizing effect.
  • Increased lymphocyte membrane fluidity was observed in patients with major thermal injury.
  • Cortisol's effects mimicked those of ethanol, a known membrane-fluidizing agent.

Conclusions:

  • Cortisol directly alters lymphocyte membrane fluidity.
  • In vitro findings correlate with in vivo observations after thermal injury.
  • This direct membrane effect may partially explain post-thermal injury cellular dysfunction and immunosuppression.

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