Influence of Gestational Age, Cesarean Section, and Type of Feeding on Fecal Human β‐Defensin 2 and Tumor Necrosis Factor‐α

Abstract

: Low fecal HBD-2 may be a risk factor in preterm infants to develop neonatal enteric disease, such as necrotizing enterocolitis.

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

“…Moreover, in our study, these reports also demonstrated positive correlation of amniotic hBD2 levels with premature rupture of membranes and microbial invasion of the amniotic cavity (25,26). During the first 2 wk of life, fecal hBD2 concentrations dropped, reaching a nadir at ~2 wk and slowly increasing from there on showing a similar postnatal dynamic as in two previous smaller studies (9,27). Concentrations of fecal hBD1 were similarly high in meconium and dropped afterwards to a very low baseline in all patients, which is consistent with several studies demonstrating the developmental regulation of hBD1 with almost no expression before 24 wk of gestational age (28,29).…”

“…Mortality rate of severe NEC was 66% (n = 4) with no further deaths in the remaining patients. A total of 732 fecal samples were available (mean 11 per individual, range [5][6][7][8][9][10][11][12][13][14].…”

“…Fecal calprotectin (Immundiagnostik, Bennsheim, Germany), hBD2 (Immundiagnostik), and hBD1 (Alpha Diagnostic, San Antonio, TX) concentrations were determined by enzyme-linked immunosorbent assays as described earlier (9,33). Extraction of antimicrobial peptides from stool samples was performed according to the manufacturer's recommendations.…”

“…Under physiological conditions, hBD1 is expressed constitutively by intestinal epithelial cells, whereas hBD2 expression was found to be induced during infection and inflammation. hBD2 exhibits potent bactericidal activity against Gram-negative bacteria and eukaryotic pathogens, such as Candida strains (8), and reduced expression has been observed previously in preterm infants as compared with full-term babies (9); the expression of hBD2 is partly dependent on Toll-like receptor 4 (TLR4) (10), which is mainly stimulated by lipopolysaccharide (LPS), the glycolipid component of the outer membrane of Gramnegative bacteria. For correct function of TLR4, in vivo binding of MD2, a 20-30-kD glycoprotein secreted by endothelial and epithelial cells to its extracellular domain, is essential (11).…”

Fecal Calprotectin Concentrations in Premature Infants Have a Lower Limit and Show Postnatal and Gestational Age Dependence

“…Together with the observation of unusually low fCP concentrations in fulminant NEC, this might indicate an impaired recruitment of granulocytes in the gastrointestinal lumen which could make these infants at risk for aberrant postnatal microbial colonization and subsequent NEC. Whereas several studies have already demonstrated a generally impaired immune response in VLBW infants [22,23,24], this idea is also supported by a recent study specifically demonstrating low fecal concentrations of the antimicrobial peptide hBD2 in premature infants [25] which also functions as a chemotactic factor for human neutrophils [26]. …”