Clostridioides difficile infection promotes gastrointestinal dysfunction in human and mice post-acute phase of the disease.

Objectives: In the US, Clostridioides difficile (C. difficile) infection (CDI) is the 8th leading cause of hospital readmission and 7th for mortality among all gastrointestinal (GI) disorders. Here, we investigated GI dysfunction post-CDI in humans and mice post-acute infection.

Adenosine receptors differentially mediate enteric glial cell death induced by Toxins A and B.

Increased risk of intestinal dysfunction has been reported in patients after infection (CDI). Enteric glial cells (EGCs), a component of the enteric nervous system (ENS), contribute to gut homeostasis. Previous studies showed that adenosine receptors, A2A and A2B, modulate inflammation during CDI.

Role of Pannexin-1-P2X7R signaling on cell death and pro-inflammatory mediator expression induced by toxins in enteric glia.

( produces toxins A (TcdA) and B (TcdB), both associated with intestinal damage and diarrhea. Pannexin-1 (Panx1) channels allows the passage of messenger molecules, such as adenosine triphosphate (ATP), which in turn activate the P2X7 receptors (P2X7R) that regulate inflammation and cell death in inflammatory bowel diseases. The aim of this study was to verify the effect of infection (CDI) in the expression of Panx1 and P2X7R in intestinal tissues of mice, as well as their role in cell death and expression induced by TcdA and TcdB in enteric glial cells (EGCs).

Host and Clostridioides difficile-Response Modulated by Micronutrients and Glutamine: An Overview.

Changes in intestinal microbiota are integral to development of ()-associated nosocomial diarrhea. Certain diets, especially Western diets, increase susceptibility to infection (CDI). Here, we discuss recent findings regarding how nutrients modulate response of the host and during infection.