Fermented milks and eicosanoid biology
Intestinal epithelial cells (IEC) are known to actively participate in the mucosal immune response through the production of cytokines and prostaglandins which are intimately involved in many immunoregulatory activities. Probiotic lactic acid bacteria can affect IEC cytokine production profiles and both fermented milk and soy products have been reported to influence IEC growth. In a study reported in the March 2005 issue of the Journal of Food Science (2005, 70 (2): M81 – M86), Fiander et al. have examined the effect of lactic acid bacteria (LAB) and fermented milks on eicosanoid production. Arachidonic acid (20:4ω6, eicosa=20 in Greek) is the premier eicosanoid precursor in mammalian cells. Eicosanoids are a group of lipid mediators which include prostaglandins and leukotrienes and are involved in numerous inflammatory and allergic reactions in the body. Gastrointestinal pathogenic bacteria like Salmonella, Yersinia and E. coli can induce the synthesis of prostaglandins and this is associated with their ability to invade epithelial cells and cause illness. Previous research has suggested that bioactive peptides (eg. beta-casomorphins) released from casein during milk fermentation by LAB can have analgesic effects, increase gastrointestinal transit times and modulate endocrine secretions. Some of these milk-derived peptides are opioid in nature, and it is known that IECs contain opioid receptors.
Two lines of human intestinal epithelial cells were used in the study. Lactobacillus rhamnosus R0011 and L. acidophilus R0052 were both used to produce samples of fermented milks. The effects of the LAB and their milk ferments on the synthesis of prostaglandin E2 (PGE2) and prostaglandin F2α (PGF2α) by the IEC cell lines were determined using a competitive enzyme immunoassay. LAB alone did not alter interleukin-induced prostaglandin synthesis by IEC, but milk fermented with L. rhamnosus R0011 significantly suppressed interleukin induced levels of PGE2 and PGF2α. Fermented milks produced with L. acidophilus R0052 showed a similar but not identical pattern of suppression, and were marginally less effective in down-regulating prostaglandin (PG) production by IECs. The addition of L. rhamnosus R0011 culture alone counteracted the suppression induced by the L. rhamnosus milk ferment. Naltrexone, an opioid receptor antagonist, blocked the suppressive effects of L. rhamnosus ferments on PG production, indicating that the bioactivity of the milk ferments could be mediated through opioid receptors in the IECs. These results suggest that the immunomodulatory effects of fermented milks are due to bioactive milk components liberated by the lactobacilli rather than the lactobacilli themselves.
I decided last summer that yoghurt wasn’t actually good for me. I find it highly addictive – much more addictive than fresh milk – and it makes me feel drugged. I crave it and feel grumpy if it is withdrawn. I also gain weight with it. I think this is why.
Here we have lactobacillus apparently liberating both opioid-like peptides and messing with prostaglandins. The prostaglandin enzymes blocked here are slightly further down the prostaglandin pathway than the ones blocked by NSAIDs (COX). I wonder if they still affect the pathway in the same way, by increasing leukotriene production?