Thermotolerance-induced goblet cell activity confers protection in post-operative gut barrier dysfunction

Aims: The aims of this research is to examine the hypothesis that the gut-barrier dysfunction which results from ischaemia-reperfusion injury and bowel-handling is prevented or decreased by prior induction of thermotolerance and whether the protective effect of thermotolerance may be due to phenomena other than heat shock protein.

Methods: Adult sprague-Dawley rats were randomized into thermotolerant (n=16) and control (n=16) groups; half of the animals in each group were subjected to bowel-handling and half to ischaemia-reperfusion. The responses of these animals were compared with respect to goblet cell type and number, oedema of the bowel wall, TNF blood levels and histopathological changes of the bowel wall.

Results: The thermotolerant animals were found to have significantly less oedema and histological damage. There was significant increase in the number of goblet cell in response to surgical insults (19.16+/-5.66 vs. 4.855+/-3.15), and specifically a greater increase in acidic goblet cells (19.42+/-4.58) as compared with neutral ones (13.28+/-5.53)(p<0.0001).

Conclusions: Thermotolerant animals were not only able to recruit or produce more goblet cells to protect the gut surface, but the greater numbers of the goblet cells in the thermotolerant were of the mature acidic type thus capable of functioning in a protective capacity.