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Published on: June 30, 2011
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
Summary
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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