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Objective: Antibiotic therapy is a major risk factor for the development of diarrhea and colitis with varying severity. Often the origin of antibiotic-associated gastrointestinal deterioration remains elusive and no specific infectious agents could be discerned.
Patients: We represent three cases of intractable high-volume diarrhea associated with combined antibiotic and steroid therapy in critically ill patients not fitting into established disease entities. Cases presented with severe apoptotic enterocolitis resembling acute intestinal graft-versus-host-disease. Microbiologic workup precluded known enteropathogens, but microbiota analysis revealed a severely depleted gut microbiota with concomitant opportunistic pathogen overgrowth.
Interventions: Fecal microbiota transplantation, performed in one patient, was associated with correction of dysbiosis, rapid clinical improvement, and healing of enterocolitis.
Conclusions: Our series represents a severe form of antibiotic-associated colitis in critically ill patients signified by microbiota depletion, and reestablishment of a physiologic gastrointestinal microbiota might be beneficial for this condition.
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http://dx.doi.org/10.1097/CCM.0000000000002310 | DOI Listing |
Sci Rep
July 2025
Department of Pediatrics, Seoul National University College of Medicine, Jongno-gu, Seoul, 03080, Republic of Korea.
The aim of this study was to determine whether there is a difference in the degree of apoptosis and the pathways leading to necrotizing enterocolitis (NEC) between preterm and full-term rat pups. To achieve this goal, we investigated the pathogenesis of NEC. premature Sprague‒Dawley (SD) rat pups delivered by cesarean section at a gestational age of 21 days (preterm group), as well as full-term SD rat pups four days after birth (full-term group).
View Article and Find Full Text PDFPediatr Res
May 2025
Division of General Pediatric Surgery and Department of Surgery, Johns Hopkins University and Johns Hopkins Children's Center, Baltimore, MD, USA.
Background: Necrotizing enterocolitis (NEC) is mediated by toll-like receptor 4 (TLR4)-induced inflammation and is preceded by reduced intestinal motility. Human milk oligosaccharides (HMOs) are non-digestible components of breast milk that prevent NEC in preclinical models. We now hypothesize that HMOs can reduce the risk of NEC through restoration of intestinal motility and reduced TLR4-mediated inflammation.
View Article and Find Full Text PDFStem Cell Res Ther
February 2025
Department of Health Sciences and Technology, SAIHST, Sungkyunkwan University, Seoul, 06355, Republic of Korea.
Background: Necrotizing enterocolitis (NEC) is a critical gastrointestinal disease in preterm infants, for which no specific treatment is established. We previously demonstrated that thrombin-preconditioned mesenchymal stromal cell-derived extracellular vesicles (thMSC-EVs) enhance protection against other neonatal tissue injuries. Therefore, this study aimed to evaluate the therapeutic potential of thMSC-EVs in modified in vitro, in vivo, and organoid models of NEC.
View Article and Find Full Text PDFFood Funct
May 2025
Department of Neonatology, Dongguan Children's Hospital Affiliated to Guangdong Medical University, No. 68, Xi Hu Third Road, Shilong Town, Dongguan, Guangdong, China.
: Necrotizing enterocolitis (NEC) is a disease with prevalent and serious intestinal inflammation that poses a significant threat to the lives of newborns. Human milk has been shown to prevent and treat the occurrence of NEC; however, the underlying mechanisms remain unclear. MAMP-1 is a significantly overexpressed endogenous peptide derived from β-casein extracted from the human milk of premature mothers, which is resistant to gastrointestinal conditions and exhibits favorable physicochemical properties.
View Article and Find Full Text PDFCurr Mol Med
January 2025
Department of Neonatology, Shenzhen People's Hospital (The Second Clinical Medical College, Jinan University; The First Affiliated Hospital, Southern University of Science and Technology), Shenzhen 518020, Guangdong, China.
Objective: This study aimed to investigate the roles of Mucin 1 (MUC1), the PI3K/AKT pathway, and enterocyte apoptosis in Necrotizing Enterocolitis (NEC).
Methods: Using an NEC Caco-2 cell model, retinoic acid treatment and MUC1 gene silencing were employed. Flow cytometry was used to assess apoptosis, while quantitative PCR and western blot analyses were conducted to evaluate the gene and protein expressions of MUC1, PI3K, Akt, and factors related to apoptotic modulation.