This study in a group of young adult women in south India shows that the probiotic yoghurt was well tolerated and that faecal excretion of secretory immunoglobulin A was significantly increased during feeding of probiotic yoghurt compared to the baseline. Although the levels decreased after probiotic yoghurt was stopped, they did not return to normal and tended to be higher than baseline levels. This suggests that the effect of the probiotic yoghurt persisted even after cessation of feeding this; there is also be a possibility that normal yoghurt contributed to elevated faecal sIgA, that was more pronounced during feeding of probiotic yoghurt. These results are likely to be generalizable. Studies in healthy children and preterm infants have shown an increase in faecal IgA excretion in response to probiotic interventions [7
]. A study in animals showed that probiotic yoghurt containing Lactobacillus casei increased IgA secretion in mice [11
]. On the other hand, a study in infants did not find any change in faecal IgA after probiotic administration [12
]. In another study, faecal IgA output in pre-term infants was increased in response to both mother's milk and to fermented formula (in which the probiotic was killed by heating) [13
Probiotics are also known to upregulate defensin expression and to increase defensin secretion from intestinal epithelium. Both lactobacilli and probiotic E. coli
have been shown to increase human beta-defensin 2 (hBD-2) secretion from CaCo-2 cells through stimulation of TLR2 and TLR5 respectively [14
]. In a feeding trial in healthy adult volunteers, the probiotic E. coli
Nissle strain increased fecal hBD-2 excretion in healthy adult volunteers [17
]. In the present study, there was no obvious effect on faecal hBD-2 excretion during the probiotic yoghurt feeding period. Thus far, an effect on human beta-defensin expression has been noted only with lactobacilli and with E. coli Nissle 2. In a study where 11 lactobacilli were tested, only 2 of the strains increased hBD-2 mRNA expression in CaCo-2 cells. The difference between lactobacilli strains in their ability to induce hBD-2 correlated with the presence of genes encoding glycosylated cell surface structures [18
]. Although we did not examine the probiotic used in this study for these genes, this appears a likely explanation for the absence of an effect on hBD-2 excretion in stool.
This study had several drawbacks. It was a non-randomised study and the participants could potentially differentiate between the two different kinds of yoghurt on the basis of smell and taste, although the nature of the two was not known to them. These were not commercially available standardized products, although we took care to make them to a standard protocol. The generalizability of these results to other products and populations is therefore not to be assumed.
The present study appears to be the first report of an effect of probiotic foods on faecal IgA in healthy adults. Increased IgA output was noted only with yoghurt containing Bb12® and not with normal yoghurt. An increase in faecal IgA may explain the ability of probiotics to prevent diarrhoeal illness in specific settings. It is possible that this may also explain beneficial effects of probiotics in preventing severe lower respiratory tract infections.