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

There is evidence that some level of protection against the adverse sequelae of surgery is provided by induction of thermotolerance; this protective effect was explored by study of several indicators of bowel wall damage in animals exposed to surgical insults. It has been argued that the mechanism of the protective effect of thermotolerance involves heat shock proteins (HSPs). We hypothesized that the protective effect of thermotolerance may be due in part to changes in the bowel wall itself, and we investigated this hypothesis in an experimental rat model.

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 insults. The responses of the thermotolerant animals and controls were compared with respect to goblet cell type and number and histopathological changes of the bowel wall.

The thermotolerant animals were found to have significantly less oedema and histological damage. There was significant increase in the number of goblet cells 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).

This suggests that the thermotolerant animals were not only able to recruit or produce more goblet cells to protect the gut surface, but that greater numbers of the goblet cells in the thermotolerant animals were of the mature acidic type and thus capable of functioning in a protective capacity. These findings provide evidence for thermotolerance-induced histological changes in the bowel wall providing a protective effect against adverse sequelae of surgery.