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Ann Thorac Surg 1999;68:1150-1153
© 1999 The Society of Thoracic Surgeons

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Original Articles

Heat shock protein suppresses the senescent lung cytokine response to acute endotoxemia

^a Section of General Thoracic Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA
^b Department of Pharmacology, Albert Einstein College of Medicine, New York, New York, USA

Address reprint requests to Dr LoCicero III, Section of Cardiothoracic Surgery, Beth Israel Deaconess Medical Center, 110 Francis St, Suite 2C, Boston, MA 02215
e-mail: locicero{at}harvarda.harvard.edu

Presented at the Poster Session of the Thirty-fifth Annual Meeting of The Society of Thoracic Surgeons, San Antonio, TX, Jan 25–29, 1999.

Background. Previous reports demonstrate that heat shock protein (HSP) can alter the pulmonary inflammatory cascade. We wished to determine if this mechanism is active in the senescent mouse.

Methods. A dose-response and time-response curve for sodium arsenite (SA) induction of HSP was constructed. Eight 25-month-old B6C3F1 mice were given either 1, 2, 4, or 6 mg/kg SA. At 4 hours, the lungs were harvested and assayed for HSP by Western blot. Next, 8 mice were given 4 mg/kg SA and the lungs harvested at either 1, 2, 4, or 6 hours after injection and assayed for HSP. Next, 12 mice were prepared: Half received 4 mg/kg SA and 4 hours later, all received 0.5 mg/kg lipopolysaccharide (LPS). After 4 hours, lungs were harvested and Interleukin-1ß mRNA was assayed by Northern blot and semiquantified by densitometry.

Results. The optimum SA dose was determined to be 4 mg/kg. The maximum HSP production was at 4 hours. Mice receiving LPS only showed a marked increase (3-fold) in IL-1 message compared with the mice pretreated with SA.

Conclusions. These data suggest that in the senescent as in the mature mouse lung, HSP downregulates the inflammatory cascade in response to LPS.

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