Update of our research project :

Hello everyone ! Today I am posting a lab note to introduce an update of our research project. Indeed, our supervisor wanted to focus on another probiotic first before going on with Bacteroides fragilis. Here is the background:

The pathogenesis of necrotizing enterocolitis (NEC) is not well characterized. Intestinal inflammation in premature neonates is likely caused by a combination of intestinal cells immaturity and gut microbiota imbalance.

In that way, a growing body of experimental and clinical evidence (mainly provided by clinical trials outside the United-States) supports the concept that probiotics may have a preventative application in NEC. It has been shown in these clinical trials that probiotics could protect premature infants against NEC. One major probiotic which has shown protective effect is Bifidobacterium infantis. This probiotic is a common commensal bacteria usually found in the healthy newborn intestine. However, the FDA (Food and Drug Administration) in the United-States does not allow the use of live probiotics in neonates yet.

Hence, this laboratory is looking for the use of the secreted factors from Bifidobacterium infantis, avoiding the use of the live probiotic, which could protect premature infants against NEC through anti-inflammatory mechanisms. It has already been demonstrated by our laboratory that secretions from Bifidobacterium infantis can prevent inflammation in immature human intestinal cells. However, the underlying mechanism is unknown and need to be demonstrated before going into clinical trials in premature infants.

Thus, the aim of our updated project will be to study the precise mechanism of action of the secreted factors from Bifidobacterium infantis on immature human intestinal cells, a model representative of the immature intestine of preterm neonates.

We hypothesize that the anti-inflammatory effect of Bifidobacterium infantis secreted factors on these cells may be mediated by the aryl hydrocarbon receptor (AhR), a nuclear receptor expressed in immune cells.

It has previously been shown that AhR activation modulates and educates the immune system to avoid excessive inflammation. This makes this receptor’s activation in early life a very relevant area of research, which has not received much attention. These observations may help in future prevention of NEC.

I attached a picture which explain our hypothesis.

Thank you !