Higher MASP-2 levels may favor complement-mediated inflammation and could thereby predispose to necrotizing enterocolitis (NEC). Determination of MASP-2 with the Hycult Biotech MASP-2 ELISA (Cat. # HK326) may help to identify infants at increased risk of NEC.

NEC is a major cause of morbidity and mortality in premature infants. Unfortunately, the exact pathophysiological mechanisms underlying NEC remain unidentified and identification of infants at risk for NEC is a challenge.

The lectin pathway of the complement system may be involved in NEC pathogenesis by generation of potentially harmful inflammatory mediators. Mannose-binding lectin-associated serine protease-2 (MASP-2) represents the common pathway for both mannose binding lectin (MBL) and ficolins.

Schlapbach and co-workers investigated the correlation between cord blood concentrations of MBL and MASP-2 and later development of NEC. Higher cord blood MASP-2 (but not MBL) levels were significantly associated with an increased risk of NEC in multivariate analysis when compared to controls.
MASP-2 cord blood concentrations were extremely low in most neonates compared to values reported from adults and children. MASP-2 deficiency, resulting in extremely low MASP-2 concentrations, suggests that the lectin pathway of complement activation is often not fully functional at birth. This may represent a protective mechanism against excessive proinflammatory stimuli during the neonatal period.

Available reagents for MASP-2 related research:

Click here for more information on Complement, Collectins

Reference:

1. Schlapbach, L et al; Higher cord blood levels of mannose-binding lectin-associated serine protease-2 in infants with necrotising enterocolitis. Pediatr Res 2008, Epub ahead of print.