Significats de intestinal homeostasis en anglès

Background: How the gut microbiota regulates intestinal homeostasis is not completely clear.

Cytoplasmic innate immune sensors, including NLRs, are central regulators of intestinal homeostasis.

We further discuss the contribution of pre-mRNA alternative splicing to barrier integrity and intestinal homeostasis.

Host sensing in the gut microbiota has been crucial in the regulation of intestinal homeostasis.

The intracellular NOD-like receptor Nlrp3 is rapidly emerging as a crucial regulator of intestinal homeostasis.

In order to maintain intestinal homeostasis, mucosal immune responses to theses microorganisms must be tightly regulated.

The host has to maintain intestinal homeostasis to keep the commensal and pathogenic bacteria under control.

Intact ATG16L1 plays an essential role in Paneth cell function and intestinal homeostasis.

The data thereby provide a novel pathway by which microbiota regulates IEC expression of AMP and intestinal homeostasis.

Recent studies furthermore support additional functions of these proteins in the control of adaptive immune responses and intestinal homeostasis.

Although Tregs are essential in mice for the maintenance of intestinal homeostasis, their role in human IBD remains unclear.

The intestinal epithelium responds to and transmits signals from the microbiota and the mucosal immune system to insure intestinal homeostasis.

Our findings suggest that Paneth cells may contribute to intestinal homeostasis by secreting a-defensins in response to certain nutrients or metabolites.

We hypothesized that its deficiency may play a role in the loss of intestinal homeostasis through the control of immunomodulatory factors.

Various studies have found that the dysfunction of intestinal homeostasis contributes to the pathogenesis of inflammatory bowel disease (IBD).

Snail family members regulate epithelial-to-mesenchymal transition (EMT) during invasion of intestinal tumours, but their role in normal intestinal homeostasis is unknown.