Human β-defensin 2 expression in ELBW infants with severe necrotizing enterocolitis

Jenke, Andreas; Zilbauer, Matthias; Postberg, Jan; Wirth, Stéfan

doi:10.1038/pr.2012.110

Cited by 43 publications

(55 citation statements)

References 33 publications

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“…In addition to the primarily recognized antimicrobial activities, hBD3 also functions as immune modulators linking innate and adaptive immunity (4,5). Analysis of intestinal resections obtained from infants with severe NEC revealed that low defensin mRNA and protein expression (6). Armogida et al (7) reported that the presence of mediators of the innate immune system in human milk, including hBD3 provided protection for the developing digestive tract of newborns.…”

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confidence: 99%

Human β-defensin-3 promotes intestinal epithelial cell migration and reduces the development of necrotizing enterocolitis in a neonatal rat model

Sheng

Cai

et al. 2014

Pediatr Res

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Background:The aim of this study was to investigate the effects of human β-defensin-3 (hBD3) on intestinal wound healing and in a neonatal rat model of necrotizing enterocolitis (NEC). Methods: Enterocyte migration and proliferation were detected in vitro and in vivo. The role of chemokine receptor CCR6 and its downstream signaling pathway was assessed. Newborn Sprague-Dawley rats were randomly divided into four groups: Control+NS, Control+hBD3, NEC+NS, and NEC+hBD3. Body weight, histological score, survival time, cytokines expression, and mucosal integrity were evaluated. results: hBD3 could stimulate enterocyte migration, but not proliferation, both in cultured enterocytes and in the NEC model. Neutralizing antibody and small interfering RNA confirmed this stimulatory effect was mediated by CCR6. Furthermore, hBD3 induced Rho activation, myosin light chain 2 phosphorylation, and F-actin accumulation. The bactericidal activity of hBD3 was maintained throughout a broad pH range. Strikingly, hBD3 administration decreased the incidence of NEC, increased the survival rate, and reduced the severity of NEC. Moreover, hBD3 reduced the proinflammatory cytokines expression in ileum and serum and preserved the intestinal barrier integrity. conclusion: This study provided evidence that the antimicrobial peptide hBD3 might participate in intestinal wound healing by promoting enterocyte migration and show beneficial effects on newborn rats with NEC.

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mentioning

confidence: 99%

Human β-defensin-3 promotes intestinal epithelial cell migration and reduces the development of necrotizing enterocolitis in a neonatal rat model

Sheng

Cai

et al. 2014

Pediatr Res

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“…This points to the immaturity of the gastrointestinal tract of preterms, including the intestinal barrier function and innate immune defense (2)(3)(4)(5). Accordingly, intestinal distress was diagnosed predominantly during the first and second week after birth (Table 1) in contrast to NEC, which was usually diagnosed during the second and third week of life.…”

Section: Discussionmentioning

confidence: 91%

Fecal S100A12

Däbritz

Foell

Wirth

et al. 2013

J. pediatr. gastroenterol. nutr.

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“…An increased DEFB-CN has been associated with psoriasis [25], [27] and chronic obstructive pulmonary disease [28]. Conversely, a reduced DEFB-CN is associated with susceptibility to celiac disease [29], chronic pancreatitis [30] and necrotizing enterocolitis [31], possibly as a result of an expected overall deficit in beta-defensin production. There are conflicting reports on the association of DEFB-CN with Crohn's disease [32], with data supporting either lower [33] or higher [34] DEFB-CN.…”

Section: Introductionmentioning

confidence: 99%

Copy Number Variation of the Beta Defensin Gene Cluster on Chromosome 8p Influences the Bacterial Microbiota within the Nasopharynx of Otitis-Prone Children

et al. 2014

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As there is increasing evidence that aberrant defensin expression is related to susceptibility for infectious disease and inflammatory disorders, we sought to determine if copy number of the beta-defensin gene cluster located on chromosome 8p23.1 (DEFB107, 106, 105, 104, 103, DEFB4 and SPAG11), that shows copy number variation as a block, was associated with susceptibility to otitis media (OM). The gene DEFB103 within this complex encodes human beta defensin-3 (hBD-3), an antimicrobial peptide (AP) expressed by epithelial cells that line the mammalian airway, important for defense of mucosal surfaces and previously shown to have bactericidal activity in vitro against multiple human pathogens, including the three that predominate in OM. To this end, we conducted a retrospective case-control study of 113 OM prone children and 267 controls aged five to sixty months. We identified the copy number of the above defined beta-defensin gene cluster (DEFB-CN) in each study subject by paralogue ratio assays. The mean DEFB-CN was indistinguishable between subjects classified as OM prone based on a recent history of multiple episodes of OM and control subjects who had no history of OM (4.4±0.96 versus 4.4±1.08, respectively: Odds Ratio [OR]: 1.16 (95% CI: 0.61, 2.20). Despite a lack of direct association, we observed a statistically significant correlation between DEFB-CN and nasopharyngeal bacterial colonization patterns. Collectively, our findings suggested that susceptibility to OM might be mediated by genetic variation among individuals, wherein a DEFB-CN less than 4 exerts a marked influence on the microbiota of the nasopharynx, specifically with regard to colonization by the three predominant bacterial pathogens of OM.

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Human β-defensin 2 expression in ELBW infants with severe necrotizing enterocolitis

Cited by 43 publications

References 33 publications

Human β-defensin-3 promotes intestinal epithelial cell migration and reduces the development of necrotizing enterocolitis in a neonatal rat model

Human β-defensin-3 promotes intestinal epithelial cell migration and reduces the development of necrotizing enterocolitis in a neonatal rat model

Fecal S100A12

Copy Number Variation of the Beta Defensin Gene Cluster on Chromosome 8p Influences the Bacterial Microbiota within the Nasopharynx of Otitis-Prone Children

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