The expression of heat shock proteins (hsp) is probably one of the most primitive mechanisms of cellular protection from stress. Pathogens such as viruses and bacteria have recently been found to induce the heat shock gene expression. In the present study hsp-72, the stress-inducible form of hsp-70, was detected by Western blotting in samples from rat distal colon (DC), proximal colon (PC), and terminal ileum (TI), but was not found in proximal small bowel (PSB) or other organs (liver, kidney, spleen, heart, and brain) of unstressed animals. The signal intensity of hsp-72 in colon (DC > PC > TI > PSB) correlates qualitatively with the presence of normal gut microflora. hsp-72 was also observed in DC, to a lesser extent in PC, but not in TI or PSB of bacteria-free or antibiotic-treated rats. Inflammatory states induced by the intravenous administration of endotoxin (1 mg/kg), the subcutaneous injection of zymosan (1 g/kg) or by cecal ligation and puncture (sepsis) failed to increase the hsp-72 levels in rat colon or other organs. These results demonstrate that hsp-72 is expressed in normal rat colon. However, the induction of hsp-72 expression may not be due solely to the presence of resident bacteria in the gut, but instead, may be the result of a more complex process.

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