RESUMO
Few studies have focused on the risk factors for necrotizing enterocolitis (NEC) in small for gestational age (SGA) infants. The aim of this study was to identify the risk factors for NEC in SGA newborns. This study included consecutive SGA neonates admitted to a tertiary hospital in Jiangxi Province, China from Jan 2008 to Dec 2022. Patients with NEC (Bell's stage ≥ II) were assigned to the NEC group. Gestational age- and birth weight-matched non-NEC infants born during the same period at the same hospital were assigned to the control group. The risk factors associated with NEC were analyzed with univariate and logistic regression models. During the study period, 2,912 SGA infants were enrolled, 150 (5.15%) of whom developed NEC. In total, 143 patients and 143 controls were included in the NEC and control groups, respectively. Logistic regression analysis revealed that sepsis (OR 2.399, 95% CI 1.271-4.527, P = 0.007) and anemia (OR 2.214, 95% CI 1.166-4.204, P = 0.015) might increase the incidence of NEC in SGA infants and that prophylactic administration of probiotics (OR 0.492, 95% CI 0.303-0.799, P = 0.004) was a protective factor against NEC. Therefore, sepsis, anemia and a lack of probiotic use are independent risk factors for NEC in SGA infants.
Assuntos
Enterocolite Necrosante , Recém-Nascido Pequeno para a Idade Gestacional , Humanos , Enterocolite Necrosante/epidemiologia , Enterocolite Necrosante/etiologia , Fatores de Risco , Recém-Nascido , Masculino , Feminino , Estudos de Casos e Controles , China/epidemiologia , Idade Gestacional , Sepse/epidemiologia , Sepse/etiologia , Modelos Logísticos , Incidência , Probióticos/administração & dosagem , Anemia/epidemiologiaRESUMO
BACKGROUND: Necrotizing enterocolitis (NEC) is a severe gastrointestinal inflammatory disease in neonates. Fucosyltransferase 2 (Fut2) regulates intestinal epithelial cell fucosylation. In this study, we aimed to investigate butyrate-mediated upregulation of Fut2 expression and the underlying mechanisms. METHODS: In vivo and in vitro models were established. SP600125 was used to inhibit the MEK4-JNK pathway, and anisomycin was used to activate the MEK4-JNK pathway. Fut2, occludin, and ZO-1 expressions were assessed. Furthermore, intestinal permeability was analyzed by FITC-Dextran. The expression of proteins in the MEK-4-JNK pathway was examined by western blotting. RESULTS: In vivo, the addition of exogenous butyrate notably upregulated Fut2, occludin, and ZO-1 expressions and reduced intestinal permeability in mice with NEC. Butyrate may increase the phosphorylation of MEK4, JNK, and c-jun, which are key components of the MEK4-JNK pathway. Additionally, SP600125 inhibited their phosphorylation, which was reversed by anisomycin treatment. In vitro, butyrate substantially increased occludin and ZO-1 expressions. Butyrate considerably increased Fut2 expression and markedly upregulated p-MEK4, p-JNK, and p-c-jun expressions. SP600125 administration decreased their expressions, while anisomycin administration increased their expressions. CONCLUSION: Butyrate upregulated Fut2 expression via activation of the MEK4-JNK pathway, improved intestinal barrier integrity, and protected neonatal mice from NEC. IMPACT: We found that exogenous butyrate could improve intestinal barrier integrity and protect against NEC in neonatal mice. Our data showed that exogenous butyrate supplementation upregulated Fut2 expression by activating the MEK4-JNK pathway. Our study provides novel insights into the pathogenesis of NEC, thereby laying an experimental foundation for future clinical research on the use of butyrate in NEC treatment.
RESUMO
Objective:To explore the effect of prenatal glucocorticoids therapy on hearing screening in premature infants Methods:Data of 693 preterm infants with gestational age of 24-34î+6weeks admitted to theJiangxi Maternal and Child Health Hospital within 24 h after birth from June 2022 to June 2023 were retrospectively analyzed. The infants were divided into the DXM group ï¼544 casesï¼ and the non-DXM group ï¼149 casesï¼ based on whether dexamethasone ï¼DXMï¼ was administered prenatally. General data of preterm infants and parturients in two groups were compared, and the effects of different doses and timing of DXM on hearing screening were analyzed. Results:In the terms of preliminary hearing screening. the pass rate of initial hearing screening in DXM group was significantly higher than that in non-DXM groupï¼53.9% vs 35.6%ï¼, with statistical significanceï¼P<0.05ï¼. Further subgroup analysis showed that the passing rate of preliminary hearing screening in adequate prenatal doseï¼=4 dosesï¼ DXM groupï¼58.1%ï¼ was significantly higher than that in insufficient groupï¼48.0%ï¼ and excessive groupï¼42.4%ï¼, with statistical significanceï¼P<0.05ï¼. Administering DXM 48 hours to 7 days before birth resulted in a higher pass rate for initial hearing screening compared to administration <48 hours or >7 days before birth ï¼56.4% vs. 48.6%ï¼, with a statistically significant difference ï¼P < 0.05ï¼. In terms of re-hearing screening, the pass rate of secondary hearing screening was not significantly correlated with DXM treatmentï¼P>0.05ï¼, but was significantly correlated with gestational age, birth weight, hospital stays, invasive mechanical ventilation, and common neonatal diseasesï¼bronchopulmonary dysplasia, respiratory distress syndromeï¼ï¼P<0.05ï¼. Among them, bronchopulmonary dysplasia was an independent risk factor forsecondary hearing screening referralï¼P<0.05ï¼. Conclusion:A single course of adequate dexamethasone use within 48 h-7 d of prenatal has a positive effect on the preliminary hearing screening of preterm infants.
Assuntos
Dexametasona , Glucocorticoides , Testes Auditivos , Recém-Nascido Prematuro , Humanos , Feminino , Glucocorticoides/administração & dosagem , Glucocorticoides/efeitos adversos , Glucocorticoides/uso terapêutico , Recém-Nascido , Dexametasona/administração & dosagem , Dexametasona/uso terapêutico , Estudos Retrospectivos , Gravidez , Masculino , Idade Gestacional , Triagem Neonatal/métodos , Cuidado Pré-Natal/métodosRESUMO
BACKGROUND: Imbalanced intestinal microbiota and damage to the intestinal barrier contribute to the development of necrotizing enterocolitis (NEC). Autoinducer-2 (AI-2) plays a crucial role in repairing intestinal damage and reducing inflammation. OBJECTIVE: This study aimed to investigate the impact of AI-2 on the expression of intestinal zonula occludens-1 (ZO-1) and occludin proteins in NEC. We evaluated its effects in vivo using NEC mice and in vitro using lipopolysaccharide (LPS)-stimulated intestinal cells. METHODS: Pathological changes in the intestines of neonatal mice were assessed using histological staining and scoring. Cell proliferation was measured using the cell counting kit-8 (CCK-8) assay to determine the optimal conditions for LPS and AI-2 interventions. Real-time quantitative polymerase chain reaction (RT-qPCR) was used to analyze the mRNA levels of matrix metalloproteinase-3 (MMP3), protease activated receptor-2 (PAR2), interleukin-1ß (IL-1ß), and IL-6. Protein levels of MMP3, PAR2, ZO-1, and occludin were evaluated using western blot, immunohistochemistry, or immunofluorescence. RESULTS: AI-2 alleviated NEC-induced intestinal damage (P < 0.05) and enhanced the proliferation of damaged IEC-6 cells (P < 0.05). AI-2 intervention reduced the mRNA and protein expressions of MMP3 and PAR2 in intestinal tissue and cells (P < 0.05). Additionally, it increased the protein levels of ZO-1 and occludin (P < 0.05), while reducing IL-1ß and IL-6 mRNA expression (P < 0.05). CONCLUSION: AI-2 intervention enhances the expression of tight junction proteins (ZO-1 and occludin), mitigates intestinal damage in NEC neonatal mice and IEC-6 cells, potentially by modulating PAR2 and MMP3 signaling. AI-2 holds promise as a protective intervention for NEC. AI-2 plays a crucial role in repairing intestinal damage and reducing inflammation.
Assuntos
Enterocolite Necrosante , Metaloproteinase 3 da Matriz , Receptor PAR-2 , Transdução de Sinais , Animais , Humanos , Camundongos , Animais Recém-Nascidos , Linhagem Celular , Proliferação de Células/efeitos dos fármacos , Modelos Animais de Doenças , Enterocolite Necrosante/patologia , Enterocolite Necrosante/tratamento farmacológico , Enterocolite Necrosante/metabolismo , Homosserina/análogos & derivados , Homosserina/farmacologia , Mucosa Intestinal/patologia , Mucosa Intestinal/efeitos dos fármacos , Mucosa Intestinal/metabolismo , Mucosa Intestinal/imunologia , Intestinos/patologia , Intestinos/efeitos dos fármacos , Lactonas/farmacologia , Lipopolissacarídeos , Metaloproteinase 3 da Matriz/metabolismo , Metaloproteinase 3 da Matriz/genética , Camundongos Endogâmicos C57BL , Ocludina/metabolismo , Ocludina/genética , Receptor PAR-2/metabolismo , Receptor PAR-2/genética , Transdução de Sinais/efeitos dos fármacos , Proteína da Zônula de Oclusão-1/metabolismo , Proteína da Zônula de Oclusão-1/genéticaRESUMO
BACKGROUND: We explored the effects of two formulas, extensively hydrolyzed formula (EHF) and amino acid-based formula (AAF), on the gut microbiota and short-chain fatty acids (SCFAs) in infants with food protein-induced enterocolitis syndrome (FPIES). METHODS: Fecal samples of thirty infants with bloody diarrhea receiving EHF or AAF feeding were collected at enrollment, diagnosis of FPIES, and four weeks after diagnosis. The gut microbiota and SCFAs were analyzed using 16 S rRNA gene sequencing and gas chromatography-mass spectrometry, respectively. RESULTS: Microbial diversity of FPIES infants was significantly different from that of the controls. FPIES infants had a significantly lower abundance of Bifidobacterium and a higher level of hexanoic acid compared with controls. In EHF-fed FPIES infants, microbial richness was significantly decreased over time; while the microbial diversity and richness in AAF-fed FPIES infants exhibited no differences at the three time points. By four weeks after diagnosis, EHF-fed FPIES infants contained a decreased abundance of Acinetobacter, whereas AAF-fed FPIES infants contained an increased abundance of Escherichia-Shigella. EHF-fed infants experienced significantly decreased levels of butyric acid and hexanoic acid at four weeks after diagnosis. CONCLUSIONS: Infants with FPIES had intestinal dysbiosis and different formulas differentially affected gut microbiota and SCFAs in FPIES infants. IMPACT: We firstly report the impacts of two different nutritional milk formulas on the gut microbial composition and SCFAs levels in infants with FPIES. We show that infants with FPIES have obvious intestinal dysbiosis and different formulas differentially affect gut microbiota and SCFAs in FPIES infants. Understanding the effects of different types of formulas on gut microbial colonization and composition, as well as the related metabolites in infants with FPIES could help provide valuable insights for making choices about feeding practices.