Butyrate is a short chain fatty acid that is produced by the bacterial fermentation of carbohydrate. It is a significant source of energy for the colonic epithelium. Moreover, it also regulates colonic mucosal growth, barrier function as well as epithelial proliferation1.
In addition, it is reported that butyrate enemas have been employed to lessen the colonic mucosal inflammation in inflammatory conditions including Ulcerative Colitis (UC) as well as radiation colitis2.
On the other hand, the heat shock proteins (Hsp) that are also known as stress proteins are imperative regarding cellular response in case of stress as well as in cellular homeostatic functions like manufacturing of protein and its transportation across membranes.
However, besides these fundamental functions, these stress proteins also play an important role in activation of immune system as well as its recognition. Therefore, they can be cytotoxic3. Several studies also supports a role for Hsp in the inflammatory response which demonstrates that Hsp participate in cytokine signal transduction as well as in the control of cytokine gene expression4.
Accordingly, scientists planned to carry out a new study in order to investigate the hypothesis that cytoprotection of colonic epithelial cells by butyrate can be arbitrated by means of modulation of heat shock protein expression. For this purpose, HT29 intestinal epithelial cell monolayers were exposed to two forms of non-lethal stress; heat or chemical with or without butyrate5.
Afterwards, cells were radio labeled with 35S-methionine and incubated at 37°C for duration of two hours. Cells were then lysed, subjected to 1D SDS-PAGE, followed by autoradiography. Moreover, the impact of initial exposure to sub-lethal heat on consequent exposure to lethal heat was also analyzed5.
During this study, non-lethal stress induced Hsp70 expression in HT29 cells that was restrained by butyrate. However, this activity of butyrate was observed only at lower amount. Inhibition of Hsp70 synthesis was also noticed by research team because of the capability of the cells to bear a second lethal heat stress.
Butyrate was found to amplify colonic epithelial cell survival by considerably decreasing Hsp70 expression. Conclusively, this research points out the useful effect of butyrate on survival of colonic epithelial cells. This beneficial aspect can occupy clinical significance in various conditions involving the colonic mucosa.
Key words: butyrate, bacterial fermentation, colonic mucosal growth, ulcerative colitis, heat shock proteins, immune activation, colonic epithelial cells, heat stress
References:
- Cook, S.I. and J.H. Sellin, 1998. Review article: Short chain fatty acids in health and disease. Aliment Pharmacol. Ther., 12: 499-507.
https://www.ncbi.nlm.nih.gov/pubmed/9678808 - Breuer, R.I., S.K. Buto, M.L. Christ, J. Bean and P. Vernia et al., 1991. Rectal irrigation with short-chain fatty acids for distal ulcerative colitis. Preliminary report. Dig. Dis. Sci., 36: 185-187.
https://link.springer.com/article/10.1007%2FBF01300754 - Wallin, R.P., A. Lundqvist, S.H. More, A. von Bonin, R. Kiessling and H.G. Ljunggren, 2002. Heat-shock proteins as activators of the innate immune system. Trends Immunol., 23: 130-135.
https://www.cell.com/trends/immunology/fulltext/S1471-4906(01)02168-8?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS1471490601021688%3Fshowall%3Dtrue - Chen, W., U. Syldath, K. Bellmann, V. Burkart and H. Kolb, 1999. Human 60-kDa heat-shock protein: a danger signal to the innate immune system. J. Immunol., 162: 3212-3219.
http://www.jimmunol.org/content/162/6/3212 - Venkatraman, . A, N.S. Nanda Kumar and B.S. Ramakrishna , 2006. Butyrate Cytoprotection of Colonic Epithelial Cells May Be Mediated Through Inhibition of Heat Shock Protein 70. Asian Journal of Cell Biology, 1: 81-92.
https://scialert.net/fulltext/?doi=ajcb.2006.81.92&org=10
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