Short-bowel syndrome represents the most common cause of intestinal failure and occurs when the remaining intestine cannot support fluid and nutrient needs to sustain adequate physiology and development without the use of supplemental parenteral nutrition. After intestinal loss or damage, the remnant bowel undergoes multifactorial compensatory processes, termed adaptation, which are largely driven by intraluminal nutrient exposure. Previous studies have provided insight into the biological processes and mediators after resection, however, there still remains a gap in the knowledge of more comprehensive mechanisms that drive the adaptive responses in these patients. Recent data support the microbiota as a key mediator of gut homeostasis and a potential driver of metabolism and immunomodulation after intestinal loss. In this review, we summarize the emerging ideas related to host-microbiota interactions in the intestinal adaptation processes.

Human intestinal organoids (HIOs) derived from pluripotent stem cells provide a valuable model for investigating human intestinal organogenesis and physiology, but they lack the immune components required to fully recapitulate the complexity of human intestinal biology and diseases. To address this issue and to begin to decipher human intestinal–immune crosstalk during development, we generated HIOs containing immune cells by transplanting HIOs under the kidney capsule of mice with a humanized immune system. We found that human immune cells temporally migrate to the mucosa and form cellular aggregates that resemble human intestinal lymphoid follicles. Moreover, after microbial exposure, epithelial microfold cells are increased in number, leading to immune cell activation determined by the secretion of IgA antibodies in the HIO lumen. This in vivo HIO system with human immune cells provides a framework for future studies on infection- or allergen-driven intestinal diseases.

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Objective To understand the nutritional intake and growth outcomes of very low birth weight infants with surgical necrotizing enterocolitis (NEC). Study design In a retrospective cohort study, linear mixed models were used to compare growth outcomes from birth to 24 months corrected age for very low birth weight (VLBW) infants with surgical NEC to those with spontaneous intestinal perforation (SIP). Kaplan-Meier curves were developed to demonstrate the duration of parenteral nutrition (PN) use. Result Height differed by surgical NEC and SIP over time (interaction p = 0.03). Surviving infants with surgical NEC had lower head circumference z-scores at 24 months. Of infants surviving surgical NEC, 71% received PN for >60 days after diagnosis. Conclusion The majority of infants with surgical NEC have a delay in achieving enteral autonomy. There was a difference in linear catch-up growth over time between infants with SIP and surgical NEC at 24 months.