Journal of Neonatal Biology

Abstract

Immunohistochemical Demonstration of Blood Group Antigen Expression in Intestinal Endothelium Links Blood Type and Necrotizing Enterocolitis

Charissa L Manuat, Sherri J Yong, Phillip J DeChristopher, Christina A Kwong, Loretto A Glynn, Omar Habeeb, Tricia L Thomson and Jonathan K Muraskas

Objectives: To determine the presence of A and B blood group antigens on vascular endothelial cells of intestinal tissue and compare tissue resected for necrotizing enterocolitis (NEC) with tissues resected for non-NEC pathologies (spontaneous intestinal perforation (SIP), intussusception, Hirschsprung disease, intestinal atresia, etc.) in an effort to implicate blood group antigen expression on bowel endothelium as a mechanism of bowel injury in NEC via a humoral immune-mediated inflammatory response.
Methods :Intestinal tissue from 21 patients with NEC and 23 non-NEC patients (5 of which were SIP) was stained with monoclonal antibodies against blood group antigens A and B. Vascular endothelial lined spaces were examined for expression of these blood group antigens and graded as 0 (no staining) to 3 (marked staining).
Results: Control group birth gestational age (GA) ranged from 26 to 40 weeks (Mdn=36.4-37.0). Both NEC and SIP groups had birth GA ranging from 24 to 37 weeks (Mdn=29.3 and Mdn=27.6, respectively). Overall, A and B blood group antigens were appropriately expressed on the endothelium of all intestinal tissue regardless of the presence of NEC. The A antigen appeared to stain more intensely than the B antigen in most tissue, except for the NEC sample from an AB blood type patient in which A and B antigens stained equally intense (grade 3). Multivariate regression analysis confirms the significantly inverse relationship between gestational age and NEC, but a significant relationship could not be established between blood group or IHC scoring of the blood group antigen expression and NEC. 1.4 Conclusions: Blood group antigens, A more than B or AB together, may increase the risk of a neonate to develop NEC in the presence of passively or actively transferred isoagglutinins.